Abstract
This study tried to explore how saponins from bitter melon (BMS) affect the glucose and lipid metabolism in palmitic acid-treated HepG2 cell and glucose-treated Caenorhabditis elegans (C. elegans). Results showed that BMS could effectively accelerate glucose consumption and elevate the levels of glycogen and ATP in palmitic acid-treated HepG2 cell, while significantly decreasing the triglyceride (TG) content. qRT-PCR data indicated that BMS might promote fatty acid β-oxidation by AMPK-ACC2-CPT1 pathway and glucose uptake by upregulating GLUT4 expression. In the model of glucose-treated C. elegans, we observed that BMS obviously inhibited fat accumulation, along with no toxicity towards some physical activities. The potential mechanism of BMS in the metabolism involved the suppression of synthesis of polyunsaturated fatty acids and enhancement of fatty acid β-oxidation. Taken together, BMS exhibited ability of regulating energy metabolism in HepG2 cell line and C. elegans.
Highlights
In the last few decades, obesity and its related metabolic disorders have emerged as public health issues worldwide [1]
Obesity is developed with the evidence of body weight gain, insulin resistance, hyperlipaemia, and so on, increasing the risk of II type diabetes, nonalcoholic fatty liver disease, and some other metabolic syndromes [2]
In vitro study suggested bitter melon triterpenoid reduced preadipocyte viability and lipid accumulation by downregulating PPARc in 3T3-L1 cells [7]; in vivo study reported that saponin extract from bitter melon significantly suppressed body weight gain and visceral fat accumulation in the PPARα- and PPARc-mediated pathways in obese mice [8]
Summary
In the last few decades, obesity and its related metabolic disorders have emerged as public health issues worldwide [1]. Obesity is developed with the evidence of body weight gain, insulin resistance, hyperlipaemia, and so on, increasing the risk of II type diabetes, nonalcoholic fatty liver disease, and some other metabolic syndromes [2]. Large amounts of mechanism studies have shown that the saponins of bitter gourd have physiological activities such as lowering blood glucose and improving insulin resistance, which are recognized as insulin-like [5, 6]. In vitro study suggested bitter melon triterpenoid reduced preadipocyte viability and lipid accumulation by downregulating PPARc in 3T3-L1 cells [7]; in vivo study reported that saponin extract from bitter melon significantly suppressed body weight gain and visceral fat accumulation in the PPARα- and PPARc-mediated pathways in obese mice [8]
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