Insulin resistance and gut health -
Diabetologia — Zhao L, Chen Y, Xia F, Abudukerimu B, Zhang W, Guo Y, et al. A glucagon-like peptide-1 receptor agonist lowers weight by modulating the structure of gut microbiota. Front Endocrinol. Forslund K, Hildebrand F, Nielsen T, Falony G, Le Chatelier E, Sunagawa S, et al. Disentangling type 2 diabetes and metformin treatment signatures in the human gut microbiota.
Rodriguez J, Hiel S, Delzenne NM. Metformin: old friend, new ways of action-implication of the gut microbiome? Curr Opin Clin Nutr Metab Care — de la Cuesta-Zuluaga J, Mueller NT, Corrales-Agudelo V, Velásquez-Mejía EP, Carmona JA, Abad JM, et al.
Metformin is associated with higher relative abundance of mucin-degrading akkermansia muciniphila and several short-chain fatty acid-producing microbiota in the gut.
Wu H, Esteve E, Tremaroli V, Khan MT, Caesar R, Mannerås-Holm L, et al. Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug.
Nat Med. Drucker DJ. Mechanisms of action and therapeutic application of glucagon-like peptide Cell Metab. Nauck MA, Meier JJ. Incretin hormones: their role in health and disease. Diabetes Obes Metab. Faerch K, Torekov SS, Vistisen D, Johansen NB, Witte DR, Jonsson A, et al.
GLP-1 response to oral glucose is reduced in prediabetes, screen-detected type 2 diabetes, and obesity and influenced by sex: the ADDITION-PRO study. Diabetes — Larsen MP, Torekov SS. Glucagon-like peptide 1: a predictor of type 2 diabetes?
J Diabetes Res. Deacon CF. Peptide degradation and the role of DPP-4 inhibitors in the treatment of type 2 diabetes. Peptides —7. Piche T, des Varannes SB, Sacher-Huvelin S, Holst JJ, Cuber JC, Galmiche JP.
Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease.
Gastroenterology — Cani PD, Dewever C, Delzenne NM. Inulin-type fructans modulate gastrointestinal peptides involved in appetite regulation glucagon-like peptide-1 and ghrelin in rats. Br J Nutr. Cani PD, Knauf C, Iglesias MA, Drucker DJ, Delzenne NM, Burcelin R.
Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon-like peptide 1 receptor. Cani PD, Hoste S, Guiot Y, Delzenne NM. Dietary non-digestible carbohydrates promote L-cell differentiation in the proximal colon of rats.
Pichette J, Fynn-Sackey N, Gagnon J. Hydrogen sulfide and sulfate prebiotic stimulates the secretion of GLP-1 and improves glycemia in male mice. Endocrinology — Bala V, Rajagopal S, Kumar DP, Nalli AD, Mahavadi S, Sanyal AJ, et al.
Front Physiol. Chimerel C, Emery E, Summers DK, Keyser U, Gribble FM, Reimann F. Bacterial metabolite indole modulates incretin secretion from intestinal enteroendocrine L cells.
Cell Rep. Yang M, Fukui H, Eda H, Kitayama Y, Hara K, Kodani M, et al. Mol Med Rep. Grasset E, Puel A, Charpentier J, Collet X, Christensen JE, Tercé F, et al. A specific gut microbiota dysbiosis of type 2 diabetic mice induces GLP-1 resistance through an enteric NO-dependent and gut-brain axis mechanism.
Li X, Zhao J, Zhang H, Chen W. Lactobacillus casei CCFM attenuates type 2 diabetes via a gut microbiota dependent mechanism.
Food Funct. CrossRef Full Text Google Scholar. Bjerg AT, Kristensen M, Ritz C, Holst JJ, Rasmussen C, Leser TD, et al. Lactobacillus paracasei subsp paracasei L. casei W8 suppresses energy intake acutely. Appetite —8. Simon MC, Strassburger K, Nowotny B, Kolb H, Nowotny P, Burkart V, et al.
Intake of Lactobacillus reuteri improves incretin and insulin secretion in glucose-tolerant humans: a proof of concept. Ryan PM, Patterson E, Kent RM, Stack H, O'Connor PM, Murphy K, et al. Recombinant incretin-secreting microbe improves metabolic dysfunction in high-fat diet fed rodents.
Sci Rep. Macfarlane GT, Macfarlane S. Bacteria, colonic fermentation, and gastrointestinal health. J AOAC Int. Cummings JH, Pomare EW, Branch WJ, Naylor CP, Macfarlane GT.
Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut —7. Wolever TM, Josse RG, Leiter LA, Chiasson JL.
Time of day and glucose tolerance status affect serum short-chain fatty acid concentrations in humans. Metabolism — Wolever TM, Spadafora P, Eshuis H. Interaction between colonic acetate and propionate in humans.
Am J Clin Nutr. Kaiko GE, Ryu SH, Koues OI, Collins PL, Solnica-Krezel L, Pearce EJ, et al. The colonic crypt protects stem cells from microbiota-derived metabolites.
Cell Lupton JR. Microbial degradation products influence colon cancer risk: the butyrate controversy. J Nutr. Puddu A, Sanguineti R, Montecucco F, Viviani GL.
Evidence for the gut microbiota short-chain fatty acids as key pathophysiological molecules improving diabetes. Mediators Inflamm. Reichardt N, Duncan SH, Young P, Belenguer A, McWilliam Leitch C, Scott KP, et al.
Phylogenetic distribution of three pathways for propionate production within the human gut microbiota. ISME J. Zhao L, Zhang F, Ding X, Wu G, Lam YY, Wang X, et al.
Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes. Science —6. De Vadder F, Kovatcheva-Datchary P, Goncalves D, Vinera J, Zitoun C, Duchampt A, et al.
Microbiota-generated metabolites promote metabolic benefits via gut-brain neural circuits. Mithieux G, Gautier-Stein A. Intestinal glucose metabolism revisited. De Vadder F, Kovatcheva-Datchary P, Zitoun C, Duchampt A, Bäckhed F, Mithieux G. Microbiota-produced succinate improves glucose homeostasis via intestinal gluconeogenesis.
Mithieux G. Gut microbiota and host metabolism: what relationship. Neuroendocrinology —6. Wang S, Li Q, Zang Y, Zhao Y, Liu N, Wang Y, et al.
Apple polysaccharide inhibits microbial dysbiosis and chronic inflammation and modulates gut permeability in HFD-fed rats. Int J Biol Macromol. Han M, Song P, Huang C, Rezaei A, Farrar S, Brown MA, et al.
Dietary grape seed proanthocyanidins GSPs improve weaned intestinal microbiota and mucosal barrier using a piglet model.
Oncotarget — Xu YH, Gao CL, Guo HL, Zhang WQ, Huang W, Tang SS, et al. J Endocrinol. Le Poul E, Loison C, Struyf S, Springael JY, Lannoy V, Decobecq ME, et al. Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation. J Biol Chem.
Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F. From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites. Kimura I, Ozawa K, Inoue D, Imamura T, Kimura K, Maeda T, et al.
The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR Nat Commun. Bjursell M, Admyre T, Göransson M, Marley AE, Smith DM, Oscarsson J, et al.
Improved glucose control and reduced body fat mass in free fatty acid receptor 2-deficient mice fed a high-fat diet. Am J Physiol Endocrinol Metab. Ang Z, Ding JL. GPR41 and GPR43 in obesity and inflammation - protective or causative? Front Immunol. Tolhurst G, Heffron H, Lam YS, Parker HE, Habib AM, Diakogiannaki E, et al.
Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Psichas A, Sleeth ML, Murphy KG, Brooks L, Bewick GA, Hanyaloglu AC, et al. The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents.
Yadav H, Lee JH, Lloyd J, Walter P, Rane SG. Beneficial metabolic effects of a probiotic via butyrate-induced GLP-1 hormone secretion. Priyadarshini M, Wicksteed B, Schiltz GE, Gilchrist A, Layden BT.
SCFA receptors in pancreatic beta cells: novel diabetes targets? Trends Endocrinol Metab. McNelis JC, Lee YS, Mayoral R, van der Kant R, Johnson AM, Wollam J, et al. GPR43 potentiates beta-cell function in obesity. Gao Z, Yin J, Zhang J, Ward RE, Martin RJ, Lefevre M, et al. Butyrate improves insulin sensitivity and increases energy expenditure in mice.
Zhang L, Du J, Yano N, Wang H, Zhao YT, Dubielecka PM, et al. Sodium butyrate protects -against high fat diet-induced cardiac dysfunction and metabolic disorders in type II diabetic mice. J Cell Biochem. Dewulf EM, Cani PD, Claus SP, Fuentes S, Puylaert PG, Neyrinck AM, et al. Insight into the prebiotic concept: lessons from an exploratory, double blind intervention study with inulin-type fructans in obese women.
Gut — van der Beek CM, Canfora EE, Kip AM, Gorissen SHM, Olde Damink SWM, van Eijk HM, et al. The prebiotic inulin improves substrate metabolism and promotes short-chain fatty acid production in overweight to obese men. Hylemon PB, Zhou H, Pandak WM, Ren S, Gil G, Dent P.
