Circadian disruption in the pathogenesis of metabolic syndrome

E. Maury*, H. K. Hong, J. Bass

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

105 Scopus citations

Abstract

Metabolic syndrome is a multifactorial process induced by a combination of genetic and environmental factors and recent evidence has highlighted that circadian disruption and sleep loss contribute to disease pathogenesis. Emerging work in experimental genetic models has provided insight into the mechanistic basis for clock disruption in disease. Indeed, disruption of the clock system perturbs both neuroendocrine pathways within the hypothalamus important in feeding and energetics, in addition to peripheral tissues involved in glucose and lipid metabolism. This review illustrates the impact of molecular clock disruptions at the level of both brain and behavior and peripheral tissues, with a focus on how such dysregulation in turn impacts lipid and glucose homeostasis, inflammation and cardiovascular function. New insight into circadian biology may ultimately lead to improved therapeutics for metabolic syndrome and cardiovascular disease in humans.

Original languageEnglish (US)
Pages (from-to)338-346
Number of pages9
JournalDiabetes and Metabolism
Volume40
Issue number5
DOIs
StatePublished - Nov 1 2014

Funding

We thank members of the Bass, Takahashi, Turek and Allada laboratories for helpful discussions. Funding: This work was supported by Alfediam (to E.M.), NIH (P01 AG011412 and R01HL097817-01 to J.B.), American Diabetes Association (to J.B.), Chicago Biomedical Consortium Searle Funds (to J.B.), Juvenile Diabetes Research Foundation (to J.B.), and the University of Chicago Diabetes Research and Training Center (P60 DK020595).

Keywords

  • Cardiovascular disease
  • Circadian rhythm
  • Metabolism

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Fingerprint

Dive into the research topics of 'Circadian disruption in the pathogenesis of metabolic syndrome'. Together they form a unique fingerprint.

Cite this