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Leptin disinhibits nonshivering thermogenesis in infants after maternal separation
Journal article   Open access   Peer reviewed

Leptin disinhibits nonshivering thermogenesis in infants after maternal separation

Mark S Blumberg, Kara Deaver and Robert F Kirby
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.276(2), pp.R606-R610
02/01/1999
DOI: 10.1152/ajpregu.1999.276.2.R606
PMID: 9950943
url
https://doi.org/10.1152/ajpregu.1999.276.2.R606View
Published (Version of record) Open Access

Abstract

Prolonged maternal separation inhibits endogenous heat production in infant mammals exposed to cold. This inhibition of thermogenesis occurs many hours before energy stores have been fully depleted. The need to protect energy resources during separation-induced starvation may be signaled by declining levels of leptin, a hormone that acts as a “fat signal” and a regulator of energy utilization; in fact, starvation reduces leptin levels in adult mice and infant rats. It is not known, however, whether leptin has a functional role during starvation in infants. Such a role may be found in the regulation of nonshivering thermogenesis by brown adipose tissue (BAT), a specialized organ that provides heat to infant mammals, including humans, during cold exposure. Heat produced by BAT allows the cold-exposed infant to prevent the detrimental effects of hypothermia on physiology and behavior and, ultimately, growth. Here we show that leptin disinhibits BAT thermogenesis during cold exposure in infant rats after 18 h of maternal separation. This finding demonstrates that leptin is more than simply an adipostat for the regulation of body weight; specifically, leptin modulates thermogenesis and energy utilization in the early postnatal period.

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