Abstract
Sirt6 is one of the sirtuin family members, a kind of NAD+-dependent histone deacetylase and ADP-ribose transferase enzyme. It has an important role in physiological and pathological processes, regulating aging, cancer, obesity, insulin resistance, inflammation, and energy metabolism. Recent studies have suggested that reduced Sirt6 action is related to obesity and diabetes. Aging and overnutrition, two major risk factors for obesity and diabetes, lead to decreased Sirt6 level and function, which results in abnormal glucose and lipid metabolism. Whole-body ablation of Sirt6 in mice results in severe hypoglycemia. Sirt6 deficiency leads to liver steatosis and promotes diet-induced obesity and insulin resistance. Sirt6 has a protective effect on obesity and diabetes. This review surveys evidence for an emerging role of Sirt6 as a regulator of metabolism in mammals and summarizes its major functions in obesity and diabetes.
Highlights
The sirtuins are a highly conserved family of NAD+-dependent deacetylases and ADP-ribosyltransferases that play an important regulatory role in the physiological and pathological processes of the organism
This review summarizes the role of Sirt6 in obesity and diabetes
Sirt6 physically interacts with Forkhead box protein O1 (FoxO1), and Sirt6 deficiency increased the acetylation and phosphorylation of FoxO1, thereby promoting its nuclear exclusion and decreasing its transcriptional activity, which downregulated Adipose TG lipase (ATGL) expression (Kuang et al, 2017)
Summary
The sirtuins are a highly conserved family of NAD+-dependent deacetylases and ADP-ribosyltransferases that play an important regulatory role in the physiological and pathological processes of the organism. Two major risk factors for obesity and diabetes, lead to decreased Sirt6 level and function and result in abnormal glucose and lipid metabolism. Fat-specific deletion of Sirt6 increased blood glucose levels and hepatic steatosis and promoted diet-induced obesity and insulin resistance (Kuang et al, 2017; Xiong et al, 2017; Yao et al, 2017).
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