Temporal Leptin to Determine Cardiovascular and Metabolic Fate throughout the Life.

Nutrients

Department of Pharmacology and Physiology, School of Medicine & Health Sciences, The George Washington University, Washington, DC 20037, USA.

Published: October 2020

AI Article Synopsis

  • * Disruptions in leptin signaling in the brain can lead to serious health issues like obesity, hypertension, and type 2 diabetes.
  • * Maternal leptin levels during pregnancy can influence the metabolic health of infants, impacting their future health based on their body fat and leptin levels in early life.

Article Abstract

Leptin links peripheral adiposity and the central nervous system (CNS) to regulate cardiometabolic physiology. Within the CNS, leptin receptor-expressing cells are a counterpart to circulating leptin, and leptin receptor-mediated neural networks modulate the output of neuroendocrine and sympathetic nervous activity to balance cardiometabolic homeostasis. Therefore, disrupted CNS leptin signaling is directly implicated in the development of metabolic diseases, such as hypertension, obesity, and type 2 diabetes. Independently, maternal leptin also plays a central role in the development and growth of the infant during gestation. Accumulating evidence points to the dynamic maternal leptin environment as a predictor of cardiometabolic fate in their offspring as it is directly associated with infant metabolic parameters at birth. In postnatal life, the degree of serum leptin is representative of the level of body adiposity/weight, a driving factor for cardiometabolic alterations, and therefore, the levels of blood leptin through the CNS mechanism, in a large part, are a strong determinant for future cardiometabolic fate. The current review focuses on highlighting and discussing recent updates for temporal dissection of leptin-associated programing of future cardiometabolic fate throughout the entire life.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7690895PMC
http://dx.doi.org/10.3390/nu12113256DOI Listing

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