Hypocaloric high-protein diet improves fatty liver and hypertriglyceridemia in sucrose-fed obese rats via two pathways
Hypocaloric high-protein diet improves fatty liver and hypertriglyceridemia in sucrose-fed obese rats via two pathways
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DOI：
10.1152/ajpendo.00014.2009
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发表时间：
2009-07-01
影响因子：
5.1
通讯作者：
Takeda, Eiji
中科院分区：
文献类型：
--
作者：
Uebanso, Takashi;Taketani, Yutaka;Takeda, Eiji
[10] Uebanso T，Taketani Y，福谷M，Sato K，Takei Y，Sato T，Sawada N，Amo K，Harada N，Arai H，Yamamoto H，Takeda E.低热量高蛋白饮食通过两种途径改善蔗糖喂养肥胖大鼠的脂肪肝和高脂血症。Am J Physiol Endocrinol Metab 297：E76-E84，2009.首次发表于2009年5月12日; doi：10.1152/ajpendo.00014.2009.-在减肥过程中用蛋白质替代某些饮食中的碳水化合物有利于脂质代谢的机制仍然不清楚。在这项研究中，我们研究了能量限制，高蛋白/低碳水化合物饮食对肥胖大鼠脂质代谢的影响。高蔗糖诱导的肥胖大鼠被随机分配到两个能量限制饮食干预之一：碳水化合物为基础的控制饮食（CD）或高蛋白饮食（HPD）。另取同龄瘦型大鼠作为正常对照。相对于CD饮食，HPD饮食对脂肪肝和高脂血症的改善显著更大。在喂食HPD的肥胖大鼠中，受成纤维细胞生长因子-21（FGF 21）调节并参与肝脏脂解和脂质利用的基因（如脂肪酶和酰基辅酶A氧化酶）的表达增加。此外，FGF 21基因表达水平（由胰高血糖素/胰岛素平衡调节）与肥胖大鼠肝脏中甘油三酯浓度升高呈负相关。相对于CD组，HPD组（与禁食动物的血浆甘油三酯水平相似）中主要受饮食碳水化合物调节的肝硬脂酰辅酶A去饱和酶-1（SCD 1）的表达也显著降低。总之，低热量高蛋白饮食相对于碳水化合物饮食有效地改善脂肪肝和高脂血症。在这些益处背后起作用的两种细胞途径包括通过FGF 21介导的肝脂解和脂质利用的刺激以及通过SCD 1调节的肝VLDL-TG产生的减少。
Uebanso T, Taketani Y, Fukaya M, Sato K, Takei Y, Sato T, Sawada N, Amo K, Harada N, Arai H, Yamamoto H, Takeda E. Hypocaloric high-protein diet improves fatty liver and hypertriglyceridemia in sucrose-fed obese rats via two pathways. Am J Physiol Endocrinol Metab 297: E76-E84, 2009. First published May 12, 2009; doi: 10.1152/ajpendo.00014.2009.-The mechanism by which replacement of some dietary carbohydrates with protein during weight loss favors lipid metabolism remains obscure. In this study, we investigated the effect of an energy-restricted, high-protein/low-carbohydrate diet on lipid metabolism in obese rats. High-sucrose-induced obese rats were assigned randomly to one of two energy-restricted dietary interventions: a carbohydrate-based control diet ( CD) or a high-protein diet (HPD). Lean rats of the same age were assigned as normal control. There was significantly greater improvement in fatty liver and hypertriglyceridemia with the HPD diet relative to the CD diet. Expression of genes regulated by fibroblast growth factor-21 (FGF21) and involved in liver lipolysis and lipid utilitization, such as lipase and acyl-CoA oxidase, increased in obese rats fed the HPD. Furthermore, there was an inverse correlation between levels of FGF21 gene expression ( regulated by glucagon/insulin balance) and increased triglyceride concentrations in liver from obese rats. Expression of hepatic stearoyl-CoA desaturase-1 (SCD1), regulated primarily by the dietary carbohydrate, was also markedly reduced in the HPD group ( similar to plasma triglyceride levels in fasting animals) relative to the CD group. In conclusion, a hypocaloric high-protein diet improves fatty liver and hypertriglyceridemia effectively relative to a carbohydrate diet. The two cellular pathways at work behind these benefits include stimulation of hepatic lipolysis and lipid utilization mediated by FGF21 and reduction of hepatic VLDL-TG production by SCD1 regulation.