Kasim-Karakas S E, Vriend H, Almario R, Chow L C, Goodman M N
Division of Endocrinology and Metabolism, University of California at Davis, Sacramento 95817, USA.
J Lab Clin Med. 1996 Aug;128(2):208-13. doi: 10.1016/s0022-2143(96)90013-x.
Frequent coexistence of insulin resistance, central obesity, and hypertriglyceridemia in the same individual suggests an underlying common pathogenesis. Insulin resistance and hypertriglyceridemia can be induced by carbohydrate feeding in rats. Golden Syrian hamsters are believed to be resistant to the metabolic effects of dietary carbohydrates. We investigated the effects of diets containing 60% fructose or sucrose on glucose and lipid metabolism in hamsters, both in the fasting state and during an intravenous glucose tolerance test. Fructose caused obesity (weight after treatment: 131 +/- 7 gm in the control group, 155 +/- 5 gm in the fructose group, 136 +/- 7 gm in sucrose group, p < 0.04). Fructose also reduced glucose disappearance rate (KG: 2.69% +/- 0.39% in the control group, 1.45% +/- 0.18% in the fructose group, p < 0.02). Sucrose caused a marginal decrease in glucose disappearance (KG: 1.93% +/- 0.21%, p = 0.08 vs the control group). Only fructose feeding increased fasting plasma nonesterified fatty acids (0.645 +/- 0.087 mEq/L in the control group, 1.035 +/- 0.083 mEq/L in the fructose group, 0.606 +/- 0.061 mEq/L in the sucrose group, p < 0.002), plasma triglycerides (84 +/- 6 mg/dl in the control group, 270 +/- 65 mg/dl in the fructose group, 94 +/- 16 mg/dl in the sucrose group, p < 0.0002), and liver triglycerides (1.88 +/- 0.38 mg/gm liver weight in the control group, 2.35 =/- 0.24 mg/gm in the fructose group, 1.41 +/- 0.13 mg/gm in the sucrose group, p < 0.04). Previous studies in the rat have suggested that dietary carbohydrates induce insulin resistance by increasing plasma nonesterified fatty acids and triglycerides, which are preferentially used by the muscles. The present report shows that sucrose also can cause some decrease in glucose disappearance in the hamster without causing hypertriglyceridemia or increasing plasma nonesterified fatty acids. Thus other mechanisms may also contribute to the insulin resistance in the hamster. These findings suggest that hamsters provide a good model for investigation of hormonal and nutritional regulation of glucose and lipid metabolism.
胰岛素抵抗、中心性肥胖和高甘油三酯血症在同一个体中经常并存，提示存在潜在的共同发病机制。在大鼠中，碳水化合物喂养可诱导胰岛素抵抗和高甘油三酯血症。金黄叙利亚仓鼠被认为对膳食碳水化合物的代谢作用具有抗性。我们研究了含60%果糖或蔗糖的饮食对仓鼠在禁食状态和静脉葡萄糖耐量试验期间葡萄糖和脂质代谢的影响。果糖导致肥胖（治疗后体重：对照组为131±7克，果糖组为155±5克，蔗糖组为136±7克，p<0.04）。果糖还降低了葡萄糖消失率（K G：对照组为2.69%±0.39%，果糖组为1.45%±0.18%，p<0.02）。蔗糖使葡萄糖消失略有减少（K G：1.93%±0.21%，与对照组相比p=0.08）。仅果糖喂养增加了空腹血浆非酯化脂肪酸（对照组为0.645±0.087mEq/L，果糖组为1.035±0.083mEq/L，蔗糖组为0.606±0.061mEq/L，p<0.002）、血浆甘油三酯（对照组为84±6mg/dl，果糖组为270±65mg/dl，蔗糖组为94±16mg/dl，p<0.0002）和肝脏甘油三酯（对照组为1.88±0.38mg/g肝脏重量，果糖组为2.35±0.24mg/g，蔗糖组为1.41±0.13mg/g，p<0.04）。先前在大鼠中的研究表明，膳食碳水化合物通过增加血浆非酯化脂肪酸和甘油三酯诱导胰岛素抵抗，而肌肉优先利用这些物质。本报告显示，蔗糖也可使仓鼠的葡萄糖消失有所减少，而不引起高甘油三酯血症或增加血浆非酯化脂肪酸。因此，其他机制也可能导致仓鼠的胰岛素抵抗。这些发现表明，仓鼠为研究葡萄糖和脂质代谢的激素和营养调节提供了一个良好的模型。
