Clock gene expression in the liver and adipose tissues of non-obese type 2 diabetic Goto-Kakizaki rats

Clin Exp Hypertens. 2009 May;31(3):201-7. doi: 10.1080/10641960902822450.


Recent studies have revealed a close relationship between the pathophysiology of metabolic syndrome, which is characterized by obesity and hyperglycemia, and the functioning of internal molecular clocks. In this study, we show that the rhythmic mRNA expression of clock genes (Clock, Bmal1, Cry1, and Dbp) is not attenuated in the liver and visceral adipose tissues of Goto-Kakizaki rats, a model of nonobese, type 2 diabetes, as compared to control Wistar rats. Our results suggest that molecular clock impairment in peripheral tissues of obese diabetic animals may be either caused by obesity-related factor(s), but not hyperglycemia, or be a cause, but not a consequence, of hyperglycemia.

MeSH terms

  • ARNTL Transcription Factors
  • Adipose Tissue / metabolism*
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors / metabolism*
  • Blood Glucose / metabolism
  • CLOCK Proteins
  • Circadian Rhythm
  • Cryptochromes
  • DNA-Binding Proteins
  • Diabetes Mellitus, Type 2 / metabolism*
  • Disease Models, Animal
  • Flavoproteins / metabolism*
  • Insulin / blood
  • Liver / metabolism*
  • Male
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Mutant Strains
  • Rats, Wistar
  • Trans-Activators / metabolism*
  • Transcription Factors


  • ARNTL Transcription Factors
  • Basic Helix-Loop-Helix Transcription Factors
  • Blood Glucose
  • Cry1 protein, rat
  • Cryptochromes
  • DBP protein, rat
  • DNA-Binding Proteins
  • Flavoproteins
  • Insulin
  • RNA, Messenger
  • Trans-Activators
  • Transcription Factors
  • CLOCK Proteins
  • Clock protein, rat