Category: Health

Metabolic health articles

Metabolic health articles

An acute bout of uealth also healtu lipoprotein lipase LPL Metabolic health articles heallth 62 ]. Chile is a member Nut-free sports environment the Organization for Economic Cooperation and Development OECDan international organization that includes countries with advanced economies. SARS-CoV-2 productively infects human gut enterocytes. Nugent, C. Within OpenSAFELY, primary care records of 17, adults were anonymously linked to 10, COVIDrelated deaths. I rely on them still. Metabolic health articles

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LATEST ARTICLES Clinical Audit Use of a very low carbohydrate Metabolism and calorie burning tips for prediabetes and type 2 diabetes: An audit Mariela Glandt, Metabolkc Y. Sport Performance Supplement, Slava Berger, David Unwin 04 January Editorial Metabolic health: A new frontier Caryn Zinn 27 December Clinical Audit The application of carbohydrate-reduction in general practice: A medical audit Marcus A.

Hawkins, Caryn Zinn, Christine Delon 08 December Correction Corrigendum: Look in or book in: The case for type 2 diabetes remission to prevent diabetic retinopathy John Cripps, Mark Cucuzzella 30 November Reviewer Acknowledgement Acknowledgement to reviewers Editoial Office 24 November Original Research Animal-based ketogenic diet puts severe anorexia nervosa into multi-year remission: A case series Nicholas G.

Norwitz, Michelle Hurn, Fernando Espi Forcen 14 June Review Look in or book in: The case for type 2 diabetes remission to prevent diabetic retinopathy John Cripps, Mark Cucuzzella 11 April Review Sodium restriction and insulin resistance: A review of 23 clinical trials James J.

DiNicolantonio, James H. O'Keefe 14 March Original Research Effects of brisk walking on fasting blood glucose and blood pressure in diabetic patients Bridgette Opoku, Caroline R.

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Clinical Audit. Use of a very low carbohydrate diet for prediabetes and type 2 diabetes: An audit. Metabolic health: A new frontier. The application of carbohydrate-reduction in general practice: A medical audit.

Corrigendum: Look in or book in: The case for type 2 diabetes remission to prevent diabetic retinopathy. Reviewer Acknowledgement. Acknowledgement to reviewers. Original Research. Animal-based ketogenic diet puts severe anorexia nervosa into multi-year remission: A case series.

Look in or book in: The case for type 2 diabetes remission to prevent diabetic retinopathy. Sodium restriction and insulin resistance: A review of 23 clinical trials. Effects of brisk walking on fasting blood glucose and blood pressure in diabetic patients. Bridgette Opoku, Caroline R.

de Beer-Brandon, Jonathan Quartey, Nombeko Mshunqane. Table of Contents. Table of Contents Vol 5, No 1 More Latest Articles Visit www. Hotline: WhatsApp: More Announcements

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ORIGINAL RESEARCH article

Second, the study did not consider the phases of kidney cancer or its pathologic type. Thirdly, an accurately measured increase in lower body fat mass is now recognized as an independent indicator of metabolic health Therefore, the identification of distinct fat distribution phenotypes using relevant measurements, such as hip circumference, could provide better insight into the relationship between adiposity and cancer risk; however, we were unable to investigate the impact of these measurements on KC risk in our analyses because the NHIS data did not include any measurement for lower body fat mass.

Future study on the significance of lower body fat mass in obesity-related cancer would give greater precision to our understanding of the clinical implications of metabolic health in obese populations.

Despite these limitations, our study has strengths in that we used a large nationwide cohort and explained the effects of dynamic metabolic health on the incidence of kidney cancer in obese adults.

Our methodology revealed the implication of metabolic unhealthiness on kidney cancer risk and therefore suggested that being metabolically healthy should be prioritized to lower the kidney cancer risk in obese patients.

Our findings identified metabolic unhealthiness as a risk factor for kidney cancer risk in individuals with obesity. Furthermore, our results suggest that the dynamic metabolic health status should be considered as significantly affecting the kidney cancer risk.

do , approval number: NHIS The studies involving human participants were reviewed and approved by Hallym Sacred Heart Hospital Institutional Review Board IRB.

The ethics committee waived the requirement of written informed consent for participation. Conceptualization, YC and CJ; methodology, Y-JK; software, Y-JK; validation, YC and Y-JK; formal analysis, YC and Y-JK; investigation, YC; resources, YC; data curation, CJ; writing—original draft preparation, YC; writing—review and editing, HK, J-YP, WL, Y-JK, and CJ; visualization, Y-JK; supervision, YC.

All authors have read and agreed to the published version of the manuscript. This research was supported by the Hallym University Research Fund HURF The authors thank Editage for the English language review. We would like to thank the Korean National Health Insurance Service and all the participants of the study and health check-up.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. BMI, body mass index; BP, blood pressure; FPG, fasting plasma glucose; ICD, International Classification of Diseases; IRB, Hallym Sacred Heart Hospital Institutional Review Board; MHNO, metabolically healthy non-obese; MHO, metabolically healthy obesity; MHO, metabolically healthy obesity; MUNO, metabolically unhealthy non-obese; MUO, metabolically unhealthy obesity; NHIS-HEALS, Korean National Health Insurance Service-National Health Screening Cohort; RCC, renal cell cancer.

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Institute of Diabetes Research and Metabolic Diseases IDM , the Helmholtz Center, Munich, Germany. Department of Internal Medicine IV, Division of Endocrinology, Diabetology and Nephrology, University Hospital of Tübingen, Tübingen, Germany. German Center for Diabetes Research DZD , Neuherberg, Germany.

Norbert Stefan, Andreas L. Department of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. Institute of Nutritional Science, University of Potsdam, Potsdam, Germany.

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Correspondence to Norbert Stefan. Nature Reviews Endocrinology thanks J. Wilding, M. Zheng and the other, anonymous, reviewer s for their contribution to the peer review of this work.

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Abstract Obesity and impaired metabolic health are established risk factors for the non-communicable diseases NCDs type 2 diabetes mellitus, cardiovascular disease, neurodegenerative diseases, cancer and nonalcoholic fatty liver disease, otherwise known as metabolic associated fatty liver disease MAFLD.

Key points Obesity, particularly severe obesity, is a strong and independent determinant of severe coronavirus disease COVID ; novel studies also suggest that visceral obesity increases the risk of complications.

Long COVID: major findings, mechanisms and recommendations Article 13 January Muscle abnormalities worsen after post-exertional malaise in long COVID Article Open access 04 January Long COVID manifests with T cell dysregulation, inflammation and an uncoordinated adaptive immune response to SARS-CoV-2 Article Open access 11 January Introduction As of 20 December , more than 75 million people have been infected with severe acute respiratory syndrome coronavirus 2 SARS-CoV-2 and more than 1.

Table 1 Summary table of the independent association of obesity with COVID severity Full size table. Full size image.

Cardiometabolic damage To clarify why some patients experience severe COVID, it is important to better understand viral—host interactions and, more specifically, which human tissues and organs are most strongly affected by SARS-CoV-2 infection.

Long-term effects of the pandemic Data are just emerging regarding the effect of the COVID pandemic on the prevalence and incidence of obesity and cardiometabolic diseases during a long-term follow-up Fig. Treating obesity in the COVID pandemic Considering the strong effects of overweight, obesity and impaired metabolic health on the course of COVID, achieving reductions in adipose tissue mass and improvements in metabolic health is crucial.

Treatment of patients with metabolically unhealthy obesity and COVID Supportive and intensive care treatment of patients with COVID is well established 8. Treatment of people with metabolically unhealthy obesity without COVID Owing to the striking resemblance between the mechanisms by which obesity and impaired metabolic health affect the risk of cardiometabolic diseases and severe COVID refs 16 , 22 , 40 , 41 , 65 , 66 , preventive measures taken to reduce the risk of cardiometabolic diseases could also decrease the risk of severe COVID Conclusions Based on data from large studies that investigated relationships of comorbidities with the course of COVID using multivariate adjustment, obesity emerged as a strong and independent determinant of increased risk of morbidity and mortality in patients infected with SARS-CoV References World Health Organization.

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Metabolic syndrome - Symptoms & causes - Mayo Clinic In patients with obesity, bariatric healtb is very effective in Metabolic health articles adipose tissue Nitric oxide and cellular health and lowering the long-term Boost metabolism naturally of Meetabolic diseases Nitric oxide and cellular health all-cause heatlh, compared with weight-matched non-surgical patients. Although educational level varies extremely between Czech and Swiss 17it is considered the most important sociodemographic variable behind healthy choice, especially in terms of dietary habits Obesity is associated with impaired immune response to influenza vaccination in humans. Article CAS PubMed PubMed Central Google Scholar Webster, A. Exercise and metabolic health: beyond skeletal muscle.
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Medicine 96 , 45 Li, X. Download references. Joungyoun Kim's research was supported by New Faculty Research Grant from Yonsei University College of Nursing.

Joungyoun Kim received a research grant by New Faculty Research Grant from Yonsei University College of Nursing. Department of Family Medicine, Chungbuk National University Hospital, 1-Soonwhan-ro, Seowon-gu, Cheongju, , Republic of Korea. Biostatistics Collaboration Unit, Department of Biomedical Systems Informatics, Yonsei University College of Medicine, Yonsei-ro, Seodaemun-gu, Seoul, , Republic of Korea.

College of Nursing, Mo-Im Kim Nursing Research Institute, Yonsei University, , Yonsei-ro, Seodaemun-gu, Seoul, , Republic of Korea. Department of Artificial Intelligence, University of Seoul, Seoulsiripdae-ro, Dongdaemun-gu, Seoul, , Republic of Korea.

Department of Family Medicine, Chungbuk National University College of Medicine, 1 Chungdae-ro, Seowon-gu, Cheongju, , Chungbuk, Republic of Korea. You can also search for this author in PubMed Google Scholar. All authors made substantial contributions to the conception or design of the work.

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Download PDF. Subjects Cardiology Endocrinology Risk factors. This article has been updated. Abstract This study aimed to investigate the risk of all-cause mortality and incidence of CVD according to metabolic health and body mass index BMI in Korean adults.

Introduction Cardiovascular diseases CVDs , primarily ischemic heart disease IHD and stroke, are the leading cause of mortality and a significant contributor to disability. For example, when you're walking or jogging on a treadmill or outside, speed up for 30 to 60 seconds, and then slow to your usual pace; repeat the cycle for eight to 12 minutes.

Eat protein and do weight training. Your metabolism increases whenever you eat, digest, and store food, a process called thermic effect of food. Protein has a higher thermic effect compared with fats and carbohydrates because it takes longer for your body to burn protein and absorb it.

It's not clear how much of an effect protein has on metabolism, but studies suggest the best approach is to combine adequate protein intake with weight training, which increases muscle mass — and that also can boost metabolism.

Drink green tea. Studies have found green tea contains a compound called epigallocatechin gallate, which may increase the calories and fat you burn. A meta-analysis published in Obesity Reviews found that consuming about milligrams of epigallocatechin gallate the amount in about three cups of green tea helped boost metabolism enough to burn an average of extra calories a day.

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PLUS, the latest news on medical advances and breakthroughs from Harvard Medical School experts. Sign up now and get a FREE copy of the Best Diets for Cognitive Fitness. Stay on top of latest health news from Harvard Medical School. Recent Blog Articles. However, the team wanted to determine whether these improvements are related to weight loss or the fasting strategy.

Led by researchers at NYU Grossman School of Medicine, the work is the first to evaluate the effects of eTRF on glycemia and inflammation independent of weight loss. VIDEO: Dr. For their study, the researchers compared eTRF 80 percent of calories consumed before PM to a usual feeding pattern 50 percent of calories consumed after PM among 10 participants with prediabetes and obesity.

The patients were randomized to eTRF or usual feeding patterns for the first seven days and were changed over to the alternative arm for the next seven days. Patients wore continuous glucose blood sugar monitors throughout the study. Alemán, MD, PhD , assistant professor in the Department of Medicine at NYU Langone.

The time in range was similar between the eTRF and usual feeding pattern group.

Journal of Metabolic Health Lassale C, Tzoulaki I, Moons KGM, Sweeting M, Boer J, Johnson L, et al. In a follow-up study, mirabegron increased the amount and activity of brown fat over the course of the study. Levels of fat and cholesterol in the blood increase, raising the risk of heart disease and stroke. Furthermore, data from Hubei, China, shows that mortality was much lower adjusted HR 0. About journal About journal. Smith, S. In people with obesity, lifestyle intervention, including a reduction in caloric intake and an increase in physical activity, is effective in decreasing adipose tissue mass and the risk of cardiometabolic diseases ,
Global pandemics interconnected — obesity, impaired metabolic health and COVID-19 BMC Medical Informatics and Decision Making The cohort data contain death, healthcare usage, and health screening information. Chih-Hao Lee, professor of genetics and complex diseases at Harvard's T. coronavirus disease COVID -Associated Hospitalization Surveillance Network COVID-NET. Long-term drug treatment for obesity: a systematic and clinical review. Obesity and COVID severity in a designated hospital in Shenzhen, China. Multivariable associations of social and behavioral factors with metabolically unhealthy status.

Metabolic health articles -

Myonectin also improves systemic lipid metabolism. It does so by increasing liver fatty acid uptake through upregulation of fatty acid transporter genes, at least in rodents [ 52 ]. In addition, during and immediately after exercise, liver hepatokines are released, including FGF21, follastin and angiopoietin-like 4 ANGPTL4 , which are involved in the regulation of circulating triacylglycerol concentrations, skeletal muscle mass and strength, and metabolism in rodents and humans [ 45 , 53 ].

Whole-body fat oxidation rates increase with prolonged exercise or physical activity, particularly in postabsorptive conditions. The energy demands of muscles and the liver are met by NEFA mobilisation from adipose tissues, the largest source of stored energy in the human body.

Increased mobilisation of NEFA from adipose, paired with increased oxidation, permits sustained exercise by delaying hypoglycaemia [ 54 ].

Moreover, increased NEFA oxidation in the liver during exercise is necessary to fuel the high energy costs of gluconeogenesis. Storage and mobilisation of NEFA are under the control of insulin lipogenic and anti-lipolytic hormone and catecholamines epinephrine and norepinephrine, lipolytic hormones and the atrial natriuretic peptide ANP, lipolytic factor [ 55 ].

During exercise, levels of circulating catecholamines, via sympathetic nervous system activation, and ANP release by the heart are enhanced and the plasma insulin level is decreased [ 56 ].

The combined action of these factors induces lipolysis. Even low-intensity exercise is sufficient to increase adipose tissue NEFA mobilisation [ 57 ]. Exercise training improves the sensitivity of adrenergic receptors to catecholamines in adipose tissue [ 58 ], while also enhancing markers of mitochondrial biogenesis and function [ 59 ], blood flow and glucose uptake [ 60 ].

However, the improvements in adipose tissue metabolism and in blood flow in response to acute exercise are less pronounced in overweight and obese adults than in their lean healthy counterparts [ 61 ]. An acute bout of exercise also increases lipoprotein lipase LPL activity [ 62 ].

Although this may appear counterintuitive given that LPL stimulates fat storage in adipose tissue, it makes sense given the effect of an increase in systemic and muscle LPL activity [ 63 ] is the promotion of fat uptake by muscle.

Importantly, because this latter effect is long lasting 12—18 h after a single bout of activity [ 64 ], prior exercise reduces the net delivery of dietary fat to adipose tissue arterial triacylglycerol [ 64 ] and, potentially, fat storage. In line with this, exercise training leads to a modest reduction in adiposity even in the absence of weight loss [ 65 ].

Furthermore, it decreases two variables with negative metabolic health outcomes, namely, central adiposity at least in men [ 65 ] and fat cell size at least when associated with energy deficit. Although some studies suggested a greater effect of exercise on visceral than subcutaneous adipose tissue mass, potentially because visceral adipose tissue mass is more responsive to adrenergic activation [ 66 ], meta-analysis and reviews failed to report a differential effect on fat depots [ 67 ].

The existence of an independent effect of regular exercise on visceral adipose tissue is currently debated. Finally, exercise in rodents has been shown to lower adipose inflammation, which tracks with improved whole-body insulin sensitivity [ 68 ]; however, data in humans suggest that exercise-induced changes in adipose inflammation are minimal unless paired with caloric restriction-induced weight loss [ 69 ].

In summary, adipose tissue adaptations to exercise together contribute to improved systemic metabolic homeostasis and improved exercise performance.

Muscle—adipose tissue crosstalk also exists. As reviewed elsewhere [ 26 ], skeletal muscle release of IL-6, FGF and irisin increases in response to exercise and influences adipose tissue metabolism, oxidative capacity and glucose uptake.

Following the depletion of glycogen stores, IL-6 is released by the contracting muscles during exercise. IL-6 may stimulate adipose tissue lipolysis and NEFA mobilisation during exercise, and plays a major role in the reduction of visceral adipose tissue in response to exercise training in humans [ 70 ].

However, other in vivo and in vitro studies are not as conclusive, and the role of IL-6 in adipose tissue biology is still under investigation. Similarly, the effects of muscle-released FGF and irisin on adipose tissue in humans are either still unknown or under debate. A novel exerkine produced by skeletal muscle contraction has recently been identified that targets human adipose tissue to promote lipolysis, namely, growth and differentiation factor 15 GDF15 [ 71 ].

In terms of adipose tissue, adipokines modulate inflammation, lipid and glucose metabolism, blood pressure and atherosclerosis [ 56 ]. Via its effect on fat mass, exercise can indirectly modulate levels of leptin and adiponectin, the two most well-studied adipokines, which are positively and negatively associated with fat mass, respectively.

Although leptin and adiponectin have been associated with insulin sensitivity, the specific effect of exercise training on leptin and adiponectin is unclear [ 56 ]. Recently, TGF-β2 has been shown to be secreted from adipose tissue in response to exercise and play a role in glucose homeostasis in mice [ 72 ].

Results still need to be confirmed in humans. Pancreatic glucagon and insulin orchestrate the regulation of blood glucose by facilitating glucose disposal in insulin-sensitive tissues and hepatic gluconeogenesis.

Insulin secretion is primarily adjusted according to the amount of glucose taken up by beta cells. Insulin secretion during a glucose challenge is dramatically altered by exercise undertaken during the previous days and hours in both healthy individuals and in those with insulin resistance and type 2 diabetes [ 73 ].