Bile acids as regulatory molecules. J Lipid Res. Holt JA, Luo G, Billin AN, Bisi J, McNeill YY, Kozarsky KF, et al. Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis. Genes Dev. Di Ciaula A, Garruti G, Lunardi Baccetto R, Molina-Molina E, Bonfrate L, Wang DQ, et al.
Bile acid physiology. Ann Hepatol. Chiang JYL, Ferrell JM. Bile acid metabolism in liver pathobiology. Gene Expr. Li Q, Yin W, Cai M, Liu Y, Hou H, Shen Q, et al. NO suppresses diet-induced insulin resistance and cholesterol accumulation through STAT5-dependent upregulation of IGF1 and CYP7A1.
Ridlon JM, Kang DJ, Hylemon PB. Bile salt biotransformations by human intestinal bacteria. Swann JR, Want EJ, Geier FM, Spagou K, Wilson ID, Sidaway JE, et al. Systemic gut microbial modulation of bile acid metabolism in host tissue compartments.
Labbé A, Ganopolsky JG, Martoni CJ, Prakash S, Jones ML. Bacterial bile metabolising gene abundance in Crohn's, ulcerative colitis and type 2 diabetes metagenomes.
PLoS ONE 9:e Martoni CJ, Labbé A, Ganopolsky JG, Prakash S, Jones ML. Changes in bile acids, FGF and sterol absorption in response to bile salt hydrolase active L. reuteri NCIMB 3 Gut Microbes — Gu Y, Wang X, Li J, Zhang Y, Zhong H, Liu R, et al.
Analyses of gut microbiota and plasma bile acids enable stratification of patients for antidiabetic treatment. Sayin SI, Wahlström A, Felin J, Jäntti S, Marschall HU, Bamberg K, et al. Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR antagonist.
Islam KB, Fukiya S, Hagio M, Fujii N, Ishizuka S, Ooka T, et al. Bile acid is a host factor that regulates the composition of the cecal microbiota in rats.
Zheng X, Huang F, Zhao A, Lei S, Zhang Y, Xie G, et al. Bile acid is a significant host factor shaping the gut microbiome of diet-induced obese mice. BMC Biol. Russell DW. The enzymes, regulation, and genetics of bile acid synthesis. Annu Rev Biochem. Wahlström A, Kovatcheva-Datchary P, Ståhlman M, Bäckhed F, Marschall HU.
Crosstalk between bile acids and gut microbiota and its impact on farnesoid X receptor signalling. Dig Dis. Cariou B, van Harmelen K, Duran-Sandoval D, van Dijk TH, Grefhorst A, Abdelkarim M, et al. The farnesoid X receptor modulates adiposity and peripheral insulin sensitivity in mice.
Parks DJ, Blanchard SG, Bledsoe RK, Chandra G, Consler TG, Kliewer SA, et al. Bile acids: natural ligands for an orphan nuclear receptor. Watanabe M, Horai Y, Houten SM, Morimoto K, Sugizaki T, Arita E, et al. Lowering bile acid pool size with a synthetic farnesoid X receptor FXR agonist induces obesity and diabetes through reduced energy expenditure.
Prawitt J, Abdelkarim M, Stroeve JH, Popescu I, Duez H, Velagapudi VR, et al. Farnesoid X receptor deficiency improves glucose homeostasis in mouse models of obesity.
Zhang Y, Ge X, Heemstra LA, Chen WD, Xu J, Smith JL, et al. Mol Endocrinol. Jiang C, Xie C, Lv Y, Li J, Krausz KW, Shi J, et al. Intestine-selective farnesoid X receptor inhibition improves obesity-related metabolic dysfunction. Shapiro H, Kolodziejczyk AA, Halstuch D, Elinav E.
Bile acids in glucose metabolism in health and disease. J Exp Med. Pathak P, Xie C, Nichols RG, Ferrell JM, Boehme S, Krausz KW, et al. Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism.
Hepatology — Kir S, Beddow SA, Samuel VT, Miller P, Previs SF, Suino-Powell K, et al. FGF19 as a postprandial, insulin-independent activator of hepatic protein and glycogen synthesis.
Science —4. Morton GJ, Matsen ME, Bracy DP, Meek TH, Nguyen HT, Stefanovski D, et al. FGF19 action in the brain induces insulin-independent glucose lowering. J Clin Invest. Benoit B, Meugnier E, Castelli M, Chanon S, Vieille-Marchiset A, Durand C, et al. Fibroblast growth factor 19 regulates skeletal muscle mass and ameliorates muscle wasting in mice.
Liu H, Hu C, Zhang X, Jia W. Role of gut microbiota, bile acids and their cross-talk in the effects of bariatric surgery on obesity and type 2 diabetes.
J Diabetes Investig. Tremaroli V, Karlsson F, Werling M, Ståhlman M, Kovatcheva-Datchary P, Olbers T, et al. Roux-en-Y gastric bypass and vertical banded gastroplasty induce long-term changes on the human gut microbiome contributing to fat mass regulation. In this Special Feature and accompanying podcast, we look at how insulin research is developing a century after the discovery of this crucial hormone.
In this edition of Medical Myths, we focus on diabetes. We discuss natural "cures," physical activity, driving, prediabetes, and more. Researchers said baricitinib, a drug used to treat rheumatoid arthritis, showed promise in a clinical trial in helping slow the progression of type 1…. A new review indicates that insulin—used to manage diabetes—can be kept at room temperature for months without losing its potency.
My podcast changed me Can 'biological race' explain disparities in health? Why Parkinson's research is zooming in on the gut Tools General Health Drugs A-Z Health Hubs Health Tools Find a Doctor BMI Calculators and Charts Blood Pressure Chart: Ranges and Guide Breast Cancer: Self-Examination Guide Sleep Calculator Quizzes RA Myths vs Facts Type 2 Diabetes: Managing Blood Sugar Ankylosing Spondylitis Pain: Fact or Fiction Connect About Medical News Today Who We Are Our Editorial Process Content Integrity Conscious Language Newsletters Sign Up Follow Us.
Medical News Today. Health Conditions Health Products Discover Tools Connect. How gut bacteria could improve insulin resistance and lower diabetes risk.
By Robby Berman — Fact checked by Sarah Myers, PharmD — Updated on September 6, Share on Pinterest Alistipes indistinctus may help protect against type 2 diabetes by improving insulin resistance. How Alistipes bacteria improves insulin resistance. Access to A. indistinctus bacteria is limited.
How bacteria help regulate metabolism. Share this article. Latest news Ovarian tissue freezing may help delay, and even prevent menopause. RSV vaccine errors in babies, pregnant people: Should you be worried?
Impaired aryl hydrocarbon receptor ligand production by the gut microbiota Is a key factor in metabolic syndrome. Cell Metab. Lim SM, Jeong JJ, Woo KH, Han MJ, Kim DH. Lactobacillus sakei OK67 ameliorates high-fat diet—induced blood glucose intolerance and obesity in mice by inhibiting gut microbiota lipopolysaccharide production and inducing colon tight junction protein expression.
Nutr Res. Li X, Wang E, Yin B, Fang D, Chen P, Wang G, et al. Effects of Lactobacillus casei CCFM on insulin resistance and gut microbiota in type 2 diabetic mice.
Balakumar M, Prabhu D, Sathishkumar C, Prabu P, Rokana N, Kumar R, et al. Singh S, Sharma RK, Malhotra S, Pothuraju R, Shandilya UK. Lactobacillus rhamnosus NCDC17 ameliorates type-2 diabetes by improving gut function, oxidative stress and inflammation in high-fat-diet fed and streptozotocin treated rats.
Beneficial Microbes. Niibo M, et al. Probiotic Lactobacillus gasseri SBT improves insulin secretion in a diabetic rat model.
J Dairy Sci. Wanchai K, et al. Probiotic Lactobacillus paracasei HII01 protects rats against obese-insulin resistance induced kidney injury and impaired renal organic anion transporter Oat3 function.
Chunchai T, et al. Decreased microglial activation through gut-brain axis by prebiotics, probiotics, or synbiotics effectively restored cognitive function in obese-insulin resistant rats. J Neuroinflamm.
Morshedi M, et al. Beneficial psychological effects of novel psychobiotics in diabetic rats: the interaction among the gut, blood, and amygdala. J Nutr Biochem. Yao F, et al. Effect of Lactobacillus paracasei N and fructooligosaccharides in nonalcoholic fatty liver disease.
Arch Med Sci. Kikuchi K, Othman MB, Sakamoto K. Sterilized bifidobacteria suppressed fat accumulation and blood glucose level. Bioch Biophys Res Commun. Aoki R, Kamikado K, Suda W, Takii H, Mikami Y, Suganuma N, et al.
A proliferative probiotic Bifidobacterium strain in the gut ameliorates progression of metabolic disorders via microbiota modulation and acetate elevation. Sci Rep. Alard J, Lehrter V, Rhimi M, Mangin I, Peucelle V, Abraham AL, et al.
Beneficial metabolic effects of selected probiotics on diet-induced obesity and insulin resistance in mice are associated with improvement of dysbiotic gut microbiota.
Environ Microbiol. Bagarolli RA, Tobar N, Oliveira AG, Araújo TG, Carvalho BM, Rocha GZ, et al. Probiotics modulate gut microbiota and improve insulin sensitivity in DIO mice. Rajkumar H, Kumar M, Das N, Kumar SN, Challa HR, Nagpal R. Effect of probiotic Lactobacillus salivarius UBL S22 and prebiotic fructo-oligosaccharide on serum lipids, inflammatory markers, insulin sensitivity, and gut bacteria in healthy young volunteers.
J Cardiovasc Pharmacol Ther. Tonucci LB, Santos KMO, Oliveira LL, Ribeiro SMR, Martino HSD. Clinical application of probiotics in type 2 diabetes mellitus: a randomized, double-blind, placebo-controlled study.
Clin Nutr. Hsieh MC, et al. The beneficial effects of Lactobacillus reuteri ADR-1 or ADR-3 consumption on type 2 diabetes mellitus: a randomized, double blinded, placebo-controlled trial. Article PubMed PubMed Central CAS Google Scholar.
Vallianou N, et al. Probiotics, prebiotics, synbiotics, postbiotics, and obesity: current evidence, controversies, and perspectives. Curr Obes Rep. Plovier H, Everard A, Druart C, Depommier C, Hul MV, Geurts L, et al. A purified membrane protein from Akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice.
Zhang Z, Mocanu V, Cai C, Dang J, Slater L, Deehan EC, et al. Impact of fecal microbiota transplantation on obesity and metabolic syndrome—a systematic review. Article CAS PubMed Central Google Scholar. Lin HV, Frassetto A, Kowalik EJJ, Nawrocki AR, Lu MM, Kosinski JR, et al. Butyrate and propionate protect against diet induced obesity and regulate gut hormones via free fatty acid.
Frost G, Sleeth ML, Sahuri-Arisoylu M, Lizarbe B, Cerdan S, Brody L, et al. The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism.
Liu WC, Yang MC, Wu YY, Chen PH, Hsu CM, Chen LW. Lactobacillus plantarum reverse diabetes-induced Fmo3 and ICAM expression in mice through enteric dysbiosis-related c-Jun NH2-terminal kinase pathways. Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, et al.
Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Ley R, et al. Human gut microbes associated with obesity. Duncan SH, Lobley GE, Holtrop G, et al. Human colonic microbiota associated with diet, obesity and weight loss.
Int J Obes. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insulin resistance.
Wang X, Ota N, Manzanillo P, Kates L, Zavala-Solorio J, Eidenschenk C, et al. Interleukin alleviates metabolic disorders and restores mucosal immunity in diabetes. Dao MC, et al. Akkermansia muciniphila and improved metabolic health during a dietary intervention in obesity: relationship with gut microbiome richness and ecology.
Stenman LK, Waget A, Garret C, Briand F, Burcelin R, Sulpice T, et al. Probiotic B and prebiotic polydextrose improve efficacy of antidiabetic drugs in mice. Diabetol Metab Syndr.
Treatment with the dipeptidyl peptidase-4 inhibitor vildagliptin improves fasting islet-cell function in subjects with type 2 diabetes. J Clin Endocrinol Metab. Mannucci E, Tesi F, Bardini G, Ognibene A, Petracca MG, Ciani S, et al.
Effects of metformin on glucagon-like peptide-1 levels in obese patients with and without Type 2 diabetes. Diabetes Nutr Metab. CAS PubMed Google Scholar.
Download references. Departamento de Epidemiologia, Faculdade de Saúde Pública, School of Public Health, University of Sao Paulo, Av. Arnaldo, , São Paulo, SP, CEP , Brazil.
You can also search for this author in PubMed Google Scholar. BIMS and DC participated in conceptualization, methodology, analysis and writing the manuscript. SRGF participated in conceptualization, methodology, validation and supervision of the analysis, review the writing and editing the manuscript.
All authors read and approved the final manuscript. Correspondence to Sandra Roberta G. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.
If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.
Reprints and permissions. Salles, B. Probiotics supplementation and insulin resistance: a systematic review. Diabetol Metab Syndr 12 , 98 Download citation. Received : 01 August Accepted : 20 October Published : 11 November Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search.
Download PDF. Ferreira ORCID: orcid. Methods This systematic review was based on PRISMA guidelines. Results Overall, results from 27 probiotic interventions Lactobacillus , Bifidobacterium , Clostridium and Akkermansia indicated significant beneficial changes in insulin resistance measures in animal studies.
Conclusion Available data regarding the effects of certain probiotics do not guarantee sustained amelioration of insulin resistance in humans. Introduction Growing rates of obesity represent a global lifestyle-related health problem [ 1 ]. Methods This review was performed based on the PRISMA guidelines Preferred Reporting Items for Systematic Reviews and Meta-Analysis.
Search strategy Searches for original research articles offered online, published in English from to January , were conducted in the electronic database of PubMed from the National Library of Medicine. Eligibility criteria Inclusion criteria were all longitudinal controlled studies with probiotics supplementing diet of animal models or humans and an available objective measurement of insulin sensitivity or resistance.
Data handling Two independent reviewers BIMS, DC assessed the titles and abstracts of all retrieved references to identify studies that potentially met eligibility criteria and eligible articles were retrieved in full text.
Flowchart of articles selection for this systematic review based on PRISMA. Full size image. Results Animal studies Main results related to glucose metabolism of 27 animal studies are shown in Table 1 and additional findings are mentioned in the text.
Table 1 Description of the included animal studies Full size table. Table 2 Description of the included clinical trials Full size table. Discussion This systematic review is the first to focus on the role of probiotics in attenuating insulin resistance, involved in prevalent diseases of the contemporary world.
Probiotic, its dose and duration of interventions Most used probiotics in research and clinical settings were species of Lactobacillus whose benefits for health have been demonstrated [ 5 , 44 , 47 ]. Probiotics and insulin resistance in animal studies All animal studies probiotic interventions reviewed had control groups and their results were appropriately compared.
Probiotics and insulin resistance in clinical trials There is mounting evidence pointing out to the role of gut dysbiosis in the pathogenesis of metabolic disorders, such as obesity, type 2 DM, MS and NAFLD [ 47 ].
Probiotics compared to antidiabetic agents Interest of the scientific community has grown regarding the application of probiotics as an adjuvant therapy for insulin resistance syndromes.
Abbreviations DM: Diabetes mellitus FOS: Fructooligosaccharides GLP: Glucagon-like peptide GPX: Glutathione peroxidase GTT: Glucose tolerance test HbA1c: Glycated hemoglobin HFD: High fat diet HOMA-IR: Homeostasis model assessment-Insulin resistance IL: Interleukin ISI: Insulin sensitivity index ITT: Insulin tolerance test IVGTT: Intravenous glucose tolerance test LPS: Lipopolysaccharide MS: Metabolic syndrome NAFLD: Non-alcoholic fatty liver disease NF-κB: Nuclear factor kappa B OGTT: Oral glucose tolerance test QUICKI: Quantitative insulin sensitivity check index SCFA: Short-chain fatty acid SOD: Superoxide dismutase TMAO: Trimethylamine N-oxide TNF-α: Tumor Necrosis Factor XOS: Xylooligosaccharides.
References GBD Obesity Collaborators. Article Google Scholar Bray G, Kim K, Wilding J, Federation WO. Article CAS PubMed Google Scholar International Diabetes Federation. Google Scholar Panwar H, Rashmi HM, Batish VK, Grover S. Article CAS PubMed Google Scholar Tonucci LB, Santos KMO, Ferreira CLLF, Ribeiro SMR, Oliveira LL, Martino HSD.
Article Google Scholar Barz ML, Anhê FF, Varin TV, Desjardins Y, Levy E, Roy D, et al. Article PubMed PubMed Central Google Scholar Lee E, Jung SR, Lee SY, Lee NK, Paik HD, Lim SI.
Article PubMed Central CAS Google Scholar Thiennimitr P, Yasom S, Tunapong W, Chunchai T, Wanchai K, Pongchaidecha A, et al. Article CAS PubMed Google Scholar Hampe CS, Roth CL.
Article CAS PubMed Google Scholar Yan X, Feng B, Li P, Tang Z, Wang L. CAS Google Scholar Kulecka M, et al. Article CAS Google Scholar Arumugam M, Raes J, Pelletier E, Le Paslier D, Yamada T, Mende DR, et al. Article CAS PubMed PubMed Central Google Scholar Wu GD, Chen J, Hoffmann C, Bittinger K, Chen YY, Keilbaugh SA, et al.
Article CAS PubMed PubMed Central Google Scholar Moraes ACF, Silva IT, Almeida-Pititto B, Ferreira SRG. Article Google Scholar Shang H, Sun J, Chen YQ.
