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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.
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
January 2021,
Journal of nutritional science and vitaminology,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
February 2016,
Nutrients,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
July 2004,
Archives of pharmacal research,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
June 2020,
Scientific reports,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
February 2020,
Cells,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
September 2013,
European journal of pharmacology,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
April 2023,
Scientific reports,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
January 2022,
Foods (Basel, Switzerland),
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
January 2016,
PloS one,
S Ikemoto, and
M Takahashi, and
N Tsunoda, and
K Maruyama, and
H Itakura, and
O Ezaki
June 2018,
Bone reports,
