Ikemoto S, Takahashi M, Tsunoda N, Maruyama K, Itakura H, Ezaki O
Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan.
Metabolism. 1996 Dec;45(12):1539-46. doi: 10.1016/s0026-0495(96)90185-7.
Mice fed a high-fat diet develop hyperglycemia and obesity. Using non-insulin-dependent diabetes mellitus (NIDDM) model mice, we investigated the effects of seven different dietary oils on glucose metabolism: palm oil, which contains mainly 45% palmitic acid (16:0) and 40% oleic acid (18:1); lard oil, 24% palmitic and 44% oleic acid; rapeseed oil, 59% oleic and 20% linoleic acid (18:2); soybean oil, 24% oleic and 54% linoleic acid; safflower oil, 76% linoleic acid; perilla oil, 58% alpha-linolenic acid; and tuna fish oil, 7% eicosapentaenoic acid and 23% docosahexaenoic acid. C57BL/6J mice received each as a high-fat diet (60% of total calories) for 19 weeks (n = 6 to 11 per group). After 19 weeks of feeding, body weight induced by the diets was in the following order: soybean > palm > or = lard > or = rapeseed > or = safflower > or = perilla > fish oil. Glucose levels 30 minutes after a glucose load were highest for safflower oil (approximately 21.5 mmol/L), modest for rapeseed oil, soybean oil, and lard (approximately 17.6 mmol/L), mild for perilla, fish, and palm oil (approximately 13.8 mmol/L), and minimal for high-carbohydrate meals (approximately 10.4 mmol/L). Only palm oil-fed mice showed fasting hyperinsulinemia (P < .001). By stepwise multiple regression analysis, body weight (or white adipose tissue [WAT] weight) and intake of linoleic acid (or n-3/n-6 ratio) were chosen as independent variables to affect glucose tolerance. By univariate analysis, the linoleic acid intake had a positive correlation with blood glucose level (r = .83, P = .02) but not with obesity (r = .46, P = .30). These data indicate that (1) fasting blood insulin levels vary among fat subtypes, and a higher fasting blood insulin level in palm oil-fed mice may explain their better glycemic control irrespective of their marked obesity; (2) a favorable glucose response induced by fish oil feeding may be mediated by a decrease of body weight; and (3) obesity and a higher intake of linoleic acid are independent risk factors for dysregulation of glucose tolerance.
喂食高脂饮食的小鼠会出现高血糖和肥胖。我们使用非胰岛素依赖型糖尿病（NIDDM）模型小鼠，研究了七种不同食用油对葡萄糖代谢的影响：棕榈油，主要含有45%的棕榈酸（16:0）和40%的油酸（18:1）；猪油，24%的棕榈酸和44%的油酸；菜籽油，59%的油酸和20%的亚油酸（18:2）；大豆油，24%的油酸和54%的亚油酸；红花油，76%的亚油酸；紫苏油，58%的α-亚麻酸；以及金枪鱼鱼油，7%的二十碳五烯酸和23%的二十二碳六烯酸。C57BL/6J小鼠分别接受每种食用油作为高脂饮食（占总热量的60%），持续19周（每组n = 6至11）。喂食19周后，不同饮食诱导的体重顺序如下：大豆油>棕榈油>或=猪油>或=菜籽油>或=红花油>或=紫苏油>鱼油。葡萄糖负荷后30分钟的血糖水平，红花油组最高（约21.5 mmol/L），菜籽油、大豆油和猪油组适中（约17.6 mmol/L），紫苏油、鱼油和棕榈油组轻度升高（约13.8 mmol/L），高碳水化合物餐组最低（约10.4 mmol/L）。只有喂食棕榈油的小鼠出现空腹高胰岛素血症（P <.001）。通过逐步多元回归分析，选择体重（或白色脂肪组织[WAT]重量）和亚油酸摄入量（或n-3/n-6比值）作为影响葡萄糖耐量的自变量。通过单因素分析，亚油酸摄入量与血糖水平呈正相关（r =.83，P =.02），但与肥胖无关（r =.46，P =.30）。这些数据表明：（1）空腹血胰岛素水平在不同脂肪亚型中有所不同，喂食棕榈油的小鼠空腹血胰岛素水平较高，这可能解释了尽管它们明显肥胖，但血糖控制较好的原因；（2）喂食鱼油诱导的良好葡萄糖反应可能是由体重减轻介导的；（3）肥胖和较高的亚油酸摄入量是葡萄糖耐量失调的独立危险因素。
