Regulation of Fatty Acid Metabolism by Cell Autonomous Circadian Clocks: Time to Fatten up on Information?

Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Journal of Biological Chemistry (Impact Factor: 4.57). 02/2011; 286(14):11883-9. DOI: 10.1074/jbc.R110.214643
Source: PubMed


Molecular, cellular, and animal-based studies have recently exposed circadian clocks as critical regulators of energy balance. Invariably, mouse models of genetically manipulated circadian clock components display features indicative of altered lipid/fatty acid metabolism, including differential adiposity and circulating lipids. The purpose of this minireview is to provide a comprehensive summary of current knowledge regarding the regulation of fatty acid metabolism by distinct cell autonomous circadian clocks. The implications of these recent findings for cardiometabolic disease and human health are discussed.

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    • "Intention to exercise is also often disrupted [66] [67]. Shiftwork and excessively long work hours disrupt sleep and metabolism [68] [69] [70] [71], in turn increasing the risk of obesity and metabolic syndrome [72]. Shiftwork interferes with exercise through physiological as well as behavioral mechanisms [73] "
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    • "In addition, changes in catabolic and anabolic pathways were reported to alter liver metabolome and improve nutrient utilization and energy expenditure (Hatori et al., 2012). However, circadian clocks located in the liver and other organs and tissues rule out a series of physiological functions including those relating to lipid metabolism (Asher & Schibler, 2011; Bass & Takahashi, 2010; Bray & Young, 2011; Eckel-Mahan et al., 2012), in all likelihood regardless of food availability, although the phases of the oscillations can be altered. The disruption of the circadian molecular clock may result in a number of metabolic disorders including obesity and diabetes (Durgan & Young, 2010; Froy, 2010; Green et al., 2008; Maury et al., 2010; Sookoian et al., 2008; Takahashi et al., 2008). "
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    ABSTRACT: Over the past decade, evidence has accumulated from basic science, clinical and epidemiological studies linking circadian mechanisms to adipose tissue biology and its related comorbidities, diabetes, metabolic syndrome and obesity. This review highlights recent in-vitro and in-vivo findings from murine, human and model organism studies. High-fat diets attenuate circadian mechanisms in murine adipose depots and these effects appear to be due to obesity rather than hyperglycemia. Deletion of circadian regulatory genes such as AMPK1 and nocturnin alter the circadian biology of adipose tissue. Unlike the mouse, circadian gene oscillation in human adipose tissue appears to be independent of BMI and diabetes status, suggesting that circadian mechanistic variation occurs across species. Clues for future directions in this emerging field come from studies of the hibernation and torpor state in mammals and infection models involving the Drosophila metabolic organ or 'fat body'. There is a growing consensus that circadian rhythms and metabolism are tightly regulated in adipose tissue and peripheral metabolic organs. Although central mechanisms are critical, autonomous clocks exist within the adipocytes themselves. Future circadian advances are likely to result from the studies of adipose tissue-specific gene deletions.
    Full-text · Article · Nov 2011
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