Obesity and metabolic syndrome in circadian Clock mutant mice

Science. 2005 May 13;308(5724):1043-5. doi: 10.1126/science.1108750. Epub 2005 Apr 21.

Abstract

The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.

Publication types

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

MeSH terms

  • Adipocytes / pathology
  • Animals
  • Body Weight
  • Brain / metabolism
  • CLOCK Proteins
  • Circadian Rhythm*
  • Dietary Fats / administration & dosage
  • Energy Intake
  • Energy Metabolism*
  • Feeding Behavior*
  • Hepatocytes / pathology
  • Hyperglycemia
  • Hyperlipidemias
  • Insulin / blood
  • Leptin / blood
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / physiopathology*
  • Mice
  • Mice, Inbred C57BL
  • Motor Activity
  • Mutation
  • Neuropeptides / genetics
  • Neuropeptides / metabolism
  • Obesity / genetics
  • Obesity / physiopathology*
  • Trans-Activators / genetics*
  • Trans-Activators / physiology*
  • Weight Gain

Substances

  • Dietary Fats
  • Insulin
  • Leptin
  • Neuropeptides
  • Trans-Activators
  • CLOCK Proteins
  • Clock protein, mouse