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首页> 外文期刊>American Journal of Physiology >Hyperglycemia compensates for diet-induced insulin resistance in liver and skeletal muscle of rats.
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Hyperglycemia compensates for diet-induced insulin resistance in liver and skeletal muscle of rats.

机译：高血糖可以补偿饮食引起的大鼠肝脏和骨骼肌胰岛素抵抗。

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摘要

High-fat and high-sucrose diets increase the contribution of gluconeogenesis to glucose appearance (glc R(a)) under basal conditions. They also reduce insulin suppression of glc R(a) 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), [6-3H]glucose was infused. In the second, a hyperglycemic period (HP), [6-3H]glucose, [6-14C]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 x kg(-1) x min(-1)) necessary to maintain arterial glucose concentrations at approximately 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 microg x g liver(-1) x min(-1) at 1 wk; 10.5 +/- 2.2 microg x g liver(-1) x min(-1) at 5 wk), indirect pathway glycogen synthesis (3.7 +/- 0.9 microg x g liver(-1) x min(-1) at 1 wk; 3.4 +/- 0.9 microg x g liver(-1) x min(-1) at 5 wk), or tracer-estimated net muscle glycogenesis (1.0 +/- 0.3 microg x g muscle(-1) x min(-1) at 1 wk; 1.6 +/- 0.3 microg x g muscle(-1) x min(-1) at 5 wk). These data suggest that hyperglycemia compensates for diet-induced insulin resistance in both liver and skeletal muscle.
机译：在基础条件下，高脂高蔗糖饮食会增加糖异生作用对葡萄糖外观（glc R（a））的贡献。在正常血糖，高胰岛素的情况下，它们还减少了glc R（a）的胰岛素抑制和胰岛素刺激的肌肉糖原合成。本研究的目的是确定在高血糖，高胰岛素的情况下，这些损伤是否影响肝脏和肌肉糖原的合成。给雄性大鼠喂食高蔗糖，高脂或低脂的淀粉对照饮食，剂量为1（n = 5-7 /组）或5 wk（n = 5-6 /组）。研究涉及两个90分钟的时间段。在第一个基础时期（BP），注入[6-3H]葡萄糖。在第二步中，注入高血糖期（HP），[6-3H]葡萄糖，[6-14C]葡萄糖和未标记的葡萄糖。血浆葡萄糖（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）和饮食中胰高血糖素（BP：81.8 +/- 1.6 ng / l; HP：74.0 +/- 1.3 ng / l）的浓度在饮食组之间或就饮食时间而言均无显着差异。各组之间的葡萄糖输注速率（mg x kg（-1）x min（-1））没有显着差异，维持动脉葡萄糖浓度约为170 mg / dl（合并平均值：1时为6.4 +/- 0.8） wk; 5 wk时为6.4 +/- 0.7），glc R（a）抑制百分比（1 wk时为44.4 +/- 7.8％; 5 wk时为63.2 +/- 4.3％），示踪剂估计的净肝糖原合成（ 1周时为7.8 +/- 1.3 microg xg肝（-1）x min（-1）; 5周时为10.5 +/- 2.2 microg xg肝（-1）x min（-1），间接途径糖原合成（ 1 wk时3.7 +/- 0.9 microg xg肝（-1）x min（-1）; 5 wk时3.4 +/- 0.9 microg xg肝脏（-1）x min（-1）或示踪剂估计的净值肌肉糖原形成（1 wk时1.0 +/- 0.3 microg xg肌肉（-1）x min（-1）; 5 wk时1.6 +/- 0.3 microg xg肌肉（-1）x min（-1））。这些数据表明，高血糖可以补偿饮食引起的肝脏和骨骼肌胰岛素抵抗。

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