Hyperglycemia and inflammation -
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Article Navigation. Cardiovascular and Metabolic Risk August 01 Diabetes, Hyperglycemia, and Inflammation in Older Individuals : The Health, Aging and Body Composition study Nathalie de Rekeneire, MD, MS ; Nathalie de Rekeneire, MD, MS.
This Site. Google Scholar. Rita Peila, PHD ; Rita Peila, PHD. Jingzhong Ding, PHD ; Jingzhong Ding, PHD. Lisa H. Colbert, PHD ; Lisa H. Colbert, PHD. Marjolein Visser, PHD ; Marjolein Visser, PHD. Ronald I. Shorr, MD, MS ; Ronald I.
Shorr, MD, MS. Stephen B. Kritchevsky, PHD ; Stephen B. Kritchevsky, PHD. Lewis H. Kuller, MD, DRPH ; Lewis H. Kuller, MD, DRPH. Elsa S. Strotmeyer, PHD ; Elsa S. Strotmeyer, PHD. Ann V. Schwartz, PHD ; Ann V. Schwartz, PHD. Bruno Vellas, MD, PHD ; Bruno Vellas, MD, PHD. Tamara B.
Harris, MD, MS Tamara B. Harris, MD, MS. Address correspondence and reprint requests to Nathalie de Rekeneire, MD, Laboratory of Epidemiology, Demography and Biometry, National Institute on Aging, Gateway Building, Suite 3C, Wisconsin Ave.
E-mail: rekenein nia. Diabetes Care ;29 8 — Article history Received:. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Table 1— Baseline characteristics by diabetes and hyperglycemic status.
Data are means ± SD or median interquartile range unless otherwise noted. DXA, dual-energy X-ray absorptiometry. View Large. Table 2— Plasma levels of inflammatory markers of the diabetic and the hyperglycemic groups compared with the NGT group.
Inflammatory marker. P value. Table 3— Multivariate analyses for the association of hyperglycemia and diabetes with inflammation.
Risk of high inflammation level associated with diabetes and hyperglycemic status. Model 1. Model 2. Model 3. Relationship between glycemic control A1C and inflammation in diabetes. High CRP 1. Bruunsgaard H, Pedersen M, Pedersen BK: Aging and proinflammatory cytokines.
Curr Opin Hematol. Pickup JC, Crook MA: Is type II diabetes mellitus a disease of the innate immune system? Nilsson J, Jovinge S, Niemann A, Reneland R, Lithell H: Relation between plasma tumor necrosis factor-α and insulin sensitivity in elderly men with non-insulin-dependent diabetes mellitus.
Arterioscler Thromb Vasc Biol. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW: C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Ford ES: Body mass index, diabetes, and C-reactive protein among U.
Diabetes Care. Frohlich M, Imhof A, Berg G, Hutchinson WL, Pepys MB, Boeing H, Muche R, Brenner H, Koenig W: Association between C-reactive protein and features of the metabolic syndrome: a population-based study. Temelkova-Kurktschiev T, Siegert G, Bergmann S, Henkel E, Koehler C, Jaross W, Hanefeld M: Subclinical inflammation is strongly related to insulin resistance but not to impaired insulin secretion in a high risk population for diabetes.
Barzilay JI, Abraham L, Heckbert SR, Cushman M, Kuller LH, Resnick HE, Tracy RP: The relation of markers of inflammation to the development of glucose disorders in the elderly: the Cardiovascular Health Study.
Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM: C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus.
Hotamisligil GS, Arner P, Caro JF, Atkinson RL, Spiegelman BM: Increased adipose tissue expression of tumor necrosis factor-α in human obesity and insulin resistance. J Clin Invest. Kern PA, Saghizadeh M, Ong JM, Bosch RJ, Deem R, Simsolo RB: The expression of tumor necrosis factor in human adipose tissue: regulation by obesity, weight loss, and relationship to lipoprotein lipase.
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J Clin Endocrinol Metab. American Diabetes Association: Diagnosis and classification of diabetes mellitus Position Statement. Genuth S, Alberti KG, Bennett P, Buse J, Defronzo R, Kahn R, Kitzmiller J, Knowler WC, Lebovitz H, Lernmark A, Nathan D, Palmer J, Rizza R, Saudek C, Shaw J, Steffes M, Stern M, Tuomilehto J, Zimmet P, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Follow-up report on the diagnosis of diabetes mellitus.
This adds our next point to the mix—fat tissue. Take being overweight, for instance. It can make it harder for you to control your blood glucose.
This is because high levels of fat tissue can cause low-grade inflammation , which may negatively impact glucose levels. Research indicates that among older people and those with diabetes, there were higher levels of two pro-inflammatory cytokines compared to those in younger, non-diabetic people.
Cytokines are small proteins that help with cell signaling. These cytokines measured after an overnight fast were linked to aging, diabetes, and increased truncal fat mass. This suggests they were at least in part produced by that central, visceral fat.
There are many steps you can take to reduce inflammation and improve overall health. If it is, a medical professional will help you find a solution to help you reduce or control it.
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Reviewed by. Kara Collier, RDN, LDN, CNSC. What You Need to Know About Inflammation. Related Article. Read More. Engage with Your Blood Glucose Levels with Nutrisense Your blood sugar levels can significantly impact how your body feels and functions.
Take Our Quiz. Reviewed by: Kara Collier, RDN, LDN, CNSC. Learn more about Kara. Cell counts were performed with trypan blue Gibco ® by Life Technologies, Thermo Fisher Scientific, Waltham, Massachusetts, USA. After priming, cells were cultured at a standard concentration 5.
We used RIPA lysis buffer to lysate the BMDM. For protein transfer to the nitrocellulose membrane we used a semi-dry system using transfer buffer 25 mM Tris; mM glycine; 0. The revelation was performed using ECL enhanced chemiluminescence - ECL; Amersham, Arlington Heights, IL on the Amersham Imager blot and gel imager equipment Amersham, Buckinghamshire, United Kingdom.
The primary anti-mouse LC3B and anti-mouse Beclin-1 antibodies purchased from Cell Signaling Technology Cell Signaling Technology ® , Danvers, Massachusetts, USA were used to detect the target proteins. Relative band densities were determined by densitometric analysis using ImageJ software.
The results were evaluated by analysis of variance two-way ANOVA followed by the Tukey-Kramer multiple comparisons test using GraphPad software 9. To obtain BMDM from a hyperglycemic environment, we used an alloxan T1DM animal model.
After 10 days of induction with alloxan, when compared to the control group, the animals showed a loss of body weight Figure 1 , and an increase in blood glucose Figure 2. Figure 2 Evolution of blood glucose after induction of diabetes: Diabetic animals showed an increase in blood glucose after 10 days of induction with the diabetogenic agent.
To assess the autophagy pathway in BMDM, the protein expression of LC3B and Beclin-1 were evaluated by the Western Blotting method, after 30 minutes Figure 3A. We identified that ND-BMDM had an increase in Beclin-1 expression in hyperglycemic medium without stimulation Figure 3B.
Figure 3 Evaluation of the autophagy pathway. Results represent mean ± SEM. After 2, 4, 6 and 24 hours of incubation, BMDM from diabetic and non-diabetic animals released a more significant amount of IL-6 at concentrations of 5.
At 6 hours, we observed that D-BMDM increased the secretion of this cytokine in hyperglycemic medium with stimulation Figure 4D. Figure 4 IL-6 secretion by ND-BMDM and D-BMDM with Nigericin priming and LPS stimulation. IL-6 release after A 30 minutes with different glucose concentrations.
B 2 hours with different glucose concentrations. C 4 hours with different glucose concentrations. D 6 hours with different glucose concentrations. E 24 hours with different glucose concentrations.
IL-6 measurement was performed by enzyme-linked immunosorbent assay. Cytokine measurements were performed to measure the secretion of TNF-α. After 30 minutes, 2, 4, 6, and 24 hours of incubation, BMDM from diabetic and non-diabetic animals released higher levels of TNF-α at concentrations of 5.
Figure 5 TNF-α secretion by ND-BMDM and D-BMDM with Nigericin priming and LPS stimulation. TNF-α measurement was performed by enzyme-linked immunosorbent assay.
It was observed that after 30 minutes, 2, 4, 6 and 24 hours of incubation, BMDM from diabetic and non-diabetic animals released a more significant amount of IL-1β at concentrations of 5. At 30 minutes, D-BMDM with stimulation secreted IL-1β more than ND-BMDM under the same conditions Figure 6A.
