Nuclear Receptors and AMPK: Resetting Metabolism
Author(s) -
Weiwei Fan,
Michael Downes,
Anne R Atkins,
Ruth T. Yu,
Ronald M. Evans
Publication year - 2011
Publication title -
cold spring harbor symposia on quantitative biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.615
H-Index - 77
eISSN - 1943-4456
pISSN - 0091-7451
DOI - 10.1101/sqb.2012.76.010470
Subject(s) - ampk , circadian rhythm , protein kinase a , endocrinology , receptor , nuclear receptor , metabolic syndrome , insulin resistance , biology , medicine , obesity , kinase , microbiology and biotechnology , gene , biochemistry , transcription factor
Obesity, and in particular central adiposity, is a key feature of metabolic syndrome, which includes trends toward increased triglycerides, insulin resistance, high blood pressure, hypercholesterolemia, and heart disease. It has a prevalence of 25% or more and is a dominant component of the health care budgets in Western societies. In addition to genetic causes, high-fat diets and disrupted sleep patterns have major influences on the development of metabolic syndrome. Recent studies have demonstrated active roles for the nuclear receptor superfamily and the energy-sensing kinase adenosine monophosphate (AMP)-activated protein kinase (AMPK) in regulating metabolism and circadian rhythm. In this chapter, we review these findings and attempt to develop a better understanding of the interplay between metabolism and circadian rhythm and their coordinated regulation by nuclear receptors and AMPK. This supraregulatory network may be considered a target for novel therapeutic applications against metabolic syndrome.
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