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低蛋白、高碳水化合物饮食会增加脂肪组织的脂质含量,而不会增加生长中的大鼠的甘油-3-磷酸或脂肪酸含量。

A low-protein, high-carbohydrate diet increases the adipose lipid content without increasing the glycerol-3-phosphate or fatty acid content in growing rats.

机构信息

Department of Chemistry, Federal University of Mato Grosso, Cuiabá, Mato Grosso, Brazil.

出版信息

Can J Physiol Pharmacol. 2010 Dec;88(12):1157-65. doi: 10.1139/Y10-096.

DOI:10.1139/Y10-096
PMID:21164562
Abstract

The amount of triacylglycerol (TAG) that accumulates in adipose tissue depends on 2 opposing processes: lipogenesis and lipolysis. We have previously shown that the weight and lipid content of epididymal (EPI) adipose tissue increases in growing rats fed a low-protein, high-carbohydrate (LPHC) diet for 15 days. The aim of this work was to study the pathways involved in lipogenesis and lipolysis, which ultimately regulate lipid accumulation in the tissue. De novo fatty acid synthesis was evaluated in vivo and was similar for rats fed an LPHC diet or a control diet; however, the LPHC-fed rats had decreased lipoprotein lipase activity in the EPI adipose tissue, which suggests that there was a decreased uptake of fatty acids from the circulating lipoproteins. The LPHC diet did not affect synthesis of glycerol-3-phosphate (G3P) via glycolysis or glyceroneogenesis. Glycerokinase activity - i.e., the phosphorylation of glycerol from the hydrolysis of endogenous TAG to form G3P - was also not affected in LPHC-fed rats. In contrast, adipocytes from LPHC animals had a reduced lipolytic response when stimulated by norepinephrine, even though the basal adipocyte lipolytic rate was similar for both of the groups. Thus, the results suggest that the reduction of lipolytic activity stimulated by norepinephrine seems essential for the TAG increase observed in the EPI adipose tissue of LPHC animals, probably by impairment of the process of activation of lipolysis by norepinephrine.

摘要

脂肪组织中甘油三酯 (TAG) 的积累量取决于 2 个相反的过程:脂肪生成和脂肪分解。我们之前已经表明,在喂养低蛋白、高碳水化合物 (LPHC) 饮食 15 天的生长大鼠中,附睾 (EPI) 脂肪组织的重量和脂质含量增加。这项工作的目的是研究参与脂肪生成和脂肪分解的途径,这些途径最终调节组织中脂质的积累。体内评估了从头脂肪酸合成,对于喂食 LPHC 饮食或对照饮食的大鼠来说是相似的;然而,LPHC 喂养的大鼠在 EPI 脂肪组织中的脂蛋白脂肪酶活性降低,这表明从循环脂蛋白中摄取脂肪酸减少。LPHC 饮食不影响通过糖酵解或甘油酮生成合成甘油-3-磷酸 (G3P)。甘油激酶活性 - 即,甘油从内源性 TAG 的水解形成 G3P 的磷酸化 - 在 LPHC 喂养的大鼠中也没有受到影响。相比之下,即使两组的基础脂肪细胞脂肪分解率相似,LPHC 动物的脂肪细胞对去甲肾上腺素的刺激的脂肪分解反应也降低了。因此,结果表明,去甲肾上腺素刺激的脂肪分解活性降低似乎是 LPHC 动物 EPI 脂肪组织中 TAG 增加的关键,可能是通过损害去甲肾上腺素激活脂肪分解的过程。

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