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Extensive metabolic disorders are present in APC(min) tumorigenesis mice.

Authors: Liu, Zhenzhen  Xiao, Yi  Zhou, Zhengxiang  Mao, Xiaoxiao  Cai, Jinxing  Xiong, Lu  Liao, Chaonan  Huang, Fulian  Liu, Zehao  Ali Sheikh, Md Sayed  Plutzky, Jorge  Huang, He  Yang, Tianlun  Duan, Qiong 
Citation: Liu Z, etal., Mol Cell Endocrinol. 2016 May 15;427:57-64. doi: 10.1016/j.mce.2016.03.004. Epub 2016 Mar 4.
Pubmed: (View Article at PubMed) PMID:26948948
DOI: Full-text: DOI:10.1016/j.mce.2016.03.004

Wnt signaling plays essential role in mesenchymal stem cell (MSC) differentiation. Activation of Wnt signaling suppresses adipogenesis, but promotes osteogenesis in MSC. Adenomatous polyposis coli (APC) is a negative regulator of ß-catenin and Wnt signaling activity. The mutation of APC gene leads to the activation of Wnt signaling and is responsible for tumorigenesis in APC(min) mouse; however, very few studies focused on its metabolic abnormalities. The present study reports a widespread metabolic disorder phenotype in APC(min) mice. The old APC(min) mice have decreased body weight and impaired adipogenesis, but severe hyperlipidemia, which mimic the phenotypes of Familial Adenomatous Polyposis (FAP), an inherited disease also caused by APC gene mutation in human. We found that the expression of lipid metabolism and free fat acids (FA) use genes in the white adipose tissue (WAT) of the APC(min) mice is much lower than those of control. The changed gene expression pattern may lead to the disability of circulatory lipid transportation and storage at WAT. Moreover, the APC(min) mice could not maintain the core body temperature in cold condition. PET-CT determination revealed that the BAT of APC(min) mice has significantly impaired ability to take up (18)FDG from the blood. Morphological studies identified that the brown adipocytes of APC(min) mice were filled with lipid droplets but fewer mitochondria. These results matched with the findings of impaired BAT function in APC(min) mice. Collectively, our study explores a new mechanism that explains abnormal metabolism in APC(min) mice and provides insights into studying the metabolic disorders of FAP patients.


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RGD Object Information
RGD ID: 13673785
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.