Key result
Resveratrol cuts albuminuria ~79% in diabetic mice by increasing AdipoR1 and AdipoR2 expression.
Why the study?
The mechanisms by which resveratrol may inhibit renal damage in type 2 diabetic nephropathy and its effects on AdipoR1 and AdipoR2 expression were not fully understood.
Does resveratrol prevent renal damage in type 2 diabetic db/db mice?
Does resveratrol prevent renal damage in type 2 diabetic db/db mice?
Resveratrol prevents diabetic nephropathy in a mouse model by ameliorating lipotoxicity, oxidative stress, and apoptosis via increasing AdipoR1 and AdipoR2 expression.
Answers are grounded in this paper and cite their sources.
Resveratrol shows promise in preclinical diabetic nephropathy models; leaves open translation to clinical use pending human trials.
BACKGROUND: Adiponectin has multiple functions including insulin sensitization, anti-inflammation and antiatherogenesis in various organs. Adiponectin activates 5'-adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)α via the adiponectin receptor (AdipoR) 1 and 2, which are critical for regulating lipids and glucose homeostasis and for controlling oxidative stress. We investigated whether resveratrol can inhibit renal damage in type 2 diabetic db/db mice and the underlying mechanisms of its effects. METHODS: Four groups of male C57 BLKS/J db/m and db/db mice and human glomerular endothelial cells (HGECs) were used. Resveratrol was administered to diabetic and nondiabetic mice by oral gavage for 12 weeks starting at 8 weeks of age. RESULTS: In db/db mice, resveratrol increased serum adiponectin levels and decreased albuminuria, glomerular matrix expansion, inflammation and apoptosis in the glomerulus. Resveratrol increased the phosphorylation of AMPK and silent information regulator T1 (SIRT1), and decreased phosphorylation of downstream effectors class O forkhead box (FoxO)1 and FoxO3a via increasing AdipoR1 and AdipoR2 in the renal cortex. Furthermore, resveratrol increased expression of PPARγ coactivator (PGC)-1α, estrogen-related receptor-1α, and phosphorylated acetyl-CoA carboxylase and decreased sterol regulatory element-binding protein 1. This effect lowered the content of nonesterified fatty acid and triacylglycerol in the kidneys, decreasing apoptosis, oxidative stress and activating endothelial nitric oxide synthase. Resveratrol prevented cultured HGECs from undergoing high-glucose-induced oxidative stress and apoptosis by activating the AMPK-SIRT1-PGC-1α axis and PPARα through increases in AdipoR1 and AdipoR2 expression. CONCLUSIONS: These results suggest that resveratrol prevents diabetic nephropathy by ameliorating lipotoxicity, oxidative stress, apoptosis and endothelial dysfunction via increasing AdipoR1 and AdipoR2 expression.
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Park et al. (2016) studied Type 2 diabetic nephropathy (n=32). Resveratrol vs. 0.5% carboxymethyl cellulose sodium salt (CMC) was evaluated on 24-h albuminuria (μg/day). Resveratrol reduced 24-hour albuminuria and ameliorated renal damage in type 2 diabetic mice by increasing AdipoR1 and AdipoR2 expression.
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