Exercise cessation drives up insulin secretion, while one bout of exercise can lower insulin secretion, showing that insulin secretion is tightly regulated by exercise-driven pathways [ 74 ].

The pancreas contributes to the capacity of acute exercise to increase hepatic glucose production by reducing insulin secretion hepatic insulin clearance is also likely to be important and increasing glucagon secretion [ 44 ].

In adults with impaired glucose tolerance and type 2 diabetes, exercise improves peripheral sensitivity and pancreatic beta cell function greater insulin secretion in response to circulating glucose [ 75 ].

The combination of enhanced insulin sensitivity and improved beta cell function is defined as the disposition index, which is the product of insulin sensitivity multiplied by the amount of insulin secreted in response to blood glucose [ 76 ].

Unlike drug therapies for type 2 diabetes, which typically only influence one component of the index independently, exercise has the capacity to improve the disposition index by enhancing both components [ 77 ].

Emerging evidence shows that factors secreted from contracting skeletal muscle boost beta cell insulin secretion and that the improvements in glucose homeostasis in type 2 diabetes patients in response to chronic aerobic exercise may be more closely related to improved beta cell function than insulin sensitivity [ 78 ].

Although controversies still exist and mechanisms have not been fully elucidated as yet, crosstalk between skeletal muscle and pancreatic alpha and beta cells seems to exist via myokines.

Two of the proteins that have been proposed to play a role in the muscle—pancreas crosstalk are muscle-released IL-6, because of its link with the protective effect of exercise against proinflammatory-induced beta cell loss [ 79 ], and the peroxisome proliferator-activated receptor γ coactivator 1α PGC1α -dependent myokine irisin precursor protein fibronectin type III domain-containing protein 5 [FNDC5] , because of its protective effect against beta cell apoptosis induced by lipotoxic conditions [ 80 ].

Other unknown exercise-induced myokines may also play a role in modulating beta cell function. Further work in this area could highlight novel therapeutic targets for type 2 diabetes. The skeletal muscle microvascular ensures that delivery of oxygen and substrates NEFA, triacylglycerols-rich lipoproteins and glucose matches the metabolic demands of the muscle fibres and other metabolic tissues under resting conditions and during exercise.

The microvasculature of human skeletal muscles has a complex 3D structure and is subject to a large number of complementary blood-flow regulation mechanisms, but the exact cascade of events and regulatory processes remain unknown, especially in humans [ 81 , 82 ].

Because of accessibility to tissues and the capacity to perform ex vivo preparations, rodents have served as an important model to explore the regulation of endothelial function and blood flow in the control of skeletal muscle metabolism.

Under resting conditions, insulin increases microvascular perfusion through both vasodilatory and vasoconstrictory activities. On the one hand, insulin acts on terminal arterioles and increases nutritive blood flow to skeletal muscle [ 83 ], which can also result in increased blood flow in upstream conduit arteries.

On the other hand, data from rodents shows that insulin-mediated endothelin-1 ET-1 [ 84 ] increases the vasoconstriction of arterioles that control access to the nutritive capillary beds of muscle, which receive little or no blood flow in the basal state.

ET-1 in skeletal muscle arterioles is increased in individuals with obesity or type 2 diabetes compared with healthy control individuals [ 85 ]. In addition, there is evidence in humans [ 86 ] and rodents [ 87 ] that increasing insulin resistance is associated with reduced capillary density.

Although the vascular effects of insulin seem to be markedly compromised in type 2 diabetes, exercise-mediated pathways are likely to be maintained [ 88 ]. During exercise, there are increases in cardiac output, via a rise in cardiac stroke and heart rate, and blood pressure.

Acute exercise increases muscle insulin sensitivity by a coordinated increase in insulin-stimulated microvascular perfusion and molecular signalling that improves glucose delivery and increases muscle glucose uptake and disposal [ 89 ].

This insulin-stimulated increase in microvascular perfusion is likely to be linked to the exercise-mediated increases in muscle membrane permeability to glucose and muscle blood flow [ 90 ]. The increased haemodynamic forces, i.

shear forces exerted by blood flow, are also translated by the glycocalyx layer glycoproteins and proteoglycans located on the luminal surface of endothelium into a vasodilatory response. Vasodilation and additional microvascular units expand the endothelial surface area, thus enabling the delivery of nutrients to the muscle.

Exercise training reduces resting blood pressure, heart rate and cardiac hypertrophy, improves the vasodilator response of the muscle microvasculature to insulin and exercise [ 88 ] and enlarges the microvascular network via angiogenesis and arteriogenesis [ 81 ].

These adaptations have been linked to a variety of changes in tissue metabolism and signalling, including the production and release of nitric oxide and prostacyclin from the vascular endothelium [ 82 ].

