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Leptin as a Mediator of Obesity-Induced Hypertension

  • Metabolism (J Proietto, Section Editor)
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Abstract

Hypertension and associated cardiovascular diseases represent the most common health complication of obesity and the leading cause of morbidity and mortality in overweight and obese patients. Emerging evidence suggests a critical role for the central nervous system particularly the brain action of the adipocyte-derived hormone leptin in linking obesity and hypertension. The preserved ability of leptin to cause cardiovascular sympathetic nerve activation despite the resistance to the metabolic actions of the hormone appears essential in this pathological process. This review describes the evidence supporting the neurogenic bases for obesity-associated hypertension with a particular focus on the neuronal and molecular signaling pathways underlying leptin’s effects on sympathetic nerve activity and blood pressure.

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Correspondence to Kamal Rahmouni.

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Balyssa B. Bell and Kamal Rahmouni declare that they have no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

Sources of Funding

The authors’ research is supported by the US National Institutes of Health (HL084207), the American Heart Association (Award #14EIA18860041), the University of Iowa Fraternal Order of Eagles Diabetes Research Center, and the University of Iowa Center for Hypertension Research.

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This article is part of the Topical Collection on Metabolism

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Bell, B.B., Rahmouni, K. Leptin as a Mediator of Obesity-Induced Hypertension. Curr Obes Rep 5, 397–404 (2016). https://doi.org/10.1007/s13679-016-0231-x

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