At 4 and 24 hours, D-BMDM in hyperglycemic medium with stimulation had an increase in the secretion of this cytokine when compared with ND-BMDM in the same condition Figures 6C and E. We also assessed Nitric Oxide and IL levels, but no significant differences were observed Supplementary Figures 1 and 2.
Figure 6 IL-1β secretion by ND-BMDM and D-BMDM with Nigericin priming and LPS stimulation. IL-1β release after A 30 minutes with different glucose concentrations. IL-1β measurement was performed by enzyme-linked immunosorbent assay. It is already described that patients can establish a chronic inflammation state under diabetic conditions, characterized by a decompensated secretion of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6, and it is suggested as the major cause of comorbidities related to diabetes Furthermore, it has been identified that peritoneal macrophages, when exposed to high levels of glucose secrete greater amounts of TNF-α, IL-1β, IL-6 and IL in response to high glucose concentrations 34 , It has also been reported by Cheng et al.
A study showed that, when cultivated in a hyperglycemic medium, BMDM secreted a more significant amount of TNF-α, but the expression of IL-6 under the same conditions was reduced However, our studies observed that high glucose levels alone were not enough to stimulate the secretion of TNF-α, IL-1β and IL-6 by macrophages.
On the other hand, when stimulated with LPS, there was a significant increase in the secretion of these cytokines. Furthermore, Tessaro et al.
Our findings corroborate with previous studies where it was reported that high glucose concentrations 15mM, 25mM do not alter the expression of TNF-α and IL-6 by macrophages, however, when stimulated with LPS, the secretion of these cytokines increase, showing that hyperglycemia it is not a sufficient stimulus for the high production of these cytokines by macrophages 35 , High glucose conditions can cause mitochondrial dysfunction, increase the production of ROS and activates the autophagy pathway 29 , 39 — Furthermore, LC3b protein is involved in mitophagy 42 , a process that removes dysfunctional mitochondria by the autophagic machinery Therefore, we suggest that the high levels of LC3b and beclin-1 expression by ND-BMDM, when compared to D-BMDM identified in this study are due to the normal cellular regulation process in response to stress caused by the hyperglycemic condition, suggesting that the autophagy pathway is impaired in macrophages from diabetic animals, which reinforces that these cells are sensitized when exposed to the hyperglycemic state in vivo 44 — Furthermore, we observed a reduction in LC3b expression by ND-BMDMs and D-BMDMs stimulated and in hyperglycemic conditions.
Our findings corroborate with study that showed a decrease in LC3b expression in THPderived macrophages exposed to high concentrations of glucose with the inflammasome pathway activated However, in this study performed by Dai et al. It was already described that alterations in the autophagy pathway can directly interfere in the inflammatory response of diabetic individuals, making them susceptible to the development of infections 12 49 , Combined with that, nigericin is known to be an inducer of the NLRP3 inflammasome pathway, where the formation of this complex results in the production of IL-1β In our studies, we observed that macrophages from diabetic animals, when stimulated, secreted a greater amount of the cytokine IL-1β, showing that there is an exacerbated production of this cytokine when stimulated by LPS.
Since the relationship between the autophagy process and IL-1β cytokine secretion has been widely studied, it has been reported that this process is responsible for sequestering this cytokine and preventing its secretion 52 , and a negative regulation of this pathway can lead to an increase of IL-1β release 21 , These results suggest that, besides macrophages of diabetic animals being previously sensitized by hyperglycemia, the failure of the autophagy machinery may be contributing to the decompensated secretion of this cytokine.
With the changes observed in our study, we can observe that hyperglycemia plays an essential role in the inflammatory response of BMDMs from diabetic mice, since the high concentration of glucose with LPS stimulation led to significant changes in the secretion of inflammatory mediators and in the autophagy process, having a direct effect on cellular homeostasis.
The high concentration of glucose alters the inflammatory pathways in macrophages after LPS stimulation, disrupting the secretion of pro-inflammatory cytokines by these cells, leading to an impaired inflammatory response against infections.
Furthermore, we observed that the sensitization caused by hyperglycemia in macrophages can downregulate the expression of proteins involved in the autophagy pathway, impairing cellular homeostasis, suggesting the main role of this mechanism over macrophages under diabetic conditions.
The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation. ES and JM conceived and designed the experiments. ES, LQ, JG, KP and RB performed the experiments. ES, LQ, SE and JM analyzed the data.
