PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance

Obesity is a risk factor for many human diseases. However, the underlying molecular causes of obesity are not well understood. Here, we report that protein tyrosine phosphatase receptor T (PTPRT) knockout mice are resistant to high-fat diet-induced obesity. Those mice avoid many deleterious side eff...

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Autores principales: Feng, Xiujing, Scott, Anthony, Wang, Yong, Wang, Lan, Zhao, Yiqing, Doerner, Stephanie, Satake, Masanobu, Croniger, Colleen M., Wang, Zhenghe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065109/
https://www.ncbi.nlm.nih.gov/pubmed/24949727
http://dx.doi.org/10.1371/journal.pone.0100783
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author Feng, Xiujing
Scott, Anthony
Wang, Yong
Wang, Lan
Zhao, Yiqing
Doerner, Stephanie
Satake, Masanobu
Croniger, Colleen M.
Wang, Zhenghe
author_facet Feng, Xiujing
Scott, Anthony
Wang, Yong
Wang, Lan
Zhao, Yiqing
Doerner, Stephanie
Satake, Masanobu
Croniger, Colleen M.
Wang, Zhenghe
author_sort Feng, Xiujing
collection PubMed
description Obesity is a risk factor for many human diseases. However, the underlying molecular causes of obesity are not well understood. Here, we report that protein tyrosine phosphatase receptor T (PTPRT) knockout mice are resistant to high-fat diet-induced obesity. Those mice avoid many deleterious side effects of high-fat diet-induced obesity, displaying improved peripheral insulin sensitivity, lower blood glucose and insulin levels. Compared to wild type littermates, PTPRT knockout mice show reduced food intake. Consistently, STAT3 phosphorylation is up-regulated in the hypothalamus of PTPRT knockout mice. These studies implicate PTPRT-modulated STAT3 signaling in the regulation of high-fat diet-induced obesity.
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spelling pubmed-40651092014-06-25 PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance Feng, Xiujing Scott, Anthony Wang, Yong Wang, Lan Zhao, Yiqing Doerner, Stephanie Satake, Masanobu Croniger, Colleen M. Wang, Zhenghe PLoS One Research Article Obesity is a risk factor for many human diseases. However, the underlying molecular causes of obesity are not well understood. Here, we report that protein tyrosine phosphatase receptor T (PTPRT) knockout mice are resistant to high-fat diet-induced obesity. Those mice avoid many deleterious side effects of high-fat diet-induced obesity, displaying improved peripheral insulin sensitivity, lower blood glucose and insulin levels. Compared to wild type littermates, PTPRT knockout mice show reduced food intake. Consistently, STAT3 phosphorylation is up-regulated in the hypothalamus of PTPRT knockout mice. These studies implicate PTPRT-modulated STAT3 signaling in the regulation of high-fat diet-induced obesity. Public Library of Science 2014-06-20 /pmc/articles/PMC4065109/ /pubmed/24949727 http://dx.doi.org/10.1371/journal.pone.0100783 Text en © 2014 Feng et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Feng, Xiujing
Scott, Anthony
Wang, Yong
Wang, Lan
Zhao, Yiqing
Doerner, Stephanie
Satake, Masanobu
Croniger, Colleen M.
Wang, Zhenghe
PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance
title PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance
title_full PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance
title_fullStr PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance
title_full_unstemmed PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance
title_short PTPRT Regulates High-Fat Diet-Induced Obesity and Insulin Resistance
title_sort ptprt regulates high-fat diet-induced obesity and insulin resistance
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065109/
https://www.ncbi.nlm.nih.gov/pubmed/24949727
http://dx.doi.org/10.1371/journal.pone.0100783
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