Abstract
This study was to explore the protective effects of Deepure tea against insulin resistance and hepatic steatosis and elucidate the potential underlying molecular mechanisms. C57BL/6 mice were fed with a high fat diet (HFD) for 8 weeks to induce the metabolic syndrome. In the Deepure tea group, HFD mice were administrated with Deepure tea at 160 mg/kg/day by gavage for 14 days. The mice in HFD group received water in the same way over the same period. The age-matched C57BL/6 mice fed with standard chow were used as normal control. Compared to the mice in HFD group, mice that received Deepure tea showed significantly reduced plasma insulin and improved insulin sensitivity. Deepure tea increased the expression of insulin receptor substrate 2 (IRS-2), which plays an important role in hepatic insulin signaling pathway. Deepure tea also led to a decrease in hepatic fatty acid synthesis and lipid accumulation, which were mediated by the downregulation of sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthesis (FAS), and acetyl-CoA carboxylase (ACC) proteins that are involved in liver lipogenesis. These results suggest that Deepure tea may be effective for protecting against insulin resistance and hepatic steatosis via modulating IRS-2 and downstream signaling SREBP-1c, FAS, and ACC.
Highlights
Nonalcoholic fatty liver disease (NAFLD) and insulin resistance are the main pathophysiological characteristic of metabolic syndrome [1], which has become a significant public health problem as a result of high fat diet and sedentary lifestyles [2, 3]
high fat diet (HFD) resulted in a significant increase in serum insulin, as compared with the control group, which was reduced as much as 43.5% by Deepure tea treatment (Figure 1(e))
This study provides evidence that short-term intake of Deepure tea protects against the development of hyperinsulinemia and NAFLD in HFD mice
Summary
Nonalcoholic fatty liver disease (NAFLD) and insulin resistance are the main pathophysiological characteristic of metabolic syndrome [1], which has become a significant public health problem as a result of high fat diet and sedentary lifestyles [2, 3]. NAFLD represents a state of lipid accumulation in hepatocytes, and its pathogenesis is associated with enhanced liver lipogenesis and hepatic insulin resistance. The liver lipogenesis can be activated by elevated plasma insulin, as seen in patients with the metabolic syndrome, type 2 diabetes, or obese individuals [4, 7]. Insulin is involved in a number of actions responsible for glucose control and lipid metabolism. Elevated insulin leads to activation of the lipid biosynthetic pathway through activation of the expression and proteolytic
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