Journal of Nutritional Biochemistry
Journal of Nutritional Biochemistry
4 years ago

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors Chronic high sucrose diet increases fibroblast growth factor 21 production and energy expenditure in mice

Excess carbohydrate intake causes obesity in humans. On the other hand, acute administration of fructose, glucose or sucrose in experimental animals has been shown to increase the plasma concentration of anti-obesity hormones such as glucagon-like peptide 1 (GLP-1) and Fibroblast growth factor 21 (FGF21), which contribute to reducing body weight. However, the secretion and action of GLP-1 and FGF21 in mice chronically fed a high sucrose diet has not been investigated. To address the role of anti-obesity hormones in response to increased sucrose intake, we analyzed mice fed a high sucrose diet, a high starch diet or a normal diet for 15 weeks. Mice fed a high sucrose diet showed resistance to body weight gain, in comparison with mice fed a high starch diet or control diet, due to increased energy expenditure. Plasma FGF21 levels were highest among the three groups in mice fed a high sucrose diet, whereas no significant difference in GLP-1 levels was observed. Expression levels of uncoupling protein 1 (UCP-1), FGF receptor 1c (FGFR1c) and β-klotho (KLB) mRNA in brown adipose tissue were significantly increased in high sucrose-fed mice, suggesting increases in FGF21 sensitivity and energy expenditure. Expression of carbohydrate responsive element binding protein (ChREBP) mRNA in liver and brown adipose tissue was also increased in high sucrose-fed mice. These results indicate that FGF21 production in liver and brown adipose tissue is increased in high sucrose diet and participates in resistance to weight gain.

Publisher URL: www.sciencedirect.com/science

DOI: S0955286317301948

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