PPARs: diverse regulators in energy metabolism and metabolic diseases - PubMed (original) (raw)

Review

PPARs: diverse regulators in energy metabolism and metabolic diseases

Yong-Xu Wang. Cell Res. 2010 Feb.

Abstract

The nuclear receptor PPARs are fundamentally important for energy homeostasis. Through their distinct yet overlapping functions and tissue distribution, the PPARs regulate many aspects of energy metabolism at the transcriptional level. Functional impairment or dysregulation of these receptors leads to a variety of metabolic diseases, while their ligands offer many metabolic benefits. Studies of these receptors have advanced our knowledge of the transcriptional basis of energy metabolism and helped us understand the pathogenic mechanisms of metabolic syndrome.

PubