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KMID : 1134820190480050515
Journal of the Korean Society of Food Science and Nutrition
2019 Volume.48 No. 5 p.515 ~ p.523
Anti-Diabetic Effects of Nobiletin in C57BL/KsJ-db/db Mice
Jung Un-Ju

Abstract
This study investigated the anti-diabetic effect of nobiletin in type 2 diabetic mice and its underlying mechanism. Male mice were divided randomly into three groups: Control C57BL/KsJ-db/db mice, age-matched lean non-diabetic db/+ mice, and nobiletin-supplemented db/db mice. The control db/db mice and db/+ mice were fed a normal diet for five weeks, and the nobiletin group were fed a normal diet containing nobiletin (0.02%, w/w) for five weeks. As expected, the db/db mice showed higher food intake and lower body weight gain. Nobiletin tended to improve the weight loss and suppressed hyperphagia. Furthermore, nobiletin decreased the plasma insulin and blood HbA1c levels, improved the glucose tolerance and insulin resistance, and inhibited the hepatic gluconeogenic enzyme activity. Although the plasma total cholesterol concentration was increased by nobiletin, the HDL-cholesterol concentration was also increased in the nobiletin group, resulting in no significant difference in the atherogenic index and HDL-cholesterol to total cholesterol ratio. No significant differences in plasma free fatty acid and triglyceride concentrations as well as hepatic cholesterol content were observed between the control db/db mice and nobiletin-supplemented db/db mice. However, nobiletin significantly decreased the hepatic triglyceride content by inhibiting the fatty acid synthase activity and activating ¥â-oxidation in the liver. Moreover, nobiletin significantly decreased the adipose tissue weight, mRNA expression of pro-inflammatory cytokines and chemokines in the adipose tissue and their circulating levels. These results suggest that nobiletin may be a useful phytochemical compound for improving the glucose intolerance, insulin resistance, hepatic steatosis, and inflammation in type 2 diabetes.
KEYWORD
nobiletin, type 2 diabetic mice, insulin resistance, hepatic steatosis, inflammation
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