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Theander-Carrillo, C.* ; Wiedmer, P.* ; Cettour-Rose, P.* ; Nogueiras, R.* ; Perez-Tilve, D.* ; Pfluger, P.T. ; Castañeda, T.R.* ; Muzzin, P.* ; Schürmann, A.* ; Szanto, I.* ; Tschöp, M.H. ; Rohner-Jeanrenaud, F.*

Ghrelin action in the brain controls adipocyte metabolism.

J. Clin. Invest. 116, 1983-1993 (2006)
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Many homeostatic processes, including appetite and food intake, are controlled by neuroendocrine circuits involving the CNS. The CNS also directly regulates adipocyte metabolism, as we have shown here by examining central action of the orexigenic hormone ghrelin. Chronic central ghrelin infusion resulted in increases in the glucose utilization rate of white and brown adipose tissue without affecting skeletal muscle. In white adipocytes, mRNA expression of various fat storage-promoting enzymes such as lipoprotein lipase, acetyl-CoA carboxylase alpha, fatty acid synthase, and stearoyl-CoA desaturase-1 was markedly increased, while that of the rate-limiting step in fat oxidation, carnitine palmitoyl transferase-1alpha, was decreased. In brown adipocytes, central ghrelin infusion resulted in lowered expression of the thermogenesis-related mitochondrial uncoupling proteins 1 and 3. These ghrelin effects were dose dependent, occurred independently from ghrelin-induced hyperphagia, and seemed to be mediated by the sympathetic nervous system. Additionally, the expression of some fat storage enzymes was decreased in ghrelin-deficient mice, which led us to conclude that central ghrelin is of physiological relevance in the control of cell metabolism in adipose tissue. These results unravel the existence of what we believe to be a new CNS-based neuroendocrine circuit regulating metabolic homeostasis of adipose tissue.
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Publication type Article: Journal article
Document type Scientific Article
Language
Publication Year 2006
HGF-reported in Year 2006
ISSN (print) / ISBN 0021-9738
e-ISSN 1558-8238
Quellenangaben Volume: 116, Issue: 7, Pages: 1983-1993 Article Number: , Supplement: ,
Publisher American Society of Clinical Investigation
Reviewing status Peer reviewed
PubMed ID 16767221
Erfassungsdatum 2020-02-24