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茵陈抑制高脂饮食喂养的C57BL/6J小鼠3T3-L1脂肪细胞中的脂质积累及肥胖。

Artemisia capillaris inhibits lipid accumulation in 3T3-L1 adipocytes and obesity in C57BL/6J mice fed a high fat diet.

作者信息

Hong Jung-Hee, Hwang Eun-Young, Kim Hyun-Jeong, Jeong Yun-Jeong, Lee In Seon

机构信息

The Center for Traditional Microorganism Resources Center, Keimyung University, Daegu, Republic of Korea.

出版信息

J Med Food. 2009 Aug;12(4):736-45. doi: 10.1089/jmf.2008.1240.

Abstract

The purpose of the current study was to determine the effect of the Artemisia capillaris ethyl acetate (ACE) fraction on diet-induced obesity and to elucidate the underlying mechanism. The ACE fraction treatment decreased the leptin level and fat accumulation in cultured 3T3-L1 adipocytes through the free fatty acids released in the medium. The ACE fraction significantly suppressed the expression of peroxisome proliferator-activated receptor-gamma in cultured 3T3-L1 adipocytes. To determine the effect of the ACE fraction on C57BL/6J male mice, the mice were separated into six groups: normal control (N), N plus 0.1 g/kg body weight ACE (NB), high fat control group (HF), HF plus 0.05 g/kg of body weight ACE (HFA), HF plus 0.1 g/kg of body weight ACE (HFB), and HF plus 0.03 g/kg of body weight rosiglitazone (RG) groups. We speculate that the HFB group exhibits a lipid-lowering effect via increased mitochondrial beta-oxidation, of which the rate-limiting enzyme is carnitine palmitoyl transferase I, the activity of which was significantly increased. Also, the activity of fatty acid synthase, a key enzyme of fatty acid synthesis, was markedly suppressed (19%) in the HFB group, as compared to the HF group, and glycerol-3-phosphate dehydrogenase activity, which is very useful in studying adipogenic differentiation in vitro, was markedly suppressed (30%) in the HFB group compared with the HF group. Furthermore, the HFB group showed lowered hepatic lipid droplet accumulation and adipose tissue weight and size. We suggest that 0.1 g of the ACE fraction/kg of body weight may exert an anti-obesity effect in C57BL/6J mice by enhancing lipid metabolism.

摘要

本研究的目的是确定茵陈蒿乙酸乙酯(ACE)部位对饮食诱导肥胖的影响,并阐明其潜在机制。ACE部位处理通过培养基中释放的游离脂肪酸降低了培养的3T3-L1脂肪细胞中的瘦素水平和脂肪积累。ACE部位显著抑制了培养的3T3-L1脂肪细胞中过氧化物酶体增殖物激活受体γ的表达。为了确定ACE部位对C57BL/6J雄性小鼠的影响,将小鼠分为六组:正常对照组(N)、N加0.1 g/kg体重ACE组(NB)、高脂对照组(HF)、HF加0.05 g/kg体重ACE组(HFA)、HF加0.1 g/kg体重ACE组(HFB)和HF加0.03 g/kg体重罗格列酮(RG)组。我们推测,HFB组通过增加线粒体β-氧化表现出降脂作用,其中限速酶是肉碱棕榈酰转移酶I,其活性显著增加。此外,与HF组相比,HFB组中脂肪酸合成的关键酶脂肪酸合酶的活性显著受到抑制(19%),而在体外研究脂肪生成分化中非常有用的甘油-3-磷酸脱氢酶活性在HFB组中与HF组相比显著受到抑制(30%)。此外,HFB组的肝脏脂质滴积累以及脂肪组织重量和大小均降低。我们认为,0.1 g/kg体重的ACE部位可能通过增强脂质代谢对C57BL/6J小鼠发挥抗肥胖作用。

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