Muscle lipid metabolism and insulin secretion are altered in insulin-resistant rats fed a high sucrose diet
Muscle lipid metabolism and insulin secretion are altered in insulin-resistant rats fed a high sucrose diet
复制标题
DOI：
10.1093/jn/133.1.127
复制
发表时间：
2003-01-01
影响因子：
4.2
通讯作者：
Lombardo, YB
中科院分区：
文献类型：
--
作者：
Chicco, A;D'Alessandro, ME;Lombardo, YB
给大鼠喂食富含蔗糖的食物（SRD）可诱导高甘油三酯血症和胰岛素抵抗。本研究的目的是测定SRD喂养3、15、30周大鼠基础状态和正糖高胰岛素钳夹后腓肠肌脂质和葡萄糖代谢变化的时间过程，分析SRD喂养大鼠周围离体胰岛葡萄糖刺激胰岛素分泌的变化及其与外周胰岛素不敏感的关系。对照组大鼠饲喂相同时间的对照日粮（CD）。食用SRD 3周后，肌肉中的长链酰基辅酶a （lacoa）水平高于喂食CD的大鼠，这是脂质代谢紊乱的早期迹象。此时糖原储存和葡萄糖氧化均未受损。此外，葡萄糖刺激胰岛素分泌的双相模式在第一个峰值明显增加，这有助于维持srd喂养大鼠的正常血糖。食用SRD 15或30周后，肌肉中的甘油三酯和lacoa水平高于喂食CD的大鼠。葡萄糖氧化以及胰岛素刺激的糖原合成酶活性和糖原储存低于喂食CD的大鼠。此外，胰岛素分泌模式的改变进一步恶化。伴有外周胰岛素抵抗和中度高血糖。我们的研究结果表明，长期喂食SRD的大鼠的血脂异常可能在该动物模型中胰岛素分泌和敏感性的进行性恶化中起重要作用。
Feeding rats a sucrose rich diet (SRD) induces hypertriglyceridemia and insulin resistance. The purposes of this study were to determine the time course of changes in lipid and glucose metabolism in the gastrocnemius muscle, both in the basal state and after the euglycemic hyperinsulinemic clamp, in rats fed a SRD for 3, 15 or 30 wk, and to analyze the changes in glucose-stimulated insulin secretion from perifused isolated islets from SRD-fed rats and their relationships to peripheral insulin insensitivity. A control group of rats was fed a control diet (CD) for the same period of time. After 3 wk of consuming the SRD, long-chain acyl CoA (LCACoA) levels in muscle were greater than in rats fed the CD, an early indication of the disturbance of lipid metabolism. Neither glycogen storage nor glucose oxidation were impaired at this time. Moreover, the biphasic patterns of glucose-stimulated insulin secretion showed a marked increase in the first peak, which helped maintain normoglycemia in SRD-fed rats. After 15 or 30 wk of consuming the SRD, triglyceride and LCACoA levels in muscles were greater than in rats fed the CD. Glucose oxidation as well as insulin-stimulated glycogen synthase activity and glycogen storage were lower than in rats fed the CD. Moreover, the altered pattern of insulin secretion further deteriorated. This was accompanied by peripheral insulin resistance and moderate hyperglycemia. Our results indicate that the dyslipemia present in rats chronically fed a SRD may play an important role in the progressive deterioration of insulin secretion and sensitivity in this animal model.