PTPRT regulates high-fat diet-induced obesity and insulin resistance.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 24949727.
- Also identified by DOI 10.1371/journal.pone.0100783 and PMC identifier 4065109.
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Abstract
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.
Medical subject headings
- Insulin Resistance
- Obesity
- Receptor-Like Protein Tyrosine Phosphatases, Class 2
- STAT3 Transcription Factor