Key result
Voglibose significantly improved hepatic steatosis, inflammation, and fibrosis in a high-fat, high-fructose diet-induced nondiabetic NAFLD mouse model by suppressing hepatic de novo lipogenesis.
Why the study?
Alpha-glucosidase inhibitors delay intestinal glucose absorption and reduce postprandial hepatic glucose intake, a mechanism considered potentially effective for treating NAFLD.
Does voglibose improve hepatic steatosis, inflammation, and fibrosis in a high-fat, high-fructose diet-induced NAFLD mouse model?
Does voglibose improve hepatic steatosis, inflammation, and fibrosis in a high-fat, high-fructose diet-induced NAFLD mouse model?
Voglibose improves high-fat, high-fructose diet-induced NAFLD in mice by suppressing hepatic de novo lipogenesis, suggesting potential therapeutic efficacy for NAFLD.
Answers are grounded in this paper and cite their sources.
Voglibose attenuates HFHFr-induced NAFLD in mice; hypothesis-generating for α-GI effects in human fatty liver disease.
The α-glucosidase inhibitor (α-GI) delays the intestinal absorption of glucose, which reduces postprandial hepatic glucose intake. This mechanism is considered to be effective in treating non-alcoholic fatty liver disease (NAFLD). Here, we investigated the effect of voglibose, an α-glucosidase inhibitor, on high-fat, high-fructose (HFHFr) diet-induced NAFLD models. Seven-week-old male C57BL/6J mice were randomly placed in a chow diet group or an HFHFr diet group. After 10 weeks, mice in the HFHFr group were randomly assigned to one of three groups: HFHFr diet with vehicle, HFHFr with voglibose, or HFHFr with pioglitazone. Each diet and treatment was continued for 10 weeks. The HFHFr diet induced severe NAFLD in terms of steatosis, hepatitis, and fibrosis. Administration of voglibose improved all aspects of NAFLD, comparable to those of pioglitazone, a positive control. In voglibose-treated mice, gene expressions of hepatic lipogenesis markers were significantly downregulated. In the in vitro experiment, reducing the influx of glucose into hepatocytes significantly reduced steatosis and de novo lipogenesis even in the presence of sufficient fructose and fat, demonstrating that the mechanism of voglibose could be effective in treating HFHFr diet-induced NAFLD. These results indicate that voglibose improves HFHFr diet-induced NAFLD by suppressing hepatic de novo lipogenesis.
No takes yet. Share an insight, caveat, or question.
Bae et al. (2022) studied Non-alcoholic fatty liver disease (NAFLD) (n=36). Voglibose vs. Vehicle (HFHFr diet) was evaluated on Hepatic steatosis, inflammation, and fibrosis (p=<0.05). Voglibose significantly improved hepatic steatosis, inflammation, and fibrosis in a high-fat, high-fructose diet-induced nondiabetic NAFLD mouse model by suppressing hepatic de novo lipogenesis.
Synapse has enriched 10 related papers. Consider them for comparative context: