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酶合成的糖原可减少饮食诱导肥胖大鼠的脂肪积累。

Enzymatically synthesized glycogen reduces lipid accumulation in diet-induced obese rats.

机构信息

Institute of Health Sciences, Ezaki Glico Co, Ltd, Osaka, Japan.

出版信息

Nutr Res. 2013 Sep;33(9):743-52. doi: 10.1016/j.nutres.2013.06.006. Epub 2013 Aug 1.

DOI:10.1016/j.nutres.2013.06.006
PMID:24034574
Abstract

Based on a recent study indicating that enzymatically synthesized glycogen (ESG) possesses a dietary, fiber-like action, we hypothesized that ESG can reduce the risk of obesity. In this study, the antiobesity effects of ESG were investigated in a model of diet-induced obesity. Male Sprague-Dawley rats were divided into 4 groups and fed a normal or high-fat diet, with or without 20% ESG, for 4 weeks. Body weight, food intake, lipid deposition in the white adipose tissues and liver, fecal lipid excretion, and plasma lipid profiles were measured. At week 3, the body fat mass was measured using an x-ray computed tomography system, which showed that ESG significantly suppressed the high-fat diet-induced lipid accumulation. Similar results were observed in the weight of the adipose tissue after the experiment. Moreover, ESG significantly suppressed the lipid accumulation in the liver but increased fecal lipid excretion. The plasma concentrations of triacylglycerol and nonesterified fatty acid were lowered after a high-fat diet, whereas the total bile acid concentration was increased by ESG. However, the hepatic messenger RNA (mRNA) levels of enzymes related to lipid metabolism were not affected by ESG. Conversely, the mRNA levels of long-chain acyl-CoA dehydrogenase and medium-chain acyl-CoA dehydrogenase were up-regulated by ESG in the muscle. These results suggest that the combined effects of increased fecal lipid excretion, increased mRNA levels of enzymes that oxidize fatty acids in the muscle, and increased total bile acid concentration in the plasma mediate the inhibitory effect of ESG on lipid accumulation.

摘要

基于最近一项研究表明,酶法合成的糖原(ESG)具有膳食纤维样作用,我们假设 ESG 可以降低肥胖的风险。在这项研究中,研究了 ESG 在饮食诱导肥胖模型中的抗肥胖作用。雄性 Sprague-Dawley 大鼠分为 4 组,分别用正常或高脂肪饮食喂养,同时或不添加 20%的 ESG,持续 4 周。测量体重、食物摄入量、白色脂肪组织和肝脏中的脂质沉积、粪便脂质排泄和血浆脂质谱。在第 3 周,使用 X 射线计算机断层扫描系统测量体脂肪量,结果表明 ESG 显著抑制了高脂肪饮食引起的脂质积累。实验结束后,脂肪组织的重量也观察到了类似的结果。此外,ESG 显著抑制了肝脏中的脂质积累,但增加了粪便脂质排泄。高脂肪饮食后血浆三酰甘油和非酯化脂肪酸浓度降低,而 ESG 增加了总胆汁酸浓度。然而,ESG 对与脂质代谢相关的酶的肝 mRNA 水平没有影响。相反,ESG 在上肌中上调了长链酰基辅酶 A 脱氢酶和中链酰基辅酶 A 脱氢酶的 mRNA 水平。这些结果表明,粪便脂质排泄增加、肌肉中氧化脂肪酸的酶的 mRNA 水平增加以及血浆中总胆汁酸浓度增加的综合作用介导了 ESG 对脂质积累的抑制作用。

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