Ghrelin action in the brain controls adipocyte metabolism

J Clin Invest. 2006 Jul;116(7):1983-93. doi: 10.1172/JCI25811. Epub 2006 Jun 8.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyl-CoA Carboxylase / genetics
  • Acetyl-CoA Carboxylase / metabolism
  • Adipocytes / cytology
  • Adipocytes / metabolism*
  • Adipose Tissue / cytology
  • Adipose Tissue / metabolism
  • Animals
  • Brain / anatomy & histology
  • Brain / metabolism*
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Eating / drug effects
  • Energy Metabolism / drug effects
  • Fatty Acid Synthases / genetics
  • Fatty Acid Synthases / metabolism
  • Ghrelin
  • Glucose / metabolism
  • Homeostasis
  • Ion Channels
  • Lipoprotein Lipase / genetics
  • Lipoprotein Lipase / metabolism
  • Male
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mice
  • Mice, Knockout
  • Mitochondrial Proteins
  • Neuropeptide Y / genetics
  • Neuropeptide Y / metabolism
  • Peptide Hormones / administration & dosage
  • Peptide Hormones / genetics
  • Peptide Hormones / metabolism*
  • Rats
  • Rats, Wistar
  • Stearoyl-CoA Desaturase / genetics
  • Stearoyl-CoA Desaturase / metabolism
  • Uncoupling Protein 1
  • Uncoupling Protein 3

Substances

  • Carrier Proteins
  • Ghrelin
  • Ion Channels
  • Membrane Proteins
  • Mitochondrial Proteins
  • Neuropeptide Y
  • Peptide Hormones
  • Uncoupling Protein 1
  • Uncoupling Protein 3
  • Scd1 protein, mouse
  • Stearoyl-CoA Desaturase
  • Fatty Acid Synthases
  • Lipoprotein Lipase
  • Acetyl-CoA Carboxylase
  • Glucose