Abstract
Increased levels of free fatty acids (FFAs) and hypertriglyceridemia are important risk factors for cardiovascular disease. The effective fraction isolated from radix astragali (RA) has been reported to alleviate hypertriglyceridemia. The mechanism of this triglyceride-lowering effect of RA is unclear. Here, we tested whether activation of the mTORC1-PPARγ signaling pathway is related to the triglyceride-lowering effect of RA. High-fat diet-induced obese (DIO) rats were fed a high-fat diet (40% calories from fat) for 9-10 weeks, and 4 g/kg/d RA was administered by gavage. RA treatment resulted in decreased fasting triglyceride levels, FFA concentrations, and adipocyte size. RA treated rats showed improved triglyceride clearance and fatty acid handling after olive oil overload. RA administration could also decrease macrophage infiltration and expression of MCP-1 and TNFα, but it may also increase the expression of PPARγ in epididymal adipose tissue from RA treated rats. Consistently, expressions of PPARγ and phospho-p70S6K were increased in differentiated 3T3-L1 adipocytes treated with RA. Moreover, RA couldnot upregulate the expression of PPARγ at the presence of rapamycin. In conclusion, the mTORC1-PPARγ signaling pathway is a potential mechanism through which RA exerts beneficial effects on the disturbance of triglyceride metabolism and dysfunction of adipose tissue in DIO rats.
Highlights
Obesity is becoming one of the most serious public health problems worldwide
Inflammatory pathways are chronically activated in both adipocytes and the macrophages that reside in adipose tissue, resulting in substantial M1 macrophage infiltration and aberrant secretion of proinflammatory cytokines [8, 9]
Adipocyte size was decreased by 34% in the epididymal fat pad in the high-fat diet-fed rats treated with Radix astragali (RA) when compared with obese rats (Figures 1(c) and 1(d))
Summary
Obesity is becoming one of the most serious public health problems worldwide. Substantial epidemiological evidence has proven that overweight and obesity raise the risk for chronic diseases, such as cardiovascular disease [1, 2], type 2 diabetes [3, 4], some cancers [5], and stroke [6]. Obesity is thought to be one of the top five global health risks for mortality, which accounts for 5% of deaths [7]. It has been well established that obesity is characterized by excessive expansion of adipose tissue, visceral adipose tissue, and is accompanied by chronic low-grade inflammation in adipose tissue, which is triggered by nutrient excess. Deranged triglyceride (TG) metabolism is partially a result of inflamed adipose tissue, resulting in hypertriglyceridemia and excessive FFA efflux from white adipose tissue [10, 11]
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