curcumin and Hyperinsulinism

The aim of the current study was to assess the effects of curcumin supplementation on glycemic status, lipid profile and high sensitivity C-reactive protein (hs-CRP) serum levels in women with polycystic ovary syndrome (PCOS).. This randomized double-blind placebo-controlled clinical trial was conducted on 60 women who were randomly assigned to the intervention or control groups using block randomization.. Infertility referral center.. Curcumin (500 mg/d) or placebo twice daily for 6 weeks.. Serum evaluation of lipid profile (triglycerides (TG), low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol concentrations, LDL/HDL-C and TG/HDL-C ratios), glycemic index (fasting blood sugar (FBS), insulin concentrations, homeostasis model of assessment insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI)) and hs-CRP levels.. Glycemic index, lipid profile and hs-CRP serum levels were measured at first and at the end of trial. Serum insulin (p = 0.020) and Quantitative Insulin Sensitivity Check Index (QUICKI) (p = 0.003) were improved significantly, while Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) (p = 0.067) improved marginally in curcumin treated group (within group analysis).. Curcumin supplementation might be beneficial for improving serum insulin and QUICKI, however, future investigations are suggested in order to draw a firm link between curcumin and glycemia control.

Topics: Adult; C-Reactive Protein; Curcumin; Dietary Supplements; Double-Blind Method; Female; Humans; Hyperinsulinism; Hyperlipidemias; Obesity; Overweight; Polycystic Ovary Syndrome

Hyperinsulinemia associated with type II diabetes mellitus (T2DM) is a risk factor for non-alcoholic steatohepatitis (NASH) and hepatic fibrosis. Hepatic stellate cells (HSCs) are the major effectors in collagen production during hepatic fibrogenesis. Elevated levels of insulin stimulate HSC activation. In addition to its anti-diabetic effects, the antioxidant curcumin, the yellow pigment in curry from turmeric, suppresses HSC activation and protects the liver from fibrogenesis in vitro and in vivo. This study aims at evaluating the effect of curcumin on insulin-induced HSC activation and further elucidating the underlying mechanisms. We report that curcumin dose-dependently eliminates insulin-induced HSC activation by suppressing expression of type I collagen gene and other key genes relevant to HSC activation. Additional experiments indicate that curcumin interrupts insulin signaling in HSCs by reducing the phosphorylation level of insulin receptor (InsR) and suppressing gene expression of InsR. Furthermore, curcumin attenuates insulin-induced oxidative stress in HSCs by inducing gene expression of glutamate-cysteine ligase (GCL), leading to de novo synthesis of glutathione and the suppression of gene expression of InsR. These results support our initial hypothesis that curcumin inhibits the effects of insulin on stimulating HSC activation by interrupting insulin signaling and attenuating oxidative stress. Our results provide novel insights into the mechanisms by which curcumin inhibits the insulin-induced HSC activation.

Topics: Animals; Cells, Cultured; Curcumin; Dose-Response Relationship, Drug; Gene Expression Regulation; Glutamate-Cysteine Ligase; Glutathione; Hepatic Stellate Cells; Hyperinsulinism; Insulin; Insulin Antagonists; Lipid Peroxidation; Male; Oxidative Stress; Phosphorylation; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Receptor, Insulin; Signal Transduction