Article CAS Google Scholar Wang G, Li X, Zhao J, Zhang H, Chen W. Article CAS PubMed Google Scholar Firouzi S, Majid HA, Ismail A, Kamaruddin NA, Barakatun-Nisak MY. Article PubMed CAS Google Scholar Andersson U, Bränning C, Ahrné S, Molin G, Alenfall J, Onning G, et al.
Article CAS PubMed Google Scholar Kondo S, Xiao JZ, Satoh T, Odamaki T, Takahashi S, Sugahara H, et al. Article CAS PubMed Google Scholar Amar J, Chabo C, Waget A, Klopp P, Vachoux C, Bermúdez-Humarán LG, et al. Article CAS PubMed PubMed Central Google Scholar Natividad JM, Lamas B, Pham HP, Michel ML, Rainteau D, Bridonneau C, et al.
Article CAS Google Scholar Soleimani A, Mojarrad MZ, Bahmani F, Taghizadeh M, Ramezani M, Tajabadi-Ebrahimi M, et al. Article CAS PubMed Google Scholar Depommier C, Everard A, Druart C, Plovier H, Hul MV, Vieira-Silva S, et al.
Article CAS PubMed PubMed Central Google Scholar Tripolt NJ, Leber B, Triebl A, Köfeler H, Stadlbauer V, Sourij H. Article CAS PubMed Google Scholar Zhang Y, Wang L, Zhang J, Li Y, He Q, Li H, et al.
Article CAS Google Scholar Zhao S, Liu W, Wang J, Shi J, Sun Y, Wang W, et al. Article PubMed Google Scholar Zhang L, Qin Q, Liu M, Zhang X, He F, Wang G. Article CAS Google Scholar Toral M, Gómez-Guzmán M, Jiménez R, Romero M, Sánchez M, Utrilla MP, et al. Article Google Scholar Hsieh FC, Lan CC, Huang TY, Chen KW, Chai CY, Chen WT, et al.
Article CAS PubMed Google Scholar Natividad JM, et al. Article CAS PubMed Google Scholar Lim SM, Jeong JJ, Woo KH, Han MJ, Kim DH. Article CAS PubMed Google Scholar Li X, Wang E, Yin B, Fang D, Chen P, Wang G, et al.
Article CAS PubMed Google Scholar Balakumar M, Prabhu D, Sathishkumar C, Prabu P, Rokana N, Kumar R, et al. Article PubMed CAS Google Scholar Singh S, Sharma RK, Malhotra S, Pothuraju R, Shandilya UK. Article CAS PubMed Google Scholar Niibo M, et al.
Article CAS Google Scholar Wanchai K, et al. Article CAS Google Scholar Chunchai T, et al. Article CAS Google Scholar Morshedi M, et al. Article CAS PubMed Google Scholar Yao F, et al. Article CAS PubMed PubMed Central Google Scholar Kikuchi K, Othman MB, Sakamoto K. Article CAS Google Scholar Aoki R, Kamikado K, Suda W, Takii H, Mikami Y, Suganuma N, et al.
Article PubMed PubMed Central Google Scholar Alard J, Lehrter V, Rhimi M, Mangin I, Peucelle V, Abraham AL, et al. Article CAS PubMed Google Scholar Bagarolli RA, Tobar N, Oliveira AG, Araújo TG, Carvalho BM, Rocha GZ, et al.
Article CAS PubMed Google Scholar Rajkumar H, Kumar M, Das N, Kumar SN, Challa HR, Nagpal R. Article PubMed CAS Google Scholar Tonucci LB, Santos KMO, Oliveira LL, Ribeiro SMR, Martino HSD.
Article CAS PubMed Google Scholar Hsieh MC, et al. Article PubMed PubMed Central CAS Google Scholar Vallianou N, et al. Article PubMed Google Scholar Plovier H, Everard A, Druart C, Depommier C, Hul MV, Geurts L, et al.
Article PubMed CAS Google Scholar Zhang Z, Mocanu V, Cai C, Dang J, Slater L, Deehan EC, et al. Article CAS PubMed Central Google Scholar Lin HV, Frassetto A, Kowalik EJJ, Nawrocki AR, Lu MM, Kosinski JR, et al.
Article CAS PubMed PubMed Central Google Scholar Frost G, Sleeth ML, Sahuri-Arisoylu M, Lizarbe B, Cerdan S, Brody L, et al. Article CAS PubMed Google Scholar Liu WC, Yang MC, Wu YY, Chen PH, Hsu CM, Chen LW.
Google Scholar Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, et al. Article CAS PubMed Google Scholar Ley R, et al. Article CAS PubMed Google Scholar Duncan SH, Lobley GE, Holtrop G, et al. Article CAS Google Scholar Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al.
Article CAS PubMed Google Scholar Wang X, Ota N, Manzanillo P, Kates L, Zavala-Solorio J, Eidenschenk C, et al. Article CAS PubMed Google Scholar Dao MC, et al.
Article PubMed CAS Google Scholar Stenman LK, Waget A, Garret C, Briand F, Burcelin R, Sulpice T, et al. Article PubMed CAS Google Scholar Mannucci E, Tesi F, Bardini G, Ognibene A, Petracca MG, Ciani S, et al.
CAS PubMed Google Scholar Download references. Author information Authors and Affiliations Departamento de Epidemiologia, Faculdade de Saúde Pública, School of Public Health, University of Sao Paulo, Av.
Ferreira Authors Bárbara Izabel Moraes Salles View author publications. View author publications. Ethics declarations Competing interests The authors declare that they have no competing interests. Additional information Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Supplementary information. Additional file 1. Detailed procedures for the systematic review including its search equations. Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4.
Thank you for Insilin nature. You are using a browser version with limited High-Quality Coconut Oil Insulin resistance and gut health CSS. To obtain the rssistance experience, we recommend you use rssistance more up to Immune-boosting antioxidants browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Insulin resistance is a key factor in the development of metabolic diseases such as type 2 diabetes. Recently, Takeuchi et al. found that carbohydrate metabolism by gut microbiota contributes to insulin resistance. Their study, published today in Natureinvolved Vegan lifestyle choices human fecal microbiomes then corroborating their results with tests on mouse models resietance obesity. Amd potential cause of diabetes has Insulon how resisfance bacteria in the gut break down carbohydrates during Citrus aurantium for digestion. Insulin resistance and gut health date, Immune-boosting antioxidants, solid Blood circulation problems and solutions of this reslstance sparse gutt to a lack of healhh data. Members of the Laboratory for Intestinal Ecosystem at RIKEN, led by Ohno, set out to begin unraveling the role of the gut microbiome and in the process discovered a type of bacteria that may help reduce insulin resistance. For their study, the team examined the metabolites in the feces of more than adults who provided these samples during a regular health checkup and compared the metabolic findings of each person with their insulin resistance level. The next step was to characterize the gut microbiota and their relationship to insulin resistance and carbohydrate levels. This analysis revealed the people with higher insulin resistance contained more from the Lachnospiraceae order of bacteria compared to other orders.Insulin resistance and gut health -
Similarly, Zhang et al. revealed that the abundance of Faecalibacterium specifically Faecalibacterium Prausnitzii , Bifidobacterium , and Blautia were lower in PCOS patient [ 52 ]. The reduction of these bacteria might lead to changes in production of short-chain free fatty acids SCFAs , which might affect the integrity of the intestinal barrier.
In fact, gram-negative bacteria are known to produce lipopolysaccharides LPS , which may induce inflammation, insulin resistance, and obesity by leaking into the blood-stream [ 49 ]. Notably, Liu et al. Qi et al. reported Bacteroides vulgatus was significantly elevated in the gut microbiota in PCOS patients, accompanied by a reduction in the levels of glycodeoxycholic and tauroursodeoxycholic acids [ 53 ].
This report indicated that bile acid metabolism was one of the critical metabolic pathways affected by the gut microbiota changes in PCOS patients.
Intestinal flora metabolism has been closely associated with the occurrence and development of diseases. The metabolic functions of intestinal microflora include the production of vitamins, short-chain free fatty acids SCFAs and conjugated linoleic acids, amino acid synthesis, bioconversion of bile acids, fermentation and hydrolysis of non-digestible foods, ammonia synthesis and detoxification [ 54 ].
Its mechanism of in relation to PCOS can be explored further by monitoring its alteration and association with metabolic indicators.
Currently, the pathogenesis of PCOS is still uncertain, and research on its etiology has maiorly focused on genetics, immunity, androgen exposure, and so forth. However, none of the above factors can fully explain the clinical manifestations of PCOS.
The signal pathway behind the insulin receptor has a crossover effect with the signal transduction of chronic subclinical inflammation [ 55 , 56 ]. Studies have revealed that the occurrence of insulin resistance is associated with endotoxemia, chronic inflammatory response, short-chain fatty acids, and bile acid metabolism.
Moreover, a significant imbalance in the intestinal flora has been observed in PCOS patients [ 57 , 58 , 59 , 60 ]. Given this, we speculated that gut microbiota might be involved in the pathogenesis of PCOS by mediating systemic low-grade inflammation and insulin resistance, affecting the changes in sex hormones, gut-brain axis, and other pathological mechanisms Fig.
