Insulin therapy stimulates lipid synthesis and improves endocrine functions of adipocytes in dietary obese C57BL/6 mice

Abstract

Aim: To evaluate whether insulin intervention could affect the metabolic and endocrine functions of adipose tissue. Methods: C57BL/6 mice were fed on a high-fat-diet for 12−16 weeks to induce insulin resistance. Insulin intervention was administered in the high-fat-diet mice for 4 weeks at 12 weeks (early insulin treatment) or 16 weeks (late insulin treatment). Intraperitoneal glucose tolerance tests were performed before and after insulin treatment. Expression levels of factors involved in the triglyceride synthesis and endocrine functions of adipose tissue including phosphoenolpyruvate carboxykinase (PEPCK-C), fatty acid synthase (FAS), aquaporin 7 (AQP7), adiponectin, visfatin, and interleukin-6 (IL-6) were determined by Western blot. Results: In the obese mice, glucose tolerance was impaired; triglyceride content was increased in the liver tissue; protein expression of FAS and adiponectin was decreased; expression of visfatin was increased in adipose tissue. After 4-week insulin treatment, glucose tolerance was improved; triglyceride content was decreased in the liver and skeletal muscle; expression of PEPCK-C, FAS, and adiponectin was increased in the adipose tissue; IL-6 and AQP7 expression was reduced in the fat. Early insulin treatment had better effect in increasing the expression of FAS and PEPCK-C and decreasing the expression of IL-6. Conclusion: These results indicate that insulin can target adipocytes for improvement of insulin sensitivity through stimulating triglyceride synthesis and partly improving endocrine functions.

Noninferiority Effects on Glycemic Control and β-Cell Function Improvement in Newly Diagnosed Type 2 Diabetes Patients: Basal Insulin Monotherapy Versus Continuous Subcutaneous Insulin Infusion Treatment

“…22 Other insulin effects such as reducing inflammation and decreasing ectopic lipid deposition might also contribute to the recovery of overall b-cell function in T2DM patients. 23,24 In addition, our results indicated that fasting blood glucose level was the main risk factor affecting b-cell function. In vitro experiments have shown that the first-phase insulin secretion of b-cells was damaged or vanished when the fasting blood glucose level was above 97 or 100 mg/dL, respectively.…”

Decreased expression of adipose CD36 and FATP1 are associated with increased plasma non-esterified fatty acids during prolonged fasting in northern elephant seal pups (Mirounga angustirostris)

“…Hormones such as apelin and insulin can inhibit lipolysis by preventing lipase activation within adipocytes. Insulin can also stimulate fatty acid synthase (FAS) to produce fatty acids and phosphoenol pyruvate carboxykinase (PEPCK-C) to generate glyceride-glycerol through glyceroneogenesis in adipose, and thus increase triglyceride stores (Holland and Hardie, 1985;Chen et al, 2010). However, fasting decreases the concentrations of both insulin and apelin in circulation (Choi et al, 2010;Yue et al, 2010;Viscarra et al, 2011b;Viscarra et al, 2011a;Yue et al, 2011).…”

Effects of High-Fat Feeding on Skeletal Muscle Gene Expression in Diabetic Goto-Kakizaki Rats

“…This conclusion is further supported by the observation of higher expression of aquaporin 7 (Aqp7) in the muscle from high fat–fed rats (Figure 4 – bottom panels). Aqp7 is an aquaglyceroporin responsible for glycerol efflux from skeletal muscle 34. The higher expression of Aqp7 at all age groups in both strains suggests a higher level of lipolysis in these muscles.…”