果糖
内科学
内分泌学
果糖1,6-二磷酸酶
果实分解
果糖激酶
小肠
新陈代谢
生物
化学
医学
生物化学
作者
Qiufang Bai,Yajin Liu,Chen-Ma Wang,Jue-Rui Wang,Yingying Feng,Xianhua Ma,Xiaohang Yang,Yanan Shi,Weiping J. Zhang
出处
期刊:Endocrinology
[Oxford University Press]
日期:2023-03-25
卷期号:164 (6)
被引量:3
标识
DOI:10.1210/endocr/bqad054
摘要
Abstract Fructose intolerance in mammals is caused by defects in fructose absorption and metabolism. Fructose-1,6-bisphosphatase 1 (FBP1) is a key enzyme in gluconeogenesis, and its deficiency results in hypoglycemia as well as intolerance to fructose. However, the mechanism about fructose intolerance caused by FBP1 deficiency has not been fully elucidated. Here, we demonstrate that hepatic but not intestinal FBP1 is required for fructose metabolism and tolerance. We generated inducible knockout mouse models specifically lacking FBP1 in adult intestine or liver. Intestine-specific deletion of Fbp1 in adult mice does not compromise fructose tolerance, as evidenced by no significant body weight loss, food intake reduction, or morphological changes of the small intestine during 4 weeks of exposure to a high-fructose diet. By contrast, liver-specific deletion of Fbp1 in adult mice leads to fructose intolerance, as manifested by substantial weight loss, hepatomegaly, and liver injury after exposure to a high-fructose diet. Notably, the fructose metabolite fructose-1-phosphate is accumulated in FBP1-deficient liver after fructose challenge, which indicates a defect of fructolysis, probably due to competitive inhibition by fructose-1,6-bisphosphate and may account for the fructose intolerance. In conclusion, these data have clarified the essential role of hepatic but not intestinal FBP1 in fructose metabolism and tolerance.
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