Crosstalk between the gut microbiota and the mammalian host in inflammation and metabolism. The gut microbiota can contribute to host insulin resistance, low-grade inflammation, and hyperandrogenism HA through a range of molecular interactions with the host and therefore can indirectly participate in the onset of PCOS.
PCOS is a female reproductive endocrine disease closely related to chronic inflammation [ 28 , 61 ]. Here, Tremellen et al. Additionally, Lindheim et al. also observed less the diversity on intestinal flora for patients with PCOS patients.
In this same study, changes in serum markers such as Zonulin, calprotectin, and LPS as a result of related to intestinal barrier damage and inflammation, such as Zonulin, calprotectin, LPS, were observed [ 18 ].
Notably, LPS produced by intestinal flora are vital molecules in the early development of inflammatory and metabolic diseases and have an endotoxin effect.
Actually, after LPS is absorbed into the blood, LPS binding protein LBP binds to CD14 toll-like receptor complex TRL-4 on the surface of innate immune cells, activates the downstream signaling pathway, the resulting immune system activation interferes with insulin receptor function, drives up serum insulin levels [ 62 ].
In PCOS patients, the expression of TNF and IL-6 is increased, which is related to IR [ 17 , 64 ]. Other studies also have shown that direct application of lipopolysaccharide to the blood circulation of mice and humans can increase fasting blood glucose and insulin levels [ 49 , 65 ].
IR and chronic inflammation are closely related, which implies that when intestinal barrier function is impaired, endotoxin produced by intestinal flora enters the blood to cause chronic ovarian inflammation and IR, hence promoting the occurrence and development of PCOS.
Gut microbiome decomposes dietary fiber to produce three major SCFAs, which include acetate, propionate, and butyrate [ 66 ]. Butyrate, in particular, including acting as an energy source for intestinal epithelial cells; and anti-inflammatory effects [ 67 ].
The SCFAs also maintain the barrier function of the intestinal mucosa. Besides, they are important signal molecules that directly activate G-protein-coupled receptor 41 GPR41 and GPR43 [ 68 ]. SCFA participates in glucose-stimulated insulin secretion from the pancreatic β-cells through interaction with the GPR41 and GPR43 receptors, improve insulin sensitivity and release of peptide hormones which control appetite [ 69 , 70 ].
Firmicutes mainly produce butyrate, whereas Bacteroides produces acetate. On the high-fat diet in mice, supplementation of SCFA butyrate prevented development of insulin resistance and obesity by increasing energy expenditure [ 71 ]. In the recent study on PCOS and intestinal bacteria, lower abundance of several kinds of gut microbiome in women with PCOS are all known to synthesize SCFAs [ 20 ].
After four weeks of probiotics intervention in patients with PCOS, the abundance of Lactobacillus increased significantly, it can generate lactic acid to promote the growth of Faecalibacterium, which produces butyric acid, Promote the secretion of insulin [ 72 ]..
These findings suggest that SCFAs protect intestinal barrier integrity and act on beta cells to promote insulin secretion, thus improving metabolism of PCOS [ 73 ]. Bile acids BAs are signaling molecules that regulate glucose metabolism and promote insulin sensitivity mainly through its receptors: farnesoid X receptor FXR and G protein-coupled bile acid receptor 1 GPBAR1.
Besides assisting in fat absorption, the combination of BAs with receptors and G protein-coupled receptors GGPCRs on the cell surface activates signal transduction.
Activation of nuclear receptor FXR improves the symptoms of hyperlipidemia and hyperglycemia in T2DM mice [ 74 ]. Sun et al. performed a metagenomic and metabolomic analysis of samples from patients who were newly diagnosed with T2DM and were treated with metformin for three days [ 60 ].
The analysis revealed a reduction in the abundance of Bacteroides fragilis and an increase in the bile acid, and glycoursodeoxy cholic acid GUDCA in the gut. Recent studies have found that altering bile acid metabolism may be valuable in the treatment of PCOS. Glycodeoxycholic acid induces intestinal group 3 innate lymphoid cell IL secretion through GATA binding protein 3, whereas IL in improves the PCOS phenotype [ 53 ].
These findings indicate that bile acids are involved in the regulation of IL production, thus affecting ovarian function and insulin sensitivity in PCOS. As an internal environmental factor, intestinal microflora interacts with the host and may affect insulin secretion in several ways, thus participating in the occurrence and development of pathophysiological processes of PCOS.
Branched-chain amino acids BCAAs was potentially harmful microbially microbial modulated metabolites. Recently, a recent study identified imidazole propionate as a microbially produced amino acid-derived metabolite and was shown to be present at higher concentrations in the portal and peripheral blood of patients with T2MD.
Additionally, it worsens glucose tolerance in mice and impairs insulin signaling at the level of insulin receptor substrate IRS [ 75 ]. Pedersen et al. found Prevotella in the human intestinal tract species was involved in the synthesis of BCAA [ 58 ].
Subsequently, the mice showed varying degrees of IR after another three weeks. Zhang et al. found that leucine and valine levels in the follicular fluid of PCOS patients with IR were significantly increased.
In the same study, higher levels of branched-chain amino acids increased the abortion rate and adverse pregnancy outcomes [ 77 ]. Prospective studies have also confirmed BCAA as a predictor of IR and diabetes [ 78 ].
The molecular mechanism of BCAA in pregnancy complications involves many signal transduction molecules, especially insulin receptor substrate 1 [ 79 ]. The possible mechanism is that the metabolic disorder of amino acids might aggravate IR by changing glucose metabolism or inducing inflammation, leading to abortion in PCOS patients.
Currently, there are few studies on the relationship between the gut microbiome and BCAA in PCOS patients, which calls for further investigation.
IR directly or indirectly promotes the synthesis and secretion of androgen. Subsequently, hyperandrogenemia stimulates decomposition of visceral adipose tissue, leading to an increase in free fatty acids, which further aggravate the levels of IR.
Such a sequence of events can ultimately form a vicious cycle between hyperandrogenemia and IR in PCOS, thus promoting the occurrence and development of PCOS. Barre et al. suggested that high intake of carbohydrate, hyperinsulinemia, hyperandrogenemia, and chronic low-grade inflammation are the four vital factors of pathophysiological changes in PCOS [ 80 ].
A metabolic dysfunction occuring predominantly in women diagnosed with hyperandrogenism and ovulatory dysfunction [ 81 , 82 ]. In the pathogenesis of PCOS, insulin resistance and hyperinsulinemia could contribute to metabolic dysregulation by upregulating the production of ovarian androgen and increasing its bioactivity through decreased production of sex hormone-binding globulin.
Excess androgen then leads to follicular development, maturation disorders, and follicular wall hyperplasia thickening which results resulting in ovulation disorders. Recently, a potential two-way interaction between sex hormones and intestinal flora has been proposed [ 83 ].
Prenatal androgen exposure can cause infant gut dysbiosis, hence altering the abundance of bacteria producing short-chain fatty acid metabolites. However, excess androgen in immature fetuses can result in long-term alterations of gut microbiota leading to an increased risk of developing PCOS [ 84 ].
Torres et al. discovered that treatment using letrozole adult mice was associated with a distinct shift in gut microbial diversity compared to its treatment in pubertal mice [ 85 ].
This finding showed that the timing of androgen exposure might influence metabolism dysregulation and the gut microbiome in PCOS, Which suggests that sex hormones can produce specific microbiota.
Choi et al. also discovered that ovariectomized mice had fewer Bacteroidetes and more Firmicutes than normal mice. Similar to ovariectomy, analysis of the microbiome of castrated mice using quantitative PCR assay showed a reduction in both Bacteroides and Ruminnococcaceae compared with the control group [ 46 , 86 ].
However, little is known about the mechanisms underlying sex steroid regulation of the gut microbiome. Further studies are needed to determine whether the changes in steroids in PCOS patients also affect the composition of intestinal microorganisms.
In recent years, studies have revealed that the pathological mechanism of PCOS is not confined to the dysfunction of the hypothalamic-pituitary-ovarian axis, but also involves the gut-brain axis. Besides, the hypothalamus is the centre of appetite regulation.
The gut-brain axis plays a critical role in the regulation of appetite, food intake, glucose metabolism, energy maintenance, and body weight. Gastrointestinal hormones mainly include growth hormone-releasing peptide Ghrelin , glucagon-like peptide-1 GLP-1 , cholecystokinin CCK , and PYY.
Gut microbiota and its metabolites cause insulin resistance and hyperinsulinemia by stimulating the secretion of gut-brain peptides and regulating inflammation pathway activation [ 24 ].
SCFAs stimulate the release of PYY and 5-HT in ileum and colon, wheres PYY inhibits gastrointestinal emptying and pancreatic secretion, slow intestinal peristalsis, and promote intestinal energy absorption [ 87 , 88 ]. Lin et al. found an inverse correlation between PYY and insulin as well as between body mass index BMI and testosterone [ 89 ].
Compared to healthy women, patients with PCOS show lowered ghrelin levels, serotonin, PYY, which has a negative correlation with PCOS related parameters, such as waist circumference and testosterone levels [ 19 ].
Bacteroidetes mainly produce acetate, which is involved in cholesterol metabolism and lipogenesis. Also, Bacteroidetes inhibit the secretion of appetite-stimulating hormone [ 90 ]. Ghrelin is a hormone secreted by the gastric mucosa that stimulates appetite and is inhibited through ingestion [ 66 , 90 ].
Although Houjeghani et al. found no difference in the ghrelin level between the PCOS group and the control group, many studies have found a negative correlation between serum ghrelin level and Homeostasis model assessment-insulin resistance HOMA-IR in PCOS patients [ 91 ]. Metformin usage in the treatment of PCOS has been associated with an increase in the levels of ghrelin, PYY, GLP-1, and GIP [ 92 ].
However, potential interactions of these treatments with the gut-brain axis in PCOS would be of much interest. Gut microbiota can be formed by LPS, BCAA branch-chain Amino acid , SCFA short-chain fatty acid , bile acid and other mediated inflammatory reactions affecting the sensitivity of insulin.
Also, gut microbiota are associated with hyperandrogenism and gut-brain axis in women with PCOS, IR still plays an important role in them. Notably, there are a vicious cycle between hyperandrogenemia and IR in PCOS, thus promoting the occurrence and development of PCOS Fig.
LPS: lipopolysaccharide; SCFA: short-chain fatty acid; BCAA: branch-chain amino acid; BA: Bile acids. Given that the vital role of intestinal flora is regulating human metabolism and energy storage, much focus has been directed to intestinal bacteria as a new target for the treatment of obesity and related metabolic diseases.
Lifestyle change involving exercise is the first step in the treatment of PCOS. Additionally, changes in diet can rapidly change the relative abundance of species making up the intestinal flora.
Actually, a low-carbohydrate diet will help increase production of short-chain fatty acids which reduces incidence of chronic inflammation [ 93 ]. Moreover, high-sugar foods may be one of the inducers of PCOS, by causing intestinal flora imbalance and triggering chronic inflammation, insulin resistance, and production of androgen [ 17 ].
Notably, the relationship between exercise and intestinal flora has also been widely studied in recent years. First, Clarke et al. compared the intestinal flora structure of athletes with that of the general population and found that exercise can help in increasing the diversity of intestinal flora [ 94 ].
Clinically, insulin sensitizers such as metformin can improve the sensitivity of insulin receptors, endometrial receptivity, and embryo implantation and development [ 95 ]. Therefore, intestinal flora plays a vital role in the hypoglycemic mechanism of metformin.
A recent study revealed that intestinal microorganisms and their metabolites regulate PCOS-related ovarian dysfunction and insulin resistance [ 53 ]. Transplantation of Bacteroides vulgatus infected fecal microbes in mice resulted in ovarian dysfunction, insulin resistance, changes in bile acid metabolism, decreased secretion of interleukin, and infertility.
Accumulating evidence has recommended probiotics, prebiotics, synbiotics as effective treatment options for PCOS patients. Ahmadi et al. showed that probiotics supplementation could reduce fasting blood glucose, serum insulin, HOMA-IR, triglyceride, and cholesterol in PCOS patients [ 96 ].
In a recent study involving probiotic intervention in PCOS patients, the consumption of probiotic Bifidobacterium Lactis V9 promoted the growth of SCFA producing microorganisms such as Faecalibacterium Praussnitzii , Butyriminas , and Akkermansia. Moreover, changes in PYY and ghrelin levels caused fluctuations in sexual hormone levels secreted by the thalamus and thalamus through the gut-brain axis [ 52 ].
Guo et al. treated PCOS rats models with Lactobacillus and fecal microbiota transplantation FMT from healthy rats.
They observed an improvement in the estrous cycles in all eight rats in the FMT group. Also, ovarian morphologies in six of the eight rats in the Lactobacillus transplantation group with decreased androgen biosynthesis were normalized. The composition of the gut microbiota was restored in both FMT and Lactobacillus treated groups.
The new composition of the gut microbiota had an increased abundance of Lactobacillus and Clostridium and a decreased abundance of Prevotella [ 7 ]. Considering these results, FMT may become a new direction in the treatment of PCOS. In recent years, research on intestinal microecology has attracted a lot of focus.
Actually, more and more studies have confirmed that intestinal flora can regulate the synthesis and secretion of insulin, and affect androgen metabolism and follicular development. These findings have enhanced our understanding, on the etiological mechanism of PCOS.
However, conflicting results on the composition and function of the gut microbiome changes in women with PCOS have only brought confusion. Nevertheless, a small sample size and regional differences have hindered current studies which aim at finding the relationship between gut microbiota and PCOS.
Therefore, it is of great importance to increase the sample size and conduct a multi-point research that can supplement the existing data and establish a localized health baseline and disease model. In addition to 16S rRNA sequencing, metagenomics and metabolomics could provide exciting insights into the relationship between the gut microbiome and the occurrence of PCOS.
Moreover, these analyses could confirm if variation in criteria of diagnosis could affect results of the gut microbiome composition in women with PCOS. Precisely, it is not known how changes in the gut microbiota occur in different PCOS phenotypes; therefore, there is need for further studies.
Actually, present studies have partially elucidated the mechanism of intestinal flora in PCOS; however, these findings lack a comprehensive understanding of the process. Also, more randomized and controlled studies will further elucidate causes leading to intestinal microflora imbalance and its role in PCOS.
The mechanism of ovulation disorder and insulin resistance in PCOS is still not precise, which has limited the development of therapeutic drugs. For instance, metformin can relieve symptoms of PCOS by positively influencing the composition and metabolites of intestinal microbiota.
compared the effects of Diane, probiotic, and berberine in the treatment of PCOS using dihydrotestosterone-induced PCOS rats [ 97 ]. Diane and probiotics restored the diversity of the gut microbiota and led the recovery of gut microbiota disorders, thus improving the reproductive function in PCOS-like rats.
Of note, several similar studies have confirmed the effectiveness of these treatments in improving disorders of intestinal flora from patients with in PCOS. However, their mechanisms of action are still unclear. Therefore, there is a need to understand how drugs metformin et al.
work so as to optimize their use in the treatment of PCOS. Despite being an exogenous genetic material, intestinal flora regulates expression of host genes, leading to the occurrence of PCOS. Additionally, as a result of being a diversified ecosystem, it participates in the occurrence and development of PCOS through multiple links and pathways.
Furthermore, following numerous ways and factors, it may affect the occurrence and development of IR in women with PCOS.
Thus, it is imperative to further detect and analyze specific functional bacterial profiles related to the occurrence and development of PCOS. This aims at providing new targets and options for individualized. Moreover, there is need for further research to determine whether the manipulation of the intestinal microbiota can be useful in the treatment of PCOS.
Lastly, it is also necessary to explore the potential use of probiotics and fecal transplant therapies in the treatment of this condition. Sahmay S, Aydogan Mathyk B, Sofiyeva N, Atakul N, Azemi A, Erel T.
Serum AMH levels and insulin resistance in women with PCOS. Eur J Obstet Gynecol Reprod Biol. Article CAS PubMed Google Scholar. Qin L, Huang CC, Yan XM, Wang Y, Li ZY, Wei XC. Long non-coding RNA H19 is associated with polycystic ovary syndrome in Chinese women: a preliminary study.
Endocr J. Zeng X, Xie YJ, Liu YT, Long SL, Mo ZC. Polycystic ovarian syndrome: correlation between hyperandrogenism, insulin resistance and obesity. Clin Chim Acta. Teede HJ, Misso ML, Costello MF, Dokras A, Laven J, Moran L, et al. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome.
Hum Reprod. Article PubMed PubMed Central Google Scholar. Macut D, Bjekic-Macut J, Rahelic D, Doknic M. Insulin and the polycystic ovary syndrome. Diabetes Res Clin Pract. Goodman NF, Cobin RH, Futterweit W, Glueck JS, Legro RS, Carmina E, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and androgen excess and Pcos society disease state clinical review: guide to the best practices in the evaluation and treatment of polycystic ovary syndrome - part 2.
Endocr Pract. Article PubMed Google Scholar. Guo Y, Qi Y, Yang X, Zhao L, Wen S, Liu Y, et al. Association between polycystic ovary syndrome and gut microbiota. PLoS One. Article PubMed PubMed Central CAS Google Scholar.
Rosenfield RL, Ehrmann DA. The pathogenesis of polycystic ovary syndrome PCOS : the hypothesis of PCOS as functional ovarian Hyperandrogenism revisited. Endocr Rev. Article CAS PubMed PubMed Central Google Scholar. Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications.
Legro RS, Arslanian SA, Ehrmann DA, Hoeger KM, Murad MH, Pasquali R, et al. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline.
