Abstract
Dietary supplementation with curcumin has been previously reported to have beneficial effects in people with insulin resistance, type 2 diabetes (T2D) and Alzheimer’s disease (AD). This study investigated the effects of dietary supplementation with curcumin on key peptides implicated in insulin resistance in individuals with high risk of developing T2D. Plasma samples from participants recruited for a randomised controlled trial with curcumin (180 mg/day) for 12 weeks were analysed for circulating glycogen synthase kinase-3 β (GSK-3β) and islet amyloid polypeptide (IAPP). Outcome measures were determined using ELISA kits. The homeostasis model for assessment of insulin resistance (HOMA-IR) was measured as parameters of glycaemic control. Curcumin supplementation significantly reduced circulating GSK-3β (−2.4 ± 0.4 ng/mL vs. −0.3 ± 0.6, p = 0.0068) and IAPP (−2.0 ± 0.7 ng/mL vs. 0.4 ± 0.6, p = 0.0163) levels compared with the placebo group. Curcumin supplementation significantly reduced insulin resistance (−0.3 ± 0.1 vs. 0.01 ± 0.05, p = 0.0142) compared with placebo group. Dietary supplementation with curcumin reduced circulating levels of IAPP and GSK-3β, thus suggesting a novel mechanism through which curcumin could potentially be used for alleviating insulin resistance related markers for reducing the risk of T2D and AD.
Highlights
Insulin resistance is of particular interest as defective insulin signalling in the brain contributes to the accumulation of amyloid beta (Aβ) and tau protein, presenting a pathophysiological link betweenAlzheimer’s disease (AD) and type 2 diabetes (T2D) [1]
The aim of this study was to determine if dietary supplementation with curcumin reduce plasma levels of peptides, glycogen synthase kinase-3 β (GSK-3β) and islet amyloid polypeptide (IAPP) that are implicated in the insulin resistance in people at a high risk of developing T2D
Twenty-nine serum samples were analysed from the COP-D trial for the primary outcome, GSK-3β, and for IAPP
Summary
Insulin resistance is of particular interest as defective insulin signalling in the brain contributes to the accumulation of amyloid beta (Aβ) and tau protein, presenting a pathophysiological link betweenAlzheimer’s disease (AD) and type 2 diabetes (T2D) [1]. Insulin resistance is of particular interest as defective insulin signalling in the brain contributes to the accumulation of amyloid beta (Aβ) and tau protein, presenting a pathophysiological link between. IAPP can induce peripheral insulin resistance by antagonising insulin activity, further linking to the overexpression of glycogen synthase kinase-3 (GSK-3) [7]. Impaired insulin signalling and subsequent hyperactivity of GSK-3 in rodent and human models have been associated with the accumulation of Aβ and tau protein in the brain [8]. Recent research has uncovered a pathophysiological link between T2D and AD involving insulin resistance and the activation of GSK-3, a serine-threonine kinase involved in a multitude of physiological processes including glycogen metabolism and microtubule stability [9,10]
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