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. 2017 Apr 12;4:20. doi: 10.3389/fcvm.2017.00020

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Copyright © 2017 Nebigil.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Prokineticin-2 (PK2)/PKR1 signaling may act as a new connector between development of obesity, diabetes and cardiovascular diseases (CVDs). PKR1 deficiency promotes WAT expansion and insulin resistance, CVD, and alters food intake in mice. Whether reduced level of PKR1 or functional mutated PKR1 involves these disorders in human needs to be studied. PK2/PKR1 signaling in central nervous system (CNS) regulates food intake. PK2 released from adipocytes controls preadipocyte conversion to adipocyte via PKR1 signaling and may affect food intake via CNS. Circulating or local PK2 signaling via PKR1 contributes development and function of heart and kidney. Whether this signaling involves heart and kidney regulation via CNS remains to be study.