Insulin Resistance, Inflammation, and Serum Fatty Acid Composition

Fernández-Real, José Manuel; Broch, Montserrat; Vendrell, Joan; Ricart, Wifredo

doi:10.2337/diacare.26.5.1362

Cited by 185 publications

(146 citation statements)

References 38 publications

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“…[41] The level of TNF-alpha in the colon of rats was almost four-fold lower after supplementation. The findings that plasma FAs composition is linked to inflammatory activity in subjects with insulin resistance [42] suggest possible associations in MHD patients. However, the current study identified only a strong association between changes in n-6 PUFAs: n-3 PUFAs ratio and TNF-alpha levels after supplementation with n-3 PUFAs.…”

mentioning

confidence: 97%

Effects of N-3 PUFAs Supplementation on Insulin Resistance and Inflammatory Biomarkers in Hemodialysis Patients

et al. 2007

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Aims/Hypothesis. It was suggested that polyunsaturated n-3 fatty acids (n-3 PUFAs) could improve insulin sensitivity and have an anti-inflammatory effects in overall population. This study investigates a possible effect of n-3 PUFAs supplementation on the insulin sensitivity and some inflammatory markers; hence, patients with chronic renal failure (CRF) on maintenance hemodialysis (MHD) are presented with insulin resistance. Methods. This study explored the ratio between red blood cells (RBC) phospholipid long chain fatty acids (LC FAs) and components of metabolic syndrome (MeS) in 35 patients (mean age 54.50 ± 11.99 years) with CRF on MHD. Furthermore, the effects of omega-3 FA eight-week's supplementation (EPA+DHA, 2.4g/d) on the MeS features and inflammatory markers TNF-alpha, IL 6, and hsCRP were examined. Results. Supplementation increased EPA and DHA levels in RBCs (p = 0.009 for EPA and p = 0.002 for DHA). Total n-6 PUFAs: n-3 PUFAs ratio tended to be lower after supplementation (p = 0.31), but not significantly. Data revealed a significant decrease of saturated FAs (SFA) (p = 0.01) as well as total SFA: n-3 PUFAs ratio during the treatment (p = 0.04). The values of serum insulin and calculated IR index-IR HOMA were reduced after supplementation (p = 0.001 for both).There was a significant decrease in the levels of all inflammatory markers (p = 0.01 for TNF alpha, p = 0.001 for IL 6, p = 0.001 for hsCRP, and p = 0.01 for ferritin). In multivariate regression analysis, only the changes in n-6 PUFAs: n-3 PUFAs ratio independently contributed to 40% of the variance in IR HOMA. The impact of changes in PUFAs level in RBCs membrane phospholipid fatty acids on inflammation markers was also registered. The changes in n-6: n-3 PUFAs ratio independently contributed to 18% of the variance in TNF alpha. Conclusion. It was concluded that the EPA and DHA moderate dose administration in the patients with CRF on MHD had a beneficial effect on insulin resistance decrease. The anti-inflammatory effects of the supplemented PUFAs were also presented.

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confidence: 97%

Effects of N-3 PUFAs Supplementation on Insulin Resistance and Inflammatory Biomarkers in Hemodialysis Patients

et al. 2007

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“…Effect of IL-6 on Insulin Signaling in Myotubes-Increases in circulating IL-6 plasma levels have been associated with insulin resistance in humans (11)(12)(13)(14), and IL-6 has been demonstrated to reduce insulin-stimulated signaling in human hepatocytes, e.g. by decreased tyrosine phosphorylation of IRS-1, by decreased association of the p85 subunit of phosphatidylinositol 3-kinase with IRS-1, by subsequently impaired phosphorylation of Akt on serine 473, and by reduced glycogen synthesis (19,20).…”

Section: Il-6 Signaling In Human Myotubes-mentioning

confidence: 99%

“…In individuals with obesity and overt type 2 diabetes, IL-6 plasma levels are 2-3-fold higher than in control subjects and are associated with reduced insulin action, i.e. insulin resistance (11)(12)(13)(14). The IL-6 production in fat and skeletal muscle tissue suggests hitherto unknown effects of IL-6 besides its role in the inflammatory network.…”

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confidence: 99%

Palmitate, but Not Unsaturated Fatty Acids, Induces the Expression of Interleukin-6 in Human Myotubes through Proteasome-dependent Activation of Nuclear Factor-κB

Weigert

Brodbeck

Staiger

et al. 2004

Journal of Biological Chemistry

249

189

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Circulating interleukin-6 (IL-6), insulin, and free fatty acid (FFA) concentrations are associated with impaired insulin action in obese and type 2 diabetic individuals. However, a causal relationship between elevated plasma FFAs and IL-6 has not been shown. Because skeletal muscle represents a major target of impaired insulin action, we studied whether FFAs may affect IL-6 expression in human myotubes. We demonstrate that specifically saturated FFAs, e.g. palmitate (0.25 mM), induce IL-6 mRNA expression and protein secretion by a proteasome-dependent mechanism that leads to a rapid and chronic activation of nuclear factor-B. Insulin, high glucose concentrations, or unsaturated FFAs did not activate IL-6 expression. In fact, the unsaturated FFA linoleate inhibited palmitate-induced IL-6 production. Because inhibition of palmitate metabolism by the acyl-CoA synthetase inhibitor triacsin C did not abolish IL-6 expression, it appears that the palmitate molecule per se exerts the observed effects. Furthermore, we show that in human myotubes, IL-6 activates the phosphorylation of signal transducer and activator of transcription 3 in concentrations similar to hepatocytes. However, no inhibitory effect of IL-6 on insulin action, determined as phosphatidylinositol 3-kinase association with insulin receptor substrate-1, Akt phosphorylation, and glycogen synthesis, was detected. We conclude that IL-6 expression may be modulated by the composition of circulating FFA, e.g. by diet, and that skeletal muscle cells could be target cells for IL-6.

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“…Insulin resistance, commonly seen in overweight individuals and in people genetically predisposed to the metabolic syndrome, and atherosclerosis have both been postulated to result from a state of chronic low-grade inflammation. [4][5][6][7] The inflammatory state has in part been attributed to secretion of cytokines from enlarged adipocytes or from macrophages that infiltrate the expanded fat depots. 5,6,8,9 However, multiple organs seem to be involved in the elevation of surrogate markers such as highsensitivity C-reactive protein (CRP) and interleukin-6 (IL-6).…”

Section: Introductionmentioning

confidence: 99%

Circulating soluble CD36 is associated with glucose metabolism and interleukin-6 in glucose-intolerant men

Handberg

López‐Bermejo²,

Bassols³

et al. 2009

Diabetes and Vascular Disease Research

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R ecently, soluble CD36 (sCD36) levels were reported to be elevated in type 2 diabetes, and to be tightly correlated with insulin resistance. Our aim was to obtain further insight into the relationship between insulin sensitivity, low-grade inflammation and sCD36.We studied glucose-tolerant (n=90) and glucose-intolerant (n=57) moderately obese men. Insulin sensitivity was measured by the frequent sample intravenous glucose tolerance test, and sCD36 by an in-house ELISA assay.In glucose-intolerant subjects, sCD36 was negatively associated with insulin sensitivity and positively with interleukin-6 (IL-6), fasting glucose, fasting triglycerides, fat-free mass and platelet count. On multiple linear regression analyses, insulin sensitivity contributed 22% of sCD36 variance, independent of age, body mass index (BMI) and IL-6, in glucose-intolerant subjects. The level of sCD36 in subjects with glycosylated haemoglobin (HbA 1C ) above the mean was higher than in those with HbA 1C values below the mean.Insulin sensitivity is a predictor of sCD36 in men with impaired glucose tolerance. IL-6 is related to sCD36 but does not predict sCD36 independent of insulin sensitivity and BMI.

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Insulin Resistance, Inflammation, and Serum Fatty Acid Composition

Cited by 185 publications

References 38 publications

Effects of N-3 PUFAs Supplementation on Insulin Resistance and Inflammatory Biomarkers in Hemodialysis Patients

Effects of N-3 PUFAs Supplementation on Insulin Resistance and Inflammatory Biomarkers in Hemodialysis Patients

Palmitate, but Not Unsaturated Fatty Acids, Induces the Expression of Interleukin-6 in Human Myotubes through Proteasome-dependent Activation of Nuclear Factor-κB

Circulating soluble CD36 is associated with glucose metabolism and interleukin-6 in glucose-intolerant men

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