Cold-induced alteration of adipokine profile in humans

K. Alexander Iwen, Eike T. Wenzel, Volker Ott, Nina Perwitz, Peter Wellhöner, Hendrik Lehnert, Christoph Dodt, Johannes Klein*

*Korrespondierende/r Autor/-in für diese Arbeit
19 Zitate (Scopus)

Abstract

Adipose tissue function and sympathetic nervous system (SNS) activity are tightly interconnected. Adipose tissue is densely innervated by the SNS. Adipokines secreted by adipose tissue are implicated in maintaining energy homeostasis, the control of blood pressure, immune system function, hemostasis, and atherosclerosis. Little is known about a direct effect of SNS activation on influencing adipose tissue endocrine function in humans. In 10 lean, healthy male volunteers, SNS was activated by whole-body exposure to cold for 2 hours; a group of 10 subjects served as controls. Vital parameters were evaluated, plasma adipokine levels were measured, and adipokine gene expression in subcutaneous abdominal adipose tissue was determined. Cold exposure caused an increase in cold sensation and a drop in body temperature and heart rate. Norepinephrine, but not epinephrine, plasma levels were elevated. Adiponectin plasma concentrations were acutely and significantly decreased. There was a trend of increased monocyte chemoattractant protein-1 plasma concentrations. Interleukin-6 and leptin levels increased and decreased, respectively, in both groups. Vascular endothelial growth factor plasma levels were unaffected. Subcutaneous adipokine gene expression was unchanged. Cold exposure caused SNS activation and differentially influenced adipokine secretion. Adiponectin levels were acutely reduced, whereas monocyte chemoattractant protein-1 concentrations tended to increase. No specific changes in leptin and IL-6 concentrations were detectable. The observed alterations appeared to be posttranscriptional because adipokine gene expression was found to be unaltered.

OriginalspracheEnglisch
ZeitschriftMetabolism: Clinical and Experimental
Jahrgang60
Ausgabenummer3
Seiten (von - bis)430-437
Seitenumfang8
ISSN0026-0495
DOIs
PublikationsstatusVeröffentlicht - 01.03.2011

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