Regulation of fatty acid metabolism by cell autonomous circadian clocks: time to fatten up on information?

Abstract

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.

FIGURE 1.

FA metabolism within metabolically relevant tissues. NEFA, non-esterified FA; MAG, monoacylglycerol; TAG, triacylglycerol; PL, phospholipid; CE, cholesterol ester; LP, lipoprotein; VLDL, very low density lipoprotein.

FIGURE 2.

Time of day-dependent oscillations in FA metabolism that are known to be influenced by circadian clocks either directly or indirectly. FAO, FA oxidation; TAG, triacylglycerol; PL, phospholipid; CE, cholesterol ester.

FIGURE 3.

Distinct high fat meal feeding regimes (A) differentially influence RER (B), adiposity (C), and glucose tolerance (D). Data were published previously in Ref. . *, p < 0.05 for early high fat feeding versus late high fat feeding.