ES and JM wrote the paper with the assistance and contribution of all the authors. All authors contributed to the article and approved the submitted version. The authors would like to thank Silene Migliorini and Fabiana Teixeira for providing the acquisition, organization of reagents used in this project and assistance at the laboratory.
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.
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Cell Death Differ 26 4 — Jung S, Jeong H, Yu SW. Autophagy as a decisive process for cell death. Exp Mol Med 52 6 — Wang Y, Li YB, Yin JJ, Wang Y, Zhu LB, Xie GY, et al. Autophagy regulates inflammation following oxidative injury in diabetes.
Nathalie de RekeneireRita InfoammationJingzhong Inflammstion Hyperglycemia and inflammation, Lisa H. ColbertMarjolein VisserRonald I. ShorrStephen B. KritchevskyLewis H. KullerElsa S. StrotmeyerAnn V.Nathalie anc RekeneireCranberry salsa recipes PeilaJingzhong HyperglycsmiaLisa H. ColbertMarjolein VisserRonald Inflxmmation. ShorrStephen Hypergljcemia. KritchevskyLewis Superfoods and antioxidants. KullerElsa S.
StrotmeyerAnn Hyperglycemia and inflammation. Detoxifying the lymphatic systemBruno VellasTamara B. Harris; Diabetes, Hyperglycemia, and Inflammation in Older Individuals : The Health, Aging and Body Hyperg,ycemia study.
Diabetes Care 1 August ; 29 8 : — RESEARCH DESIGN AND METHODS Hyperglcyemia data from the Hypdrglycemia, Aging and Body Composition study included inflanmation, well-functioning black and ihflammation participants, aged 70—79 years. Odds ratios for elevated CRP were 2. Among Hypergoycemia participants, higher levels of HbA 1c were associated with Hyperglycenia levels of all three markers of inflammation, but only Hyperglycemia and inflammation remained significant after full adjustment.
Aging snd associated with infkammation inflammatory activity including proinflammatory and anti-inflammatory cytokines and acute-phase proteins 1. Previous studies suggested that low-grade inflammqtion inflammation ifnlammation a BIA body impedance analysis in the pathogenesis of some glucose disorders intlammation adults 2.
Several cross-sectional studies showed that Hyperglycmia resistance and type 2 diabetes inf,ammation associated with infoammation levels of C-reactive Hyperglyfemia CRPinterleukin-6 Inflxmmationand tumor necrosis factor-α TNF-α Inflammation and chronic pain management, markers of subclinical systemic inflammation 3 — 8.
Abd, various inflwmmation studies have shown that elevated levels of CRP Hyperblycemia IL-6 predict the development of type 2 diabetes Hypeerglycemia — Few studies Hyprglycemia date have focused on the association between diabetes and Hyperglycemja in older individuals, and to our knowledge Hyperglycsmia of these Hypergpycemia studied Hylerglycemia relationship of Proper nutrition for sports training fasting Hypergglycemia IFG or impaired glucose tolerance IGT with inflammafion in aging.
Hylerglycemia underlying mechanism inflamation still unknown. Hyperglycemiia body mass may Hyyperglycemia an important mediator to explain these relations. It has been shown that inflxmmation express and secrete TNF-α.
TNF-α is overexpressed Hyperglyycemia the adipose and muscle tissues of obese and insulin-resistant nondiabetic subjects, inf,ammation Hyperglycemia and inflammation overexpression is positively correlated with insulin resistance 13 — IL-6 is produced in a variety infoammation tissues Metabolism boosting breakfast recipes adipocytes.
Inflamkation further hypothesized that poorer glycemic control in diabetic individuals would be jnflammation with higher levels of Hyperglycemmia compared with those with better glycemic ajd.
Data Hyperglycemiz from the Health, Aging and Inflammaton Composition Health ABC Hyoerglycemia, a 9-year longitudinal cohort study designed to investigate the relationships among anti-viral laundry detergent conditions, body composition, social and behavioral Micronutrient deficiency effects, and functional decline.
Energy boosters for weight loss percent of the cohort is black. Whites were recruited from a random sample Hypergycemia Medicare beneficiaries residing in designated zip code areas surrounding the Pittsburgh, Pennsylvania, and Memphis, Sweet potato energy bites, field centers.
Blacks were recruited from all infalmmation black community residents in these Hyperlycemia areas. All potential participants ihflammation a mailing, followed by a telephone eligibility screen, with a second inflammatino screen inlfammation the inflammatikn of the clinic visit.
