Hyperglycemia compensates for diet-induced insulin resistance in liver and skeletal muscle of rats
Hyperglycemia compensates for diet-induced insulin resistance in liver and skeletal muscle of rats
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DOI：
10.1152/ajpregu.2001.281.5.r1380
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发表时间：
2001-11-01
影响因子：
2.8
通讯作者：
Pagliassotti, MJ
中科院分区：
文献类型：
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作者：
Commerford, SR;Bizeau, ME;Pagliassotti, MJ
高脂肪和高糖饮食增加的基础条件下的葡萄糖外观（glc Ra）的葡萄糖生成的贡献。它们还减少血糖正常、高胰岛素血症条件下glc Ra的胰岛素抑制和胰岛素刺激的肌糖原合成。本研究的目的是确定在高血糖、高胰岛素血症条件下，这些损伤是否影响肝脏和肌肉糖原合成。雄性大鼠喂食高蔗糖、高脂肪或低脂肪淀粉对照饲料1周（n = 5-7/组）或5周（n = 5-6/组）。研究涉及两个90分钟的时间段。在第一个基础期（BP），输注[6-H-3]葡萄糖。在第二组中，输注高血糖期（HP）、[6-H-3]葡萄糖、[6-C-14]葡萄糖和未标记葡萄糖。血糖（BP：111.2 +/- 1.5 mg/dl; HP：172.3 +/- 1.5 mg/dl）、胰岛素（BP：2.5 +/- 0.2 ng/ml; HP：4.9 +/- 0.3 ng/ml）和胰高血糖素（BP：81.8 +/- 1.6 ng/l; HP：74.0 +/- 1.3纳克/升）的浓度在饮食组之间或在饮食时间方面没有显著差异。各组间葡萄糖输注速率（mg . kg（-1）。维持动脉葡萄糖浓度在170 mg/dl附近所需的时间（min（-1（合并平均值：1周时6.4 +/- 0.8; 5周时6.4 +/- 0.7），glc R-a抑制百分比（1周时44.4 ± 7.8%; 5周时63.2 ± 4.3%），示踪剂估计的净肝糖原合成（7.8 ± 1.3 μ g.g肝（-1）。1周时min（-1）; 10.5 +/- 2.2 μ g. g肝（-1）。min（-1），间接途径糖原合成（3.7 ± 0.9 μ g. g肝（-1）。1周时min（-1）; 3.4 ± 0.9 μ g. g肝（-1）。min（-1）5周），或示踪剂估计的净肌肉糖原生成（1.0 +/- 0.3 μ g. g肌肉（-1）。1周时min（-1）; 1.6 +/- 0.3 μ g. g肌肉（-1）。min（-1）。这些数据表明，高血糖补偿肝脏和骨骼肌中的饮食诱导的胰岛素抵抗。
High-fat and high-sucrose diets increase the contribution of gluconeogenesis to glucose appearance (glc Ra) under basal conditions. They also reduce insulin suppression of glc Ra and insulin-stimulated muscle glycogen synthesis under euglycemic, hyperinsulinemic conditions. The purpose of the present study was to determine whether these impairments influence liver and muscle glycogen synthesis under hyperglycemic, hyperinsulinemic conditions. Male rats were fed a high-sucrose, high-fat, or low-fat, starch control diet for either 1 (n = 5-7/group) or 5 wk (n = 5-6/group). Studies involved two 90-min periods. During the first, a basal period (BP), [6-H-3] glucose was infused. In the second, a hyperglycemic period (HP), [6-H-3] glucose, [6-C-14] glucose, and unlabeled glucose were infused. Plasma glucose (BP: 111.2 +/- 1.5 mg/dl; HP: 172.3 +/- 1.5 mg/dl), insulin (BP: 2.5 +/- 0.2 ng/ml; HP: 4.9 +/- 0.3 ng/ml), and glucagon (BP: 81.8 +/- 1.6 ng/l; HP: 74.0 +/- 1.3 ng/l) concentrations were not significantly different among diet groups or with respect to time on diet. There were no significant differences among groups in the glucose infusion rate (mg . kg(-1) . min(-1)) necessary to maintain arterial glucose concentrations at similar to 170 mg/dl (pooled average: 6.4 +/- 0.8 at 1 wk; 6.4 +/- 0.7 at 5 wk), percent suppression of glc R-a (44.4 +/- 7.8% at 1 wk; 63.2 +/- 4.3% at 5 wk), tracer-estimated net liver glycogen synthesis (7.8 +/- 1.3 mug.g liver(-1) . min(-1) at 1 wk; 10.5 +/- 2.2 mug . g liver(-1) . min(-1) at 5 wk), indirect pathway glycogen synthesis (3.7 +/- 0.9 mug . g liver(-1) . min(-1) at 1 wk; 3.4 +/- 0.9 mug . g liver(-1) . min(-1) at 5 wk), or tracer-estimated net muscle glycogenesis (1.0 +/- 0.3 mug . g muscle(-1) . min(-1) at 1 wk; 1.6 +/- 0.3 mug . g muscle(-1) . min(-1) at 5 wk). These data suggest that hyperglycemia compensates for diet-induced insulin resistance in both liver and skeletal muscle.