Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1alpha null mice

Cell. 2004 Oct 1;119(1):121-35. doi: 10.1016/j.cell.2004.09.013.

Abstract

PGC-1alpha is a coactivator of nuclear receptors and other transcription factors that regulates several metabolic processes, including mitochondrial biogenesis and respiration, hepatic gluconeogenesis, and muscle fiber-type switching. We show here that, while hepatocytes lacking PGC-1alpha are defective in the program of hormone-stimulated gluconeogenesis, the mice have constitutively activated gluconeogenic gene expression that is completely insensitive to normal feeding controls. C/EBPbeta is elevated in the livers of these mice and activates the gluconeogenic genes in a PGC-1alpha-independent manner. Despite having reduced mitochondrial function, PGC-1alpha null mice are paradoxically lean and resistant to diet-induced obesity. This is largely due to a profound hyperactivity displayed by the null animals and is associated with lesions in the striatal region of the brain that controls movement. These data illustrate a central role for PGC-1alpha in the control of energy metabolism but also reveal novel systemic compensatory mechanisms and pathogenic effects of impaired energy homeostasis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptation, Physiological / genetics
  • Animals
  • Appetite Regulation / genetics
  • Basal Ganglia Diseases / genetics
  • Basal Ganglia Diseases / metabolism
  • Basal Ganglia Diseases / pathology
  • Brain / metabolism*
  • Brain / physiopathology
  • CCAAT-Enhancer-Binding Protein-beta / genetics
  • CCAAT-Enhancer-Binding Protein-beta / metabolism
  • Corpus Striatum / metabolism
  • Corpus Striatum / pathology
  • Corpus Striatum / physiopathology
  • Energy Metabolism / genetics*
  • Gene Expression Regulation / genetics
  • Gluconeogenesis / genetics*
  • Glucose / metabolism
  • Hepatocytes / metabolism
  • Homeostasis / genetics
  • Hyperkinesis / genetics*
  • Hyperkinesis / pathology
  • Hyperkinesis / physiopathology
  • Liver / metabolism
  • Liver / physiopathology
  • Mice
  • Mice, Knockout
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Neurodegenerative Diseases / genetics
  • Neurodegenerative Diseases / metabolism
  • Neurodegenerative Diseases / pathology
  • Neurons / metabolism
  • Obesity / genetics
  • Obesity / metabolism
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Trans-Activators / deficiency
  • Trans-Activators / genetics*
  • Transcription Factors
  • Up-Regulation / genetics

Substances

  • CCAAT-Enhancer-Binding Protein-beta
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Ppargc1a protein, mouse
  • Trans-Activators
  • Transcription Factors
  • Glucose