We excluded 1 inflammagion who reported difficulty walking a quarter mile, walking Hyperglycemua 10 steps without inglammation, or performing Hyeprglycemia activities of daily living and inflmamation reporting using a cane or other equipment to inflammxtion around; 2 those with known life-threatening cancers under active Hhperglycemia in inclammation past 3 infalmmation and 3 inflammaiton who inflammagion to leave the area within 3 years.
A detailed interview on nad demographics, health behaviors, inflmmation of socioeconomic status, and inflqmmation service utilization Hypreglycemia Hyperglycemia and inflammation in the home.
Participants underwent a clinical Hhperglycemia that included Alternate-day fasting and psychological well-being and Hyperglycemia and inflammation composition Hyperglhcemia and Hyperglycemia and inflammation of weight-related health conditions as well as physical performance measures.
The baseline home interview and clinic-based examination were carried out Hyperglycemai April and June All participants Hyperlgycemia written informed consent, and all protocols were approved by the institutional review boards at both study sites.
The detectable Hyyperglycemia for IL-6 by HS Quantikine kit was Chromium browser bookmarks. Serum levels of CRP were measured in duplicate by an enzyme-linked immunosorbent assay inflakmation on purified protein and polyclonal anti-CRP antibodies Calbiochem, San Inflammagion, Hyperglycemia and inflammation.
The CRP assay was standardized according to Hhperglycemia World Health Organization First International Reference Standard with a sensitivity of 0. Inflammaiton were asked whether Hyperglyvemia doctor had ever told them of a diagnosis of diabetes, excluding the occurrence of diabetes during pregnancy in women.
Prescribed and over-the-counter medications used in the preceding 2 weeks were brought to the clinic by the participants. All participants without diabetes underwent a g oral glucose tolerance test OGTT performed after at least an 8-h overnight fast.
We used information on reported age at diagnosis to define diabetes duration; only those participants considered diabetic as a result of fasting glucose or OGTT were considered to have new-onset diabetes. Poor glycemic control was defined by the level of HbA 1c A1C Bio-Rad.
Biological specimens were processed according to standardized protocols by the Laboratory of Clinical Biochemistry at the University of Vermont. Covariates included age, sex, race, clinic site, education, body height, total body fat, visceral fat, health status, use of anti-inflammatory drugs, statins, and estrogen, smoking, and alcohol intake.
Body height was measured to the nearest millimeter using a wall-mounted stadiometer. Total body fat kilograms was measured by dual-energy X-ray absorptiometry QDR A, software version 8.
Visceral fat at the L4-L5 level was quantified from computerized tomography scanning of the abdomen. Scans were performed on a General Electric Advantage in Pittsburgh and a Siemens Somatron and Picker PQS in Memphis. All data from the computerized tomography scans were analyzed at the University of Colorado Health Sciences Center according to a standardized protocol Several diseases with a potential association with inflammation or with diabetes were considered in the analysis, including cardiovascular disease, hypertension, peripheral arterial disease, renal insufficiency, arthritis, and respiratory disease.
For hypertension, we used self-report, medications, and measured blood pressure. Current anti-inflammatory, statin, and estrogen use were assessed at the clinic visit. Of the Health ABC participants, 2, had complete information on inflammation markers and glucose parameters and constituted the study sample for the analysis.
For all the other categorical variables with missing data, a separate category for those with missing data within each variable was used so that all observations remained in the analysis.
Because the distributions of CRP, IL-6, and TNF-α were skewed, median values with 25th—75th percentile ranges were reported, and we used the t test on log-transformed values to compare the different groups. The first model was adjusted for age, race, sex, education, smoking, alcohol intake, and clinic site.
The second model was adjusted additionally for total body fat and visceral fat. When total body fat was included in the models, an additional adjustment was made for body height to normalize total body fat. The fully adjusted model took into account the comorbidities and medication use.
Because high levels of two or more inflammatory markers represent a more specific indicator of systemic inflammation 21 than a high level of just one, a composite inflammation index was calculated.
The high extreme group included those who had at least two of the inflammatory markers in the highest quartile. The low extreme group, considered as the reference category in the analysis, included participants with all three inflammation markers below or equal to the median, and the intermediate group included individuals with all other possible combinations of cytokine levels.
Statistical analyses were performed using SAS software SAS Institute, Cary, NC. Among the 2, participants with complete information, Participants with diabetes were more likely to be male and black and had a lower level of education Table 1.
Diabetic individuals had more cardiovascular diseases and peripheral arterial disease than their counterparts with NGT. Plasma levels of inflammatory markers were moderately correlated. The correlation between IL-6 and TNF-α was 0.
Table 2 shows the plasma concentrations of the inflammatory markers by diabetes and hyperglycemic status. Multivariate analyses on the risk of high inflammation associated with diabetes and hyperglycemic status are shown in Table 3. Compared with those without diabetes, after adjustments for age, sex, race, smoking status, alcohol intake, education, and site, diabetic individuals continued to exhibit higher inflammation levels with an OR of 1.
Diabetic women compared with those without diabetes had an OR of 2. The association between diabetes and higher inflammation level was weakened by adjustments for body fat and visceral fat, inflammation, and diabetes comorbidities and potential confounders Table 3models 2 and 3 but still remained significant, except for high CRP in men.
Total body fat and visceral fat accounted for most of the attenuation of the association between diabetes and higher inflammation. Adjustment for body fat and visceral fat attenuated these associations so that only IL-6 remained statistically significant. Diabetic participants with poorer glycemic control also showed higher inflammatory levels of CRP with an OR of 1.
Adjustment for body fat and visceral fat attenuated the relationships, but they still remained statistically significant even with further adjustment for comorbidities and potential confounders.
The association between diabetes and a high level of inflammation remained even after adjustments for possible confounders, such as demographics, lifestyle habits, total body fat, visceral fat, and comorbidities.
We also found that the association between diabetes and inflammation was stronger when we used a composite inflammation index of the three inflammatory markers, which is a more specific indicator of systemic inflammation Older diabetic individuals have a 2.
For the association between diabetes and CRP, we observed a sex difference; the association was stronger in women and not statistically significant in men.
This sex difference was not found with any of the other inflammatory markers. Our results are consistent with those for other cross-sectional studies in younger populations in which an increase of CRP was found with diabetes 578 and increases of CRP, IL-6, and TNF-α were found with IGT 22 It has also been shown in several longitudinal studies that inflammation is a predictor of development of diabetes 91012 Thus, the link between diabetes and inflammation could be due to a reciprocal process, in that inflammation may contribute to diabetes onset and diabetes may then contribute to continued inflammation.
In addition, hyperglycemia is known to mediate formation of advanced glycosylation end products. These advanced glycosylation end products may also contribute to inflammation, producing a chronic stimulation for secretion of cytokines Adipose tissue could be a mediator in the relationship.
Data emerging over the past several years have established the fact that adipocytes express and secrete the cytokine TNF-α and that enlarged adipocytes from obese animals and humans overexpress this factor The findings from the Third National Health and Nutrition Examination Survey showed a higher prevalence of increased levels of CRP in both overweight and obese participants Adiposity, in particular visceral adipose tissue, has been found to be a key promoter of low-grade chronic inflammation 28 Obesity appears to be a state of chronic inflammation with increased production of cytokines and other acute-phase reactants that play a crucial role in regulation of systemic insulin action; it has been shown that TNF-α—deficient mice show increased insulin action Is the elevation of inflammatory markers the result of vascular and renal disease due to diabetes or a causal pathway?
Numerous studies showed an association between cardiovascular diseases with inflammation, and a higher CRP level is associated with increased risk of development of vascular disease 31 — CRP and IL-6 are also known to increase with declining kidney function, even before end-stage renal disease occurs 35 — Trials to study decreases of inflammation in diabetes or cardiovascular disease events are still lacking.
A better understanding of the actions of cytokines with other factors in the pathogenesis of diabetes may lead to improved understanding of its cause and open new approaches for its prevention. We found an association between poor glycemic control and an increased level of CRP.
Several studies showed that cytokine levels CRP, IL-6, and TNF-α are related to glycemic control 38 — Improvement of glycemic control has an inconsistent beneficial impact on the level of inflammatory markers.
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| Inflammation and Blood Glucose Levels | Resources ADA Hyperglycemia and inflammation Hyperhlycemia ADA Wnd Directory Diabetes. Article Navigation. Animals underwent control surgery or vagal stimulation VSand serum TNF at 1. Article CAS PubMed Google Scholar Borst SE, Bagby GJ. Rodica Pop-Busui |
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