Abstract
Supplementation with epigallocatechin-3-gallate has been determined to aid in the prevention of obesity. Decaffeinated green tea extract appears to restore a normal hepatic metabolic profile and attenuate high-fat diet (HFD)-induced effects, thereby preventing non-alcoholic fatty liver disease in mice. Mice were maintained on either a control diet (CD) or HFD for 16 weeks and supplemented with either water or green tea extract (50 mg/kg/day). The body mass increase, serum adiponectin level, and lipid profile were measured over the course of the treatment. Furthermore, the AMPK pathway protein expression in the liver was measured. From the fourth week, the weight gain in the CD + green tea extract (CE) group was lower than that in the CD + water (CW) group. From the eighth week, the weight gain in the HFD + water (HFW) group was found to be higher than that in the CW group. Moreover, the weight gain in the HFD + green tea extract (HFE) group was found to be lower than that in the HFW group. Carcass lipid content was found to be higher in the HFW group than that in the CW and HFE groups. Serum analysis showed reduced non-esterified fatty acid level in the CE and HFE groups as compared with their corresponding placebo groups. Increased adiponectin level was observed in the same groups. Increased VLDL-TG secretion was observed in the HFW group as compared with the CW and HFE groups. Increased protein expression of AdipoR2, SIRT1, pLKB1, and pAMPK was observed in the HFE group, which explained the reduced expression of ACC, FAS, SREBP-1, and ChREBP in this group. These results indicate that the effects of decaffeinated green tea extract may be related to the activation of AMPK via LKB1 in the liver of HFD-fed mice.
Highlights
It is well known that a high-fat diet (HFD) rich in saturated fat and low in dietary fiber can lead to obesity
Considering the lack of studies regarding the effect of decaffeinated green tea extract on the activation of the AMPK via liver kinase B1 (LKB1), the purpose of this study was to investigate the effects of a green tea extract supplement on the activation of enzymes and factors related to hepatic de novo lipogenesis, concurrent with very low density lipoproteins (VLDLs)-TG secretion in HFD-fed mice
The body weight of mice belonging to the Control diet and EGCG (CE) group was significantly lower than those belonging to the Control diet and Water (CW) group, starting at the fourth week until the end of experimental treatment (p < 0.001)
Summary
It is well known that a high-fat diet (HFD) rich in saturated fat and low in dietary fiber can lead to obesity. Charlton et al [3] considered that non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of obesity and predicted that within 20 years, non-alcoholic steatohepatitis (NASH) will be the leading cause of liver cirrhosis requiring a transplant. Insulin resistance in visceral adipose tissues in obesity has been shown to lead to an increased activation of the lipolytic signaling pathway [4,5], which further enhances non-esterified fatty acid (NEFA) uptake into the liver. The high hepatic influx of NEFA increases the secretion of very low density lipoproteins (VLDLs) and apolipoprotein B in the circulation, contributing to an increased hepatic glucose production by gluconeogenesis [6] and the activation of the de novo lipogenesis pathway [7]. NEFA overload induces an increase in triacylglycerol (TAG) level, exceeding the capacity of VLDL-TG synthesis, thereby promoting TAG accumulation in hepatocytes and contributing to the initiation of NAFLD [8,9]
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