Striffler J S, Polansky M M, Anderson R A
Beltsville Human Nutrition Research Center, US Department of Agriculture, Agricultural Research Service, MD 20705-2350, USA.
Metabolism. 1999 Aug;48(8):1063-8. doi: 10.1016/s0026-0495(99)90207-x.
The hypothesis that the insulin secretory hyperresponsiveness observed in rats with diet-induced insulin resistance may be a basic characteristic of dietary chromium (Cr) deficiency was evaluated. Two groups of weanling rats were fed ad libitum a purified diet containing 64% sucrose, 20% casein, 5% corn oil, and the recommended levels of vitamins and minerals without added Cr. Cr-deficient (-Cr) rats were provided with distilled drinking water only, while Cr-supplemented (+Cr) rats received water containing 5 ppm Cr as CrCl3. A third group of rats fed a commercial chow diet served as sucrose controls. Effects of Cr deficiency were assessed by comparing fasting levels of glucose, insulin, and plasma lipids in blood samples collected biweekly from the -Cr and +Cr groups over a 3-month period. Both groups of rats fed the low-Cr sucrose diet developed a transient hyperinsulinemia and hyperlipidemia relative to the chow-fed control rats. There were significant effects of Cr supplementation on plasma triglycerides during the initial 2 weeks of dietary adaptation. Effects of the low-Cr diet were evaluated after the 12-week period by comparing the insulin response area and glucose clearance during a 40-minute intravenous glucose tolerance test (IVGTT). The rates of glucose clearance (KG) in -Cr and +Cr rats were similar (4.2 +/- 1.0 and 4.3 +/- 0.8%/min, respectively) and were comparable to the K(G) in chow-fed rats (4.6 +/- 0.8). In contrast, insulin secretory responses in -Cr rats were exaggerated (area, 14,083 +/- 3,399 microU/mL x min), being twofold greater (P < .05) relative to the +Cr group (6,183 +/- 864). The insulin secretory response area in chow-fed rats (7,081 +/- 408 microU/mL x min) was similar to the value in the +Cr group. These observations provide support for the hypothesis that Cr deficiency can lead to elevated insulin secretory responses to glucose.
对饮食诱导的胰岛素抵抗大鼠中观察到的胰岛素分泌高反应性可能是膳食铬（Cr）缺乏的基本特征这一假说进行了评估。两组断乳大鼠随意进食含64%蔗糖、20%酪蛋白、5%玉米油以及推荐水平的维生素和矿物质但未添加铬的纯化饮食。缺铬（-Cr）组大鼠仅提供蒸馏水，而补铬（+Cr）组大鼠饮用含5 ppm Cr（以CrCl3形式）的水。第三组喂食商业混合饲料的大鼠作为蔗糖对照组。通过比较在3个月期间每两周从-Cr组和+Cr组采集的血样中的空腹血糖、胰岛素和血浆脂质水平，评估铬缺乏的影响。相对于喂食混合饲料的对照大鼠，两组喂食低铬蔗糖饮食的大鼠均出现短暂的高胰岛素血症和高脂血症。在饮食适应的最初2周内，补铬对血浆甘油三酯有显著影响。在12周后，通过比较40分钟静脉葡萄糖耐量试验（IVGTT）期间的胰岛素反应面积和葡萄糖清除率，评估低铬饮食的影响。-Cr组和+Cr组大鼠的葡萄糖清除率（KG）相似（分别为4.2±1.0和4.3±0.8%/分钟），与喂食混合饲料的大鼠的K（G）相当（4.6±0.8）。相比之下，-Cr组大鼠的胰岛素分泌反应增强（面积为14,083±3,399微单位/毫升×分钟），比+Cr组（6,183±864）高出两倍（P<.05）。喂食混合饲料的大鼠的胰岛素分泌反应面积（7,081±408微单位/毫升×分钟）与+Cr组的值相似。这些观察结果支持了铬缺乏可导致对葡萄糖的胰岛素分泌反应升高这一假说。
