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Tumor suppressor RIZ1 in obesity and the PI3K/AKT/mTOR pathway.

Authors: Xie, X  Man, X  Zhu, Z  Yuan, D  Huang, S 
Citation: Xie X, etal., Obesity (Silver Spring). 2016 Feb;24(2):389-97. doi: 10.1002/oby.21364. Epub 2015 Dec 26.
Pubmed: (View Article at PubMed) PMID:26709097
DOI: Full-text: DOI:10.1002/oby.21364

OBJECTIVE: The aim of this study was to investigate the shared molecular pathways of obesity and cancer by exploring the role of RIZ1 in obesity and the phospatidylinositol 3-kinase (PI3K)/V-Akt murine thymoma viral oncogene homolog (PKB) (AKT)/mechanistic target of rapamycin (mTOR) pathway. METHODS: Male wild type (WT) and Riz1(-/-) mice (KO) were fed a standard diet (STD) or a high-fat (HF) diet for up to 8 months. These mice were studied for phenotypic and molecular changes. RESULTS: Riz1(-/-) mice gained more weight on a HF diet compared to WT mice, with higher free fatty acid and increased visceral fat. Metabolic cage analysis of Riz1(-/-) mice showed lower oxygen consumption but no changes in food intake and ambulatory activity. Riz1(-/-) mice showed impaired glucose regulation but no change in insulin sensitivity. RNA-seq and quantitative RT-PCR analysis found altered expression in certain glycolysis and ATP production genes such as Ubiad1, Atp5g2, and Cyp4a12. The PI3K/AKT/mTOR pathway was activated in the Riz1(-/-) mice fed a HF diet with higher Akt3 mRNA levels and increased phosphorylation of AKT (Ser473), mTOR, and S6. CONCLUSIONS: The results identify RIZ1 as an important regulator of both Akt3 transcription and AKT phosphorylation and suggest a role for RIZ1 in HF-induced obesity and the AKT pathway.

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CRRD Object Information
CRRD ID: 11535661
Created: 2016-09-21
Species: All species
Last Modified: 2016-09-21
Status: ACTIVE



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