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高脂饮食通过增加肝脏葡萄糖生成,使链脲佐菌素处理的大鼠的代谢控制恶化。

A high-fat diet worsens metabolic control in streptozotocin-treated rats by increasing hepatic glucose production.

作者信息

Traianedes K, Proietto J, O'Dea K

机构信息

Department of Human Nutrition, Deakin University, Geelong, Victoria, Australia.

出版信息

Metabolism. 1992 Aug;41(8):846-50. doi: 10.1016/0026-0495(92)90165-7.

DOI:10.1016/0026-0495(92)90165-7
PMID:1640861
Abstract

The aim of this study was to determine the mechanism by which a high-fat diet exacerbates the diabetes produced by a low dose of streptozotocin (STZ). The glucose clamp technique was used to determine hepatic glucose production (HGP) and the disappearance rate (Rd) of glucose, basally and during insulin infusions of 1.0 and 3.0 mU/kg/min in control of STZ-treated rats fed either a low-fat or high-fat diet. Fasting plasma glucose in the high fat-STZ (HFS) group was significantly higher than in any of the other groups: low fat-STZ (LFS), high-fat controls (HFC), or low-fat controls (LFC) (18.1 +/- 1.6 v 8.1 +/- 0.8 mmol/L, P less than .001; 6.0 +/- 0.2 mmol/L, P less than .001; 5.4 +/- 0.1 mmol/L, P less than .001, respectively). Basal HGP was markedly higher in the HFS group compared with each of the other three groups (98.8 +/- 5.9 v 61.4 +/- 3.7, P less than .001; 42.9 +/- 1.6, P less than .001; 39.6 +/- 1.3 mumol/kg/min, P less than .001; HFS v LFS, HFC, and LFC, respectively). Following insulin infusion, no differences were observed in HGP between the LFC and LFS groups at either insulin dose. However, HGP was not suppressed to control levels in either of the high-fat diet groups, and this defect was more marked in the HFS group. It is concluded that a high-fat diet exacerbates mild STZ diabetes primarily by increasing HGP.

摘要

本研究的目的是确定高脂饮食加剧低剂量链脲佐菌素(STZ)所致糖尿病的机制。采用葡萄糖钳夹技术,在基础状态以及以1.0和3.0 mU/kg/min的速率输注胰岛素期间,测定低脂或高脂饮食喂养的STZ处理大鼠的肝葡萄糖生成(HGP)和葡萄糖消失率(Rd)。高脂-STZ(HFS)组的空腹血糖显著高于其他任何组:低脂-STZ(LFS)组、高脂对照组(HFC)或低脂对照组(LFC)(分别为18.1±1.6 vs 8.1±0.8 mmol/L,P<0.001;6.0±0.2 mmol/L,P<0.001;5.4±0.1 mmol/L,P<0.001)。与其他三组相比,HFS组的基础HGP显著更高(分别为98.8±5.9 vs 61.4±3.7,P<0.001;42.9±1.6,P<0.001;39.6±1.3 μmol/kg/min,P<0.001;HFS vs LFS、HFC和LFC)。输注胰岛素后,LFC组和LFS组在任一胰岛素剂量下的HGP均未观察到差异。然而,高脂饮食组中的任何一组HGP均未被抑制至对照水平,且该缺陷在HFS组中更为明显。结论是,高脂饮食主要通过增加HGP来加剧轻度STZ糖尿病。

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