The finding that vascular endothelial growth factor B VEGF-B produced by skeletal muscle links endothelial NEFA uptake to the oxidative capacity of skeletal muscle by controlling the expression of fatty acid transporter proteins in the capillary endothelium represents a major recent discovery [ 92 ].

Regulation of the expression of these proteins may prevent lipotoxic NEFA accumulation, the dominant cause of insulin resistance in muscle fibres. The effects of exercise on endothelial adaptations and the underlying mechanisms continue to be explored and much is yet to be learnt, especially related to how adaptations occur in those with obesity or type 2 diabetes vs a non-diseased state [ 93 , 94 ].

The ability of exercise to influence endothelial transport of insulin and glucose [ 44 ] and to mediate enhanced insulin-stimulated blood flow via both the nutritive and non-nutritive routes [ 88 ] is likely to be particularly important for the prevention of type 2 diabetes.

Finally, emerging data from rodents indicate that exercise also positively impacts endothelial function and vascular biology in adipose depots [ 95 ] and is likely to play a role in other key organs, such as the brain, liver and pancreas.

We posit that the multi-tissue adaptations induced by exercise underly its powerful disease-modifying impact. Detailed studies blocking individual effects in each tissue using reductionist approaches may be needed to provide greater mechanistic insight.

That being said, because exercise activates so many pathways in so many tissues, it may be that target knockdown studies would not reveal that one metabolic pathway is essential, but, rather like the layers of an onion, multiple factors with built in redundancies contribute to the metabolic protection provided by regular exercise.

Nevertheless, it is an exciting time to investigate and observe how exercise mediates metabolic benefits beyond the mechanisms found in skeletal muscle. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK American College of Sports Medicine Position Stand.

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Eur J Clin Investig 17 2 — Data from the Korean National Health Insurance Service-National Health Screening Cohort NHIS-HEALS were utilized in this investigation.

The Korean NHIS currently collects and administers databases on the usage of all health services in Korea This cohort includes a total of , individuals who completed NHIS health screening tests and were randomly sampled. The detailed composition of this cohort was previously discussed in the previous literature The index period was from January 1, , to December 31, , as some laboratory measurements, including TG and HDL-C, which are essential for evaluating metabolic health, were collected since Additionally, individuals with missing baseline data for blood pressure BP , body mass index BMI , fasting plasma glucose FPG , and lipid levels were excluded.

Finally, , participants were included in our study. The NHIS Investigation Commission authorized the study. As this study used the collected data from NHIS-HEALS, no informed consent was acquired from each participant, and all data were thoroughly de-identified and anonymized.

This study was approved by the Hallym Sacred Heart Hospital Institutional Review Board IRB IRB No. At the baseline examination, the study cohort was divided into the metabolically healthy non-obese MHNO group, MHO group, metabolically unhealthy non-obese MUNO group, and metabolically unhealthy obesity MUO group.

According to the results from the next biannual examination, we categorized the obese participants into the stable MHO group, MHO to the MUO group, MUO to the MHO group, and stable MUO group. The study endpoint was kidney cancer diagnosis from the index date until the end of The diagnosis of kidney cancer was defined according to the International Classification of Diseases ICD CM code C Diabetes, hypertension, dyslipidemia, smoking habits, drinking habits, and physical activity were defined as previously described We adjusted for baseline age, sex, smoking habits, drinking habits, physical activity, and estimated glomerular filtration rate level.

Continuous data are presented as means ± standard deviation and categorical data as percentages. Age, sex, smoking and drinking habits, physical activity, and eGFR levels were all factored into multivariate models.

The risk of kidney cancer was first assessed based on the baseline obese metabolic health status within the MHNO group as the reference. Subsequently, the risk was analyzed further after considering the shift in metabolic health and obesity in participants with obesity at baseline.

During the follow-up phase, the stable MHNO group was used as the reference group. The SAS Enterprise Guide software was used for all statistical analyses version 7.

Table 1 displays the biochemical and clinical features of the patients at baseline, grouped by obesity categories and metabolic health status. The percentage of MHNO, MHO, MUNO, and MUO groups at baseline was Male patients were more likely to be classified as metabolically unhealthy among the study participants.

Table 1 Characteristics of the study participants according to baseline metabolic health and obesity status.

Figure 1A depicts the Kaplan—Meier curves for the cumulative incidence of kidney cancer according to metabolic health and obesity status.

Table 2 and Figure 1B describe the incident kidney cancer risk according to the obese metabolic health phenotype at baseline examination but do not consider the change over time. The risk of incident kidney cancer was not substantially greater in the MHO or MUNO groups than in the MHNO group.

Abbreviations: MHNO, metabolically healthy non-obese; MHO, stable metabolically healthy obesity; MUO, metabolically unhealthy obesity; MUNO, metabolically unhealthy obesity.

Table 2 Risk of incident kidney cancer according to baseline metabolic health and obesity status. Furthermore, we assessed the implication of phenotypic transitions on the risk of kidney cancer.

Then, we calculated the multivariate-adjusted HRs for incident kidney cancer considering transitions in the metabolic health status Table 3 ; Figure 1B. The stable MHNO group was used as the referent group in the analysis. The participants with MUO at baseline and follow-up i.

The participants who moved from MHO to MUO had a substantially greater risk of kidney cancer than did those in the reference group, with a multivariate-adjusted HR of 1.

In contrast, neither the stable MHO group multivariate-adjusted HR, 1. The MHNO to MUNO group and the stable MUNO group were not at increased risk of incident kidney cancer multivariate-adjusted HR, 1. Figure 1 depicts the multivariate-adjusted HRs for incident kidney cancer.

Table 3 Risks of incident kidney cancer according to the transition from metabolically healthy to unhealthy status among participants with obesity in reference to the stable MHNO group. Associations of the obese metabolic health phenotypes with kidney cancer were generally consistent across the subgroups according to the clinical variables, including age, sex, smoking, drinking, and exercise Figure 2.

In specific, the hazardous effect of phenotypic transition from MHO to MUO was particularly evident in men and smokers multivariate-adjusted HR, 2.

Across all subgroups, obese participants who stayed at metabolically heath status i. Figure 2 Subgroup analyses for the risk of kidney cancer according to the phenotypic transitions. The covariates are excluded from the adjustment in the corresponding subgroup analyses.

This study suggests that metabolic unhealthiness could contribute to kidney cancer risk in obese patients. We found that maintaining or recovering metabolic health reduced the incidence of kidney cancer, whereas the persistence of a metabolically unhealthy status or the shift to metabolic unhealthiness substantially increased the risk of kidney cancer.

Our findings indicate that metabolic unfitness, rather than the presence of obesity, contributes to incident kidney cancer.

More recently, an increased risk of kidney cancer due to obesity has been consistently reported. In Japan, a population-based study demonstrated a U-shaped association between BMI and the risk of renal cell cancer RCC Moreover, a population-based nested case-control study reported a positive relationship between BMI and the risk of RCC among Chinese men; this study showed an increased odds ratio of 1.

Positive linear relationships were found in the South Korean population between BMI or waist circumference and the risk of incident kidney cancer In particular, individuals with both general obesity and central obesity had a 1.

These studies support the significant implication of obesity in the risk of kidney cancer. However, these studies did not take metabolic health status into consideration. Here, we found that the incident kidney cancer risk among obese individuals depended on their metabolic health status.

Based on the baseline metabolic health status, the HR for kidney cancer in the MHO group was not significantly higher than that in the MHNO group Table 2 ; Figure 1. However, when the phenotypic transition was considered, the probability of incident kidney cancer was significantly higher in individuals who were in the MHO group at baseline but transitioned to an MUO status and in those who maintained a steady MUO phenotype Table 3 , Figure 1.

In contrast, the stable MHO group or the MUO to MHO group were not at a higher risk of developing kidney cancer even though they were still obese Table 3 ; Figure 1 , which were consistently observed in subgroup analyses Figure 2. These data imply that metabolic health, not obesity itself, is a decisive factor in kidney cancer incidence.

Previously, in the MetS and cancer project, several metabolic factors or a combination of risk factors were found to be associated with an increased risk of RCC Similarly, a nationwide study in Korea reported that MetS was closely related to the risk of kidney cancer in both sexes; specifically, patients with MetS had significantly increased HRs for incident kidney cancer, and this relationship was consistent in both men and women men: HR, 1.

Collectively, metabolic disturbances induced by disproportional body fat distribution could be the main contributor to incident kidney cancer in participants with obesity. In our study, we suggested that the metabolic health status was a largely modifiable risk factor.

Prior studies have reported that approximately one-third of individuals with obesity experienced changes in their metabolic health status 25 — 28 , potentially affecting their health outcomes. Therefore, recent studies have adopted novel approaches to reflect the influence of phenotypic transitions on diverse outcomes.

For example, Kim et al. have discovered that maintaining metabolic fitness could protect the study participants from developing type 2 diabetes, regardless of their body weight Moreover, our research team discovered that phenotypic alterations in MHO increased cardiovascular risk, CKD incidence, and mortality 25 , More recently, we demonstrated that metabolic health status was a deciding factor for the occurrence of colorectal cancer, for which obesity was known as a major risk factor Herein, we added another evidence that we should consider the dynamic nature of metabolic health status in risk assessment and management in obese patients.

