Abstract
Mangoes (Mangifera indica L.) are one of the most important tropical foods. The seed is one of the main by-products of mango processing. Therefore, it is important to find an economically viable use for this waste (e.g., as a food additive or supplement with high nutraceutical value). We investigated the anti-obesity effects of mango seed kernel extract with hot water (MSKE-W) in 3T3-L1 adipocytes and in a high fat diet (HFD)-induced obesity rat model. MSKE-W caused a significant decrease in the activity of glycerol 2-phosphate dehydrogenase in 3T3-L1 adipocytes without eliciting cell cytotoxicity and inhibited cellular lipid accumulation through down-regulation of transcription factors such as PPARγ and C/EBPα. In the animal model, rats fed an HFD containing 1% MSKE-W gained less weight than rats fed an HFD alone. The visceral fat mass in rats fed an HFD containing 1% MSKE-W tended to be lower than that in rats fed an HFD alone. Furthermore, histological examination of rat livers from an HFD showed steatohepatitis. However, rats on an HFD containning 1% MSKE-W showed no histopathological changes in liver tissue. Our results indicate that MSKE-W influences anti-obesity effects, both in vitro and in vivo, and suggest that MSKE-W provides a novel preventive potential against obesity.
Highlights
Adipose tissue, as a metabolic and endocrine organ, plays critical roles in the regulation of energy balance, lipid metabolism and insulin action [1]
Adipogenesis is a process beginning with fibroblast-like preadipocytes that leads to eventual mature adipocytes, and it is regulated by two key families of adipogenic transcription factors, CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor γ (PPARγ)
Cell viability of 3T3-L1 preadipocytes was examined with various concentrations of mango seed kernel extract with hot water (MSKE-W) by neutral red assay
Summary
As a metabolic and endocrine organ, plays critical roles in the regulation of energy balance, lipid metabolism and insulin action [1]. Adipocytes have been emerging as a potential pharmacological target for obesity, diabetes and cardiovascular disease [3]. Adipogenesis is a process beginning with fibroblast-like preadipocytes that leads to eventual mature adipocytes, and it is regulated by two key families of adipogenic transcription factors, CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor γ (PPARγ). Both of these factors are necessary to promote the terminal or mature adipocyte phenotype. PPARγ and C/EBPα act synergistically to induce the expression of genes that are necessary for the generation and maintenance of the adipogenic phenotype such as lipid accumulation [5]
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