J Clin Endocrinol Metab. Rotterdam EA-SPcwg. Revised consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome PCOS. Hum Reprod ;19 1 — Jiao N, Baker SS, Nugent CA, Tsompana M, Cai L, Wang Y, et al.
Gut microbiome may contribute to insulin resistance and systemic inflammation in obese rodents: a meta-analysis. Physiol Genomics. Hartstra AV, Bouter KE, Backhed F, Nieuwdorp M. Insights into the role of the microbiome in obesity and type 2 diabetes.
Diabetes Care. Scheithauer TP, Dallinga-Thie GM, de Vos WM, Nieuwdorp M, van Raalte DH. Causality of small and large intestinal microbiota in weight regulation and insulin resistance.
Mol Metab. Sun L, Hu W, Liu Q, Hao Q, Sun B, Zhang Q, et al. Metabonomics reveals plasma metabolic changes and inflammatory marker in polycystic ovary syndrome patients. J Proteome Res. Vrieze A, Van Nood E, Holleman F, Salojarvi J, Kootte RS, Bartelsman JF, et al. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome.
Tremellen K, Pearce K. Dysbiosis of gut microbiota DOGMA --a novel theory for the development of polycystic ovarian syndrome. Med Hypotheses. Lindheim L, Bashir M, Munzker J, Trummer C, Zachhuber V, Leber B, et al.
Alterations in gut microbiome composition and barrier function are associated with reproductive and metabolic defects in women with polycystic ovary syndrome PCOS : a pilot study.
Liu R, Zhang C, Shi Y, Zhang F, Li L, Wang X, et al. Dysbiosis of gut microbiota associated with clinical parameters in polycystic ovary syndrome. Front Microbiol. PubMed PubMed Central Google Scholar. Torres PJ, Siakowska M, Banaszewska B, Pawelczyk L, Duleba AJ, Kelley ST, et al.
Gut microbial diversity in women with polycystic ovary syndrome correlates with Hyperandrogenism. Insenser M, Murri M, Del Campo R, Martinez-Garcia MA, Fernandez-Duran E, Escobar-Morreale HF.
Gut microbiota and the polycystic ovary syndrome: influence of sex, sex hormones, and obesity. Zeng B, Lai Z, Sun L, Zhang Z, Yang J, Li Z, et al. Endocrinology — Bala V, Rajagopal S, Kumar DP, Nalli AD, Mahavadi S, Sanyal AJ, et al. Front Physiol.
Chimerel C, Emery E, Summers DK, Keyser U, Gribble FM, Reimann F. Bacterial metabolite indole modulates incretin secretion from intestinal enteroendocrine L cells.
Cell Rep. Yang M, Fukui H, Eda H, Kitayama Y, Hara K, Kodani M, et al. Mol Med Rep. Grasset E, Puel A, Charpentier J, Collet X, Christensen JE, Tercé F, et al. A specific gut microbiota dysbiosis of type 2 diabetic mice induces GLP-1 resistance through an enteric NO-dependent and gut-brain axis mechanism.
Li X, Zhao J, Zhang H, Chen W. Lactobacillus casei CCFM attenuates type 2 diabetes via a gut microbiota dependent mechanism. Food Funct. CrossRef Full Text Google Scholar. Bjerg AT, Kristensen M, Ritz C, Holst JJ, Rasmussen C, Leser TD, et al.
Lactobacillus paracasei subsp paracasei L. casei W8 suppresses energy intake acutely. Appetite —8. Simon MC, Strassburger K, Nowotny B, Kolb H, Nowotny P, Burkart V, et al. Intake of Lactobacillus reuteri improves incretin and insulin secretion in glucose-tolerant humans: a proof of concept.
Ryan PM, Patterson E, Kent RM, Stack H, O'Connor PM, Murphy K, et al. Recombinant incretin-secreting microbe improves metabolic dysfunction in high-fat diet fed rodents.
Sci Rep. Macfarlane GT, Macfarlane S. Bacteria, colonic fermentation, and gastrointestinal health. J AOAC Int. Cummings JH, Pomare EW, Branch WJ, Naylor CP, Macfarlane GT. Short chain fatty acids in human large intestine, portal, hepatic and venous blood.
Gut —7. Wolever TM, Josse RG, Leiter LA, Chiasson JL. Time of day and glucose tolerance status affect serum short-chain fatty acid concentrations in humans. Metabolism — Wolever TM, Spadafora P, Eshuis H. Interaction between colonic acetate and propionate in humans.
Am J Clin Nutr. Kaiko GE, Ryu SH, Koues OI, Collins PL, Solnica-Krezel L, Pearce EJ, et al. The colonic crypt protects stem cells from microbiota-derived metabolites.
Cell Lupton JR. Microbial degradation products influence colon cancer risk: the butyrate controversy. J Nutr.
Puddu A, Sanguineti R, Montecucco F, Viviani GL. Evidence for the gut microbiota short-chain fatty acids as key pathophysiological molecules improving diabetes. Mediators Inflamm. Reichardt N, Duncan SH, Young P, Belenguer A, McWilliam Leitch C, Scott KP, et al.
Phylogenetic distribution of three pathways for propionate production within the human gut microbiota. ISME J. Zhao L, Zhang F, Ding X, Wu G, Lam YY, Wang X, et al. Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes.
Science —6. De Vadder F, Kovatcheva-Datchary P, Goncalves D, Vinera J, Zitoun C, Duchampt A, et al. Microbiota-generated metabolites promote metabolic benefits via gut-brain neural circuits.
Mithieux G, Gautier-Stein A. Intestinal glucose metabolism revisited. De Vadder F, Kovatcheva-Datchary P, Zitoun C, Duchampt A, Bäckhed F, Mithieux G.
Microbiota-produced succinate improves glucose homeostasis via intestinal gluconeogenesis. Mithieux G. Gut microbiota and host metabolism: what relationship.
Neuroendocrinology —6. Wang S, Li Q, Zang Y, Zhao Y, Liu N, Wang Y, et al. Apple polysaccharide inhibits microbial dysbiosis and chronic inflammation and modulates gut permeability in HFD-fed rats.
Int J Biol Macromol. Han M, Song P, Huang C, Rezaei A, Farrar S, Brown MA, et al. Dietary grape seed proanthocyanidins GSPs improve weaned intestinal microbiota and mucosal barrier using a piglet model. Oncotarget — Xu YH, Gao CL, Guo HL, Zhang WQ, Huang W, Tang SS, et al.
J Endocrinol. Le Poul E, Loison C, Struyf S, Springael JY, Lannoy V, Decobecq ME, et al. Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation. J Biol Chem.
Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F. From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites.
Kimura I, Ozawa K, Inoue D, Imamura T, Kimura K, Maeda T, et al. The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR Nat Commun. Bjursell M, Admyre T, Göransson M, Marley AE, Smith DM, Oscarsson J, et al.
Improved glucose control and reduced body fat mass in free fatty acid receptor 2-deficient mice fed a high-fat diet. Am J Physiol Endocrinol Metab. Ang Z, Ding JL. GPR41 and GPR43 in obesity and inflammation - protective or causative? Front Immunol. Tolhurst G, Heffron H, Lam YS, Parker HE, Habib AM, Diakogiannaki E, et al.
Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Psichas A, Sleeth ML, Murphy KG, Brooks L, Bewick GA, Hanyaloglu AC, et al. The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents.
Yadav H, Lee JH, Lloyd J, Walter P, Rane SG. Beneficial metabolic effects of a probiotic via butyrate-induced GLP-1 hormone secretion. Priyadarshini M, Wicksteed B, Schiltz GE, Gilchrist A, Layden BT. SCFA receptors in pancreatic beta cells: novel diabetes targets?
Trends Endocrinol Metab. McNelis JC, Lee YS, Mayoral R, van der Kant R, Johnson AM, Wollam J, et al. GPR43 potentiates beta-cell function in obesity.
Gao Z, Yin J, Zhang J, Ward RE, Martin RJ, Lefevre M, et al. Butyrate improves insulin sensitivity and increases energy expenditure in mice.
Zhang L, Du J, Yano N, Wang H, Zhao YT, Dubielecka PM, et al. Sodium butyrate protects -against high fat diet-induced cardiac dysfunction and metabolic disorders in type II diabetic mice. J Cell Biochem. Dewulf EM, Cani PD, Claus SP, Fuentes S, Puylaert PG, Neyrinck AM, et al.
Insight into the prebiotic concept: lessons from an exploratory, double blind intervention study with inulin-type fructans in obese women. Gut — van der Beek CM, Canfora EE, Kip AM, Gorissen SHM, Olde Damink SWM, van Eijk HM, et al.
The prebiotic inulin improves substrate metabolism and promotes short-chain fatty acid production in overweight to obese men. Hylemon PB, Zhou H, Pandak WM, Ren S, Gil G, Dent P.
Bile acids as regulatory molecules. J Lipid Res. Holt JA, Luo G, Billin AN, Bisi J, McNeill YY, Kozarsky KF, et al. Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis.
Genes Dev. Di Ciaula A, Garruti G, Lunardi Baccetto R, Molina-Molina E, Bonfrate L, Wang DQ, et al. Bile acid physiology. Ann Hepatol. Chiang JYL, Ferrell JM. Bile acid metabolism in liver pathobiology. Gene Expr. Li Q, Yin W, Cai M, Liu Y, Hou H, Shen Q, et al. NO suppresses diet-induced insulin resistance and cholesterol accumulation through STAT5-dependent upregulation of IGF1 and CYP7A1.
Ridlon JM, Kang DJ, Hylemon PB. Bile salt biotransformations by human intestinal bacteria. Swann JR, Want EJ, Geier FM, Spagou K, Wilson ID, Sidaway JE, et al.
Systemic gut microbial modulation of bile acid metabolism in host tissue compartments. Labbé A, Ganopolsky JG, Martoni CJ, Prakash S, Jones ML. Bacterial bile metabolising gene abundance in Crohn's, ulcerative colitis and type 2 diabetes metagenomes.
PLoS ONE 9:e Martoni CJ, Labbé A, Ganopolsky JG, Prakash S, Jones ML. Changes in bile acids, FGF and sterol absorption in response to bile salt hydrolase active L. reuteri NCIMB 3 Gut Microbes — Gu Y, Wang X, Li J, Zhang Y, Zhong H, Liu R, et al. Analyses of gut microbiota and plasma bile acids enable stratification of patients for antidiabetic treatment.
Sayin SI, Wahlström A, Felin J, Jäntti S, Marschall HU, Bamberg K, et al. Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR antagonist.
Islam KB, Fukiya S, Hagio M, Fujii N, Ishizuka S, Ooka T, et al. Bile acid is a host factor that regulates the composition of the cecal microbiota in rats. Zheng X, Huang F, Zhao A, Lei S, Zhang Y, Xie G, et al. Bile acid is a significant host factor shaping the gut microbiome of diet-induced obese mice.
BMC Biol. Russell DW. The enzymes, regulation, and genetics of bile acid synthesis. Annu Rev Biochem. Wahlström A, Kovatcheva-Datchary P, Ståhlman M, Bäckhed F, Marschall HU. Crosstalk between bile acids and gut microbiota and its impact on farnesoid X receptor signalling.
Dig Dis. Cariou B, van Harmelen K, Duran-Sandoval D, van Dijk TH, Grefhorst A, Abdelkarim M, et al. The farnesoid X receptor modulates adiposity and peripheral insulin sensitivity in mice. Parks DJ, Blanchard SG, Bledsoe RK, Chandra G, Consler TG, Kliewer SA, et al.
Bile acids: natural ligands for an orphan nuclear receptor. Watanabe M, Horai Y, Houten SM, Morimoto K, Sugizaki T, Arita E, et al. Lowering bile acid pool size with a synthetic farnesoid X receptor FXR agonist induces obesity and diabetes through reduced energy expenditure.
Prawitt J, Abdelkarim M, Stroeve JH, Popescu I, Duez H, Velagapudi VR, et al. Farnesoid X receptor deficiency improves glucose homeostasis in mouse models of obesity. Zhang Y, Ge X, Heemstra LA, Chen WD, Xu J, Smith JL, et al.
Mol Endocrinol. Jiang C, Xie C, Lv Y, Li J, Krausz KW, Shi J, et al. Intestine-selective farnesoid X receptor inhibition improves obesity-related metabolic dysfunction. Shapiro H, Kolodziejczyk AA, Halstuch D, Elinav E. Bile acids in glucose metabolism in health and disease.
J Exp Med. Pathak P, Xie C, Nichols RG, Ferrell JM, Boehme S, Krausz KW, et al. Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism.
Hepatology — Kir S, Beddow SA, Samuel VT, Miller P, Previs SF, Suino-Powell K, et al. FGF19 as a postprandial, insulin-independent activator of hepatic protein and glycogen synthesis.
Science —4. Morton GJ, Matsen ME, Bracy DP, Meek TH, Nguyen HT, Stefanovski D, et al. FGF19 action in the brain induces insulin-independent glucose lowering. J Clin Invest. Benoit B, Meugnier E, Castelli M, Chanon S, Vieille-Marchiset A, Durand C, et al.
Fibroblast growth factor 19 regulates skeletal muscle mass and ameliorates muscle wasting in mice. Liu H, Hu C, Zhang X, Jia W. Role of gut microbiota, bile acids and their cross-talk in the effects of bariatric surgery on obesity and type 2 diabetes. J Diabetes Investig. Tremaroli V, Karlsson F, Werling M, Ståhlman M, Kovatcheva-Datchary P, Olbers T, et al.
Roux-en-Y gastric bypass and vertical banded gastroplasty induce long-term changes on the human gut microbiome contributing to fat mass regulation.
Jansen PL, van Werven J, Aarts E, Berends F, Janssen I, Stoker J, et al. Alterations of hormonally active fibroblast growth factors after Roux-en-Y gastric bypass surgery.
Bleau C, Karelis AD, St-Pierre DH, Lamontagne L. Crosstalk between intestinal microbiota, adipose tissue and skeletal muscle as an early event in systemic low-grade inflammation and the development of obesity and diabetes. Diabetes Metab Res Rev. Torres S, Fabersani E, Marquez A, Gauffin-Cano P.
Adipose tissue inflammation and metabolic syndrome. The proactive role of probiotics. Eur J Nutr. Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB. Adipose tissue remodeling: its role in energy metabolism and metabolic disorders.
Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Gérard C, Brown KA. Obesity and breast cancer - Role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue.
Mol Cell Endocrinol. Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and metabolism. Hotamisligil GS. Inflammation and metabolic disorders. Nature —7. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insulin resistance.
Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice.
de La Serre CB, Ellis CL, Lee J, Hartman AL, Rutledge JC, Raybould HE. Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation. Am J Physiol Gastrointest Liver Physiol. Vors C, Pineau G, Drai J, Meugnier E, Pesenti S, Laville M, et al.
Postprandial endotoxemia linked with chylomicrons and lipopolysaccharides handling in obese versus lean men: a lipid dose-effect trial. J Clin Endocrinol Metab.
Osbak PS, Bindslev N, Hansen MB. Relationships between body mass index and short-circuit current in human duodenal and colonic mucosal biopsies. Acta Physiol. Kim SH, Plutzky J. Brown fat and browning for the treatment of obesity and related metabolic disorders. Diabetes Metab J.
Prattichizzo F, De Nigris V, Spiga R, Mancuso E, La Sala L, Antonicelli R, et al. Inflammageing and metaflammation: the yin and yang of type 2 diabetes. Ageing Res Rev. Esser N, Legrand-Poels S, Piette J, Scheen AJ, Paquot N.
The other authors on this study are Guillaume Jospin at the Genome Center, University of California, Davis; Kristy Brownell and Barbara Laraia at the University of California, San Francisco and the University of California, Berkeley; and Elissa Epel at the University of California, San Francisco.
What is 'gut health' and why is it important? Mapping the pathway to gut health in HIV and SIV infections New paper proposes diversity, equity and inclusion measures to combat structural health inequities.
search Search All UC Davis Health. Main Menu add. close Main Menu. Main Menu remove. Giving Careers. search Search. Search All UC Davis Health. Conditions and Treatments Maps, Locations and Parking Appointments and Referrals About Patient Care. Primary Care Specialty Care A-Z Care Centers Telehealth Services Find a Provider.
Refer a Patient Featured Specialties Find a Provider or Faculty Residency Programs and Fellowships Clinical Studies Career Opportunities Professional Development Clinical News. UC Davis Health Responds Noticias en Español Feature Stories Blogs and Podcasts Publications Health Highlights Newsletter Videos Social Media For Journalists Public Reporting.
UC Davis Health News Headlines Gut bacteria differences between Black and white women Insulin resistance and diabetes Insulin is a hormone that helps blood sugar enter the cells to be used for energy. Social determinants of health and racial differences in the gut microbiome The researchers indicated that race and ethnic differences in the gut microbiome are likely a reflection of environmental influences such as diet, rather than genetics.
Related stories: What is 'gut health' and why is it important?
Researchers led by Hiroshi Ohno at the RIKEN Center for Pre-race nutrition planning Medical Sciences IMS in Japan reeistance discovered a type of gut bacteria that might help improve insulin resistance, and thus resistqnce Immune-boosting antioxidants the development of healgh and type-2 Blood circulation problems and solutions. The Strengthen immunity naturally, published Insulon 30 in the Blood circulation problems and solutions journal Natureinvolved genetic and metabolic analysis of human fecal microbiomes and then corroborating experiments in obese mice. Insulin is a hormone released by the pancreas in response to blood sugar. Normally, it helps get the sugar into the muscles and liver so that they can use the energy. When someone develops insulin resistance, it means that insulin is prevented from doing its job, and as a result, more sugar stays in their blood and their pancreas continues to make more insulin. Insulin resistance can lead to obesity, pre-diabetes, and full-blown type-2 diabetes.
0 thoughts on “Insulin resistance and gut health”