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Review
. 2013 Jul;62(7):889-97.
doi: 10.1016/j.metabol.2012.12.014. Epub 2013 Jan 26.

Cellular mechanisms regulating fuel metabolism in mammals: role of adipose tissue and lipids during prolonged food deprivation

Jose Abraham Viscarra  1 , Rudy Martin Ortiz
Affiliations
Review

Cellular mechanisms regulating fuel metabolism in mammals: role of adipose tissue and lipids during prolonged food deprivation

Jose Abraham Viscarra et al. Metabolism. 2013 Jul.

Abstract

Food deprivation in mammals results in profound changes in fuel metabolism and substrate regulation. Among these changes are decreased reliance on the counter-regulatory dynamics by insulin-glucagon due to reduced glucose utilization, and increased concentrations of lipid substrates in plasma to meet the energetic demands of peripheral tissues. As the primary storage site of lipid substrates, adipose tissue must then be a primary contributor to the regulation of metabolism in food deprived states. Through its regulation of lipolysis, adipose tissue influences the availability of carbohydrate, lipid, and protein substrates. Additionally, lipid substrates can act as ligands to various nuclear receptors (retinoid x receptor (RXR), liver x receptor (LXR), and peroxisome proliferator-activated receptor (PPAR)) and exhibit prominent regulatory capabilities over the expression of genes involved in substrate metabolism within various tissues. Therefore, through its control of lipolysis, adipose tissue also indirectly regulates the utilization of metabolic substrates within peripheral tissues. In this review, these processes are described in greater detail and the extent to which adipose tissue and lipid substrates regulate metabolism in food deprived mammals is explored with comments on future directions to better assess the contribution of adipose tissue to metabolism.

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Conflict of interest statement

Disclosure: Authors have no conflicts of interest to disclose.

Figures

Figure 1
Figure 1
Comparison of the changes to key metabolic parameters in mammals under postprandial, postabsorptive, fasting, and starving conditions.
Figure 2
Figure 2
Schematic of the simplified A) complete hydrolysis of triacylglycerols and subsequent re-esterification, and B) the proposed partial hydrolysis of triglycerides and subsequent re-esterification of monoacylglycerols and diacylglycerols. Solid lines denote direct effects, dashed lines denote indirect effects. Short downward pointing arrows denote a decrease. Abbreviations: AMPK, AMP kinase; ATGL, adipose triglyceride lipase; BCAA, branched chain amino acids; DAG, diacylglycerol; DGAT, diglyceride acyltransferase; FA-CoA, fatty acyl-CoA; FFA, free fatty acid; G3P, glycerol-3-phosphate; HSL, hormone-sensitive lipase; MAG, monoacylglycerol; MGAT, monoglyceride acyltransferase; MGL, monoglyceride lipase; PEPCK-c, phosphoenolpyruvate carboxykinase cytosolic; TAG, triacylglycerol; TCA, tricarboxylic acid
See this image and copyright information in PMC

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