Lemonnier D, Suquet J P, Aubert R, De Gasquet P, Pequignot E
Diabete Metab. 1975 Jun;1(2):77-85.
Lean mice were made obese by feeding, ad libitum, a high-lard diet. They showed an increased fat cell size and number which were maintained when this diet was replaced by the control high-carbohydrate diet for 10 weeks. Obese fed mice showed normal glucose and insulin serum levels, but insulinaemia was elevated after an overnight fast. The insulinaemic response after intraperitoneal injection of glucose was insignificant. Thus hyperinsulinism is not a prerequisite for the development of obesity. High-fat diet influenced, in vitro, glucose metabolism of adipose tissue, liver and muscle: basal lipogenesis was markedly reduced in adipose tissue and liver, and glucose oxidation was decreased in muscle. Insulin sensitivity was reduced by increased fat cell size. De novo formation of fatty acids in liver and adipose tissue did not contribute to the development of obesity. The increased lipoprotein lipase activity of the large fat cells suggested that obesity resulted from a direct storage of dietary fatty acids esterified by glycerol formed from circulating glucose.
通过随意喂食高脂饮食，使瘦小鼠变得肥胖。它们的脂肪细胞大小和数量增加，当这种饮食被对照高碳水化合物饮食替代10周时，这些指标仍保持不变。喂食肥胖的小鼠血清葡萄糖和胰岛素水平正常，但过夜禁食后胰岛素血症升高。腹腔注射葡萄糖后的胰岛素血症反应不明显。因此，高胰岛素血症不是肥胖发生的先决条件。高脂饮食在体外影响脂肪组织、肝脏和肌肉的葡萄糖代谢：脂肪组织和肝脏中的基础脂肪生成明显减少，肌肉中的葡萄糖氧化减少。脂肪细胞大小增加降低了胰岛素敏感性。肝脏和脂肪组织中脂肪酸的从头合成对肥胖的发生没有作用。大脂肪细胞中脂蛋白脂肪酶活性的增加表明，肥胖是由循环葡萄糖形成的甘油酯化的膳食脂肪酸直接储存所致。
