Ghrelin action in the brain controls adipocyte metabolism

Theander-Carrillo, C.

doi:10.1172/jci25811

Cited by 465Regulation of Appetite and ObesityAdipose Tissue and MetabolismAdipokines, Inflammation, and Metabolic Diseases

Ghrelin action in the brain controls adipocyte metabolism

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Theander-Carrillo, C.·2006·Journal of Clinical Investigation

DOI 10.1172/jci25811PMC PMC1474815

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Abstract

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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The effects of ghrelin on adiposity require intact sympathetic nervous system signaling.
“The effects of ghrelin on adiposity have been shown to require intact sympathetic nervous system signaling 53.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [53]

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Authors: Theander-Carrillo, C.
Affiliations: University of Geneva (CH)
Corresponding author: Theander-Carrillo, C.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2006-07-03
Volume: 116
Issue: 7
Pages: 1983-1993
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci25811
PMC: PMC1474815
OpenAlex: W2144925128
Cited by: 465
References: 73
Citations by year: 2026: 2 · 2025: 10 · 2024: 15 · 2023: 12 · 2022: 13 · 2021: 26 · 2020: 21 · 2019: 19 · 2018: 14 · 2017: 26 · 2016: 18 · 2015: 26 · 2014: 22 · 2013: 36 · 2012: 32
FWCI: 14.85
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Science Foundation
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (105889, 3100A0)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords: ghrelin, adipocyte metabolism, white adipose tissue, brown adipose tissue, glucose utilization, lipoprotein lipase, ACACA, fatty acid synthase, stearoyl-CoA desaturase 1, uncoupling proteins, thermogenesis, sympathetic nervous system, neuroendocrine regulation, metabolic homeostasis
MeSH terms: Uncoupling Protein 3, Uncoupling Protein 1, Acetyl-CoA Carboxylase, Adipose Tissue, Animals, Brain, Carrier Proteins, Eating, Energy Metabolism, Glucose, Homeostasis, Ion Channels, Lipoprotein Lipase, Male, Membrane Proteins, Neuropeptide Y, Stearoyl-CoA Desaturase, Rats, Wistar, Adipocytes, Mice, Knockout, Mitochondrial Proteins, Peptide Hormones, Mice, Rats, Ghrelin, Fatty Acid Synthases

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Ghrelin action in the brain controls adipocyte metabolism

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