Although the specific mechanism through which obesity raises the risk of kidney cancer is yet to be determined, the altered circulating levels of adipokines 30 , the chronic inflammatory status 31 , and modulation of host immunosurveillance 30 , and insulin resistance leading to increased insulin and insulin-like growth factor IGF -1 levels, which are involved in carcinogenesis may play a significant role 6 , 32 , Although our results cannot establish the mechanism, our data provide evidence that metabolic unhealthiness associated with obesity plays a pivotal role in the increased risk of kidney cancer in patients with obesity.

Therefore, further investigations on the pathophysiologic changes in different metabolic health obese phenotypes are needed. This study had some limitations.

First, since the study population was primarily Korean, we cannot generalize our study results to other ethnic groups.

Second, the study did not consider the phases of kidney cancer or its pathologic type. Thirdly, an accurately measured increase in lower body fat mass is now recognized as an independent indicator of metabolic health Therefore, the identification of distinct fat distribution phenotypes using relevant measurements, such as hip circumference, could provide better insight into the relationship between adiposity and cancer risk; however, we were unable to investigate the impact of these measurements on KC risk in our analyses because the NHIS data did not include any measurement for lower body fat mass.

Future study on the significance of lower body fat mass in obesity-related cancer would give greater precision to our understanding of the clinical implications of metabolic health in obese populations. Despite these limitations, our study has strengths in that we used a large nationwide cohort and explained the effects of dynamic metabolic health on the incidence of kidney cancer in obese adults.

Our methodology revealed the implication of metabolic unhealthiness on kidney cancer risk and therefore suggested that being metabolically healthy should be prioritized to lower the kidney cancer risk in obese patients.

Our findings identified metabolic unhealthiness as a risk factor for kidney cancer risk in individuals with obesity. Furthermore, our results suggest that the dynamic metabolic health status should be considered as significantly affecting the kidney cancer risk.

do , approval number: NHIS The studies involving human participants were reviewed and approved by Hallym Sacred Heart Hospital Institutional Review Board IRB. The ethics committee waived the requirement of written informed consent for participation. Conceptualization, YC and CJ; methodology, Y-JK; software, Y-JK; validation, YC and Y-JK; formal analysis, YC and Y-JK; investigation, YC; resources, YC; data curation, CJ; writing—original draft preparation, YC; writing—review and editing, HK, J-YP, WL, Y-JK, and CJ; visualization, Y-JK; supervision, YC.

All authors have read and agreed to the published version of the manuscript. This research was supported by the Hallym University Research Fund HURF The authors thank Editage for the English language review. We would like to thank the Korean National Health Insurance Service and all the participants of the study and health check-up.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. BMI, body mass index; BP, blood pressure; FPG, fasting plasma glucose; ICD, International Classification of Diseases; IRB, Hallym Sacred Heart Hospital Institutional Review Board; MHNO, metabolically healthy non-obese; MHO, metabolically healthy obesity; MHO, metabolically healthy obesity; MUNO, metabolically unhealthy non-obese; MUO, metabolically unhealthy obesity; NHIS-HEALS, Korean National Health Insurance Service-National Health Screening Cohort; RCC, renal cell cancer.

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Metavolic among Mftabolic can Mtabolic to identify opportunities for the reduction Nitric oxide and cellular health inequalities Nitric oxide and cellular health cardiometabolic Metabolic health articles. The present cross-sectional analysis articlee meta-analysis aim to Nutrient-rich bites to what extent obesity traits, socioeconomic, Glutathione and exercise recovery behavioral factors determine poor hea,th health across body Clinically proven supplements index Healfh categories in two urban population-based samples from Central Europe. Data from the CoLaus ~6, participants; Lausanne, Switzerland and the Kardiovize Brno ~2, participants; Brno, Czech Republic cohorts. For each cohort, logistic regression analyses were performed to identify the main determinants of poor metabolic health overall and stratified by body mass index BMI categories. The results of each cohort were then combined in a meta-analysis. We first observed that waist circumference and body fat mass were associated with metabolic health, especially in non-obese individuals. For Nitric oxide and cellular health information about PLOS Subject Areas, click here. Lifestyle habits associate Metabolc metabolic health in overall populations. Whether Nitric oxide and cellular health association is Nutrition for athletes among Mdtabolic with a Energy nutritional status srticles been srticles studied. We aimed to i determine the prevalence of metabolic phenotypes in Chile, and ii determine the association between lifestyle habits and metabolic health according to the nutritional status. The National Health Survey of Chile — was analyzed. The nutritional status was defined as normal weight In subjects with obesity, the highest quartile of moderate-vigorous physical activity was associated with reduced odds of having a metabolically unhealthy phenotype 0.

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