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PI3K signaling: A key pathway in the control of sympathetic traffic and arterial pressure by leptin
Journal article   Open access   Peer reviewed

PI3K signaling: A key pathway in the control of sympathetic traffic and arterial pressure by leptin

Shannon M Harlan and Kamal Rahmouni
Molecular metabolism (Germany), Vol.2(2), pp.69-73
04/2013
DOI: 10.1016/j.molmet.2013.03.004
PMCID: PMC3817392
PMID: 24199153
url
https://doi.org/10.1016/j.molmet.2013.03.004View
Published (Version of record) Open Access

Abstract

The adipocyte-derived hormone, leptin, is a master regulator of energy homeostasis. Leptin action in the central nervous system also contributes to arterial pressure regulation through its capacity to increase renal sympathetic outflow. The accumulating evidence pointing to a key role for leptin in the adverse sympathetic and cardiovascular consequences of excessive adiposity highlight the importance of understanding the mechanisms underlying the sympathetic and cardiovascular effects of leptin. The ability of the leptin receptor to stimulate various intracellular pathways allows leptin to regulate physiological processes in a specific manner. In this review, we examine the role of the PI3K pathway emanating from the leptin receptor in mediating the sympathetic and arterial pressure effects of leptin. We also discuss the relevance of PI3K signaling for obesity-induced hypertension through its role in mediating selective leptin resistance.
Energy homeostasis PI3K Cardiovascular function Autonomic nervous system Leptin

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