Cold-Induced Sympathoexcitation and Adipokine Profiles in Humans

Cold-Induced Sympathoexcitation and Adipokine Profiles in Humans

A study published in the journal Metabolism suggests that the sympathetic nervous system (SNS) and its activation during cold-induced stress activation may play an important role in the regulation of adipokine secretion.

Adipose tissue, in tight interconnection with the SNS, has a key role in maintaining energy homeostasis, blood pressure control, immunoregulation, hemostasis, and atherosclerosis.

However, few reports on SNS activation and subsequent changes of adipokine profiles in humans have been published.

In this study, K. Iwen and co-workers demonstrate that cold exposure in humans is associated with increased norepinephrine, but not epinephrine, plasma levels; decreased adiponectin plasma concentrations; and a trend of increased monocyte chemoattractant protein–1 (MCP-1) plasma concentrations but no specific changes in leptin, IL-6 and VEGF levels.

Adiponectin, specifically expressed in differentiated adipocytes, correlates negatively with obesity and insulin resistance in humans. It enhances insulin sensitivity, normalizes lipid abnormalities and causes weight loss in mice models.

Importantly, several lines of evidence indicate an anti-inflammatory and antiatherogenic role of adiponectin. Furthermore, obesity is associated with elevated levels of MCP-1, expressed and secreted by adipocytes, which lead to adipose tissue infiltration by macrophages.

This may represent the first report on the acute effect of sympathoexcitation on MCP-1 levels in humans.

The authors also discuss the relevance of their findings to the pathophysiology of SNS and adipokines in patients with metabolic syndrome.

SOURCE: Metabolism 2010 Apr 26, [Epub ahead of print]

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Source: Cover Image: Schematic depiction of the pleiotropic effects of adiponectin and leptin. Credit: researchgate.net; https://www.researchgate.net/figure/258204098_fig2_Fig-2-Schematic-depiction-of-the-pleiotropic-effects-of-adiponectin-and-leptin; Public domain

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