Key result
Resveratrol alleviates insulin resistance and reduces proinflammatory cytokines in high-fat diet-fed mice.
Why the study?
Obesity-induced glucose metabolism disorder is associated with chronic inflammation and insulin resistance, and the effects of resveratrol on insulin signaling and inflammation in adipose tissue under high-fat diet conditions were investigated.
Does resveratrol improve insulin signaling and reduce the inflammatory response in visceral white adipose tissue in high-fat diet-fed mice?
Does resveratrol improve insulin signaling and reduce the inflammatory response in visceral white adipose tissue in high-fat diet-fed mice?
Resveratrol administration protects against abnormal glucose metabolism and inflammatory adaptations in visceral white adipose tissue in a mouse model of high-fat diet-induced obesity.
RES may attenuate adipose inflammation and insulin resistance in obese mice; leaves open clinical translation pending human trials.
BACKGROUND: Obesity-induced glucose metabolism disorder is associated with chronic, low-grade, systemic inflammation and is considered a risk factor for diabetes and metabolic syndrome. Resveratrol (RES), a natural anti-inflammatory compound, is observed to improve glucose tolerance and insulin sensitivity in obese rodents and humans. This study aimed to test the effects of RES administration on insulin signaling and the inflammatory response in visceral white adipose tissue (WAT) caused by a high-fat diet (HFD) in mice. METHODS: A total of 40 wild-type C57BL/6 male mice were divided into four groups (10 in each group): the standard chow diet (STD) group was fed a STD; the HFD group was fed a HFD; and the HFD-RES/L and HFD-RES/H groups were fed a HFD plus RES (200 and 400 mg/kg/day, respectively). The L and H in RES/L and RES/H stand for low and high, respectively. Glucose tolerance, insulin sensitivity, circulating inflammatory biomarkers and lipid profile were determined. Quantitative PCR and Western blot were used to determine the expression of CC-chemokine receptor 2 (CCR2), other inflammation markers, glucose transporter 4 (GLUT4), insulin receptor substrate 1 (IRS-1) and pAkt/Akt and to assess targets of interest involving glucose metabolism and inflammation in visceral WAT. RESULTS: HFD increased the levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol and proinflammatory cytokines in serum, decreased the high-density lipoprotein cholesterol level in serum, and induced insulin resistance and WAT inflammation in mice. However, RES treatment alleviated insulin resistance, increased the expressions of pAkt, GLUT4 and IRS-1 in WAT, and decreased serum proinflammatory cytokine levels, macrophage infiltration and CCR2 expression in WAT. CONCLUSION: Our results indicated that WAT CCR2 may play a vital role in macrophage infiltration and the inflammatory response during the development of insulin resistance in HFD-induced obesity. These data suggested that administration of RES offers protection against abnormal glucose metabolism and inflammatory adaptations in visceral WAT in mice with HFD-induced obesity.
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Ding et al. (2018) studied High-fat diet-induced obesity and insulin resistance (n=40). Resveratrol vs. High-fat diet alone (and standard chow diet) was evaluated on Insulin resistance, inflammatory biomarkers, and expression of CCR2, GLUT4, IRS-1, and pAkt/Akt in visceral white adipose tissue. Resveratrol treatment alleviated insulin resistance, increased pAkt, GLUT4, and IRS-1 expression, and decreased serum proinflammatory cytokines and CCR2 expression in high-fat diet-fed mice.
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