PTPRJ Inhibits Leptin Signaling, and Induction of PTPRJ in the Hypothalamus Is a Cause of the Development of Leptin Resistance View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Takafumi Shintani, Satoru Higashi, Ryoko Suzuki, Yasushi Takeuchi, Reina Ikaga, Tomomi Yamazaki, Kenta Kobayashi, Masaharu Noda

ABSTRACT

Leptin signaling in the hypothalamus plays a crucial role in the regulation of body weight. Leptin resistance, in which leptin signaling is disrupted, is a major obstacle to the improvement of obesity. We herein demonstrated that protein tyrosine phosphatase receptor type J (Ptprj) is expressed in hypothalamic neurons together with leptin receptors, and that PTPRJ negatively regulates leptin signaling by inhibiting the activation of JAK2, the primary tyrosine kinase in leptin signaling, through the dephosphorylation of Y813 and Y868 in JAK2 autophosphorylation sites. Leptin signaling is enhanced in Ptprj-deficient mice, and they exhibit lower weight gain than wild-type mice because of a reduced food intake. Diet-induced obesity and the leptin treatment up-regulated PTPRJ expression in the hypothalamus, while the overexpression of PTPRJ induced leptin resistance. Thus, the induction of PTPRJ is a factor contributing to the development of leptin resistance, and the inhibition of PTPRJ may be a potential strategy for improving obesity. More... »

PAGES

11627

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-017-12070-7

DOI

http://dx.doi.org/10.1038/s41598-017-12070-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1091665823

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28912580


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