Diallyl disulfide suppresses weight gain, adipogenesis, and matrix metalloproteinases (MMPs) expression in high-fat-diet-induced obese animal model

二烯丙基二硫化物可抑制高脂饮食诱导的肥胖动物模型中的体重增加、脂肪生成和基质金属蛋白酶(MMPs)表达。

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Abstract

BACKGROUND/OBJECTIVES: Excessive adipogenesis and angiogenesis, mediated by matrix metalloproteinases (MMPs), contribute to the development of obesity-related complications. Diallyl disulfide (DADS), an organosulfur compound derived from garlic, has been reported to exhibit anti-obesity properties, but studies on the expression of MMPs as an anti-obesity effect of DADS are limited. This study investigated the potential role of DADS in regulating weight gain, adipogenesis, and MMP expression in mice fed a high-fat diet. MATERIALS/METHODS: Six-week-old male C57BL/6N mice were divided into 4 groups: a normal-fat diet (NF), a high-fat diet (HF), a high-fat diet supplemented with 12.5 mg/kg DADS (HFDADS12.5), and a high-fat diet supplemented with 25 mg/kg DADS (HFDADS25) for 14 weeks. This study measured plasma lipid concentrations, glycerol-3-phosphate dehydrogenase (GPDH) activity, mRNA expression of transcription factors related to adipocyte differentiation in the liver, and the mRNA expression and concentrations of MMP-2 and MMP-9 in epididymal adipose tissue. The plasma concentrations of adiponectin and leptin were also measured. RESULTS: DADS intake significantly reduced the body weight gain and epididymal adipose tissue weight (P < 0.05). The GPDH activity, mRNA expressions of the transcription factors related to adipocyte differentiation, the mRNA expression and concentrations of MMP-2 and MMP-9, and plasma leptin concentration were significantly higher in the HF group than in the NF group, but they were significantly lower in the DADS intake groups (P < 0.05). The plasma adiponectin concentrations were lower in the HF group than the NF group, but they were significantly higher in the HFDADS25 group (P < 0.05). CONCLUSION: DADS suppressed body weight gain and adipogenesis, potentially by inhibiting MMP-2 and MMP-9 in mice fed a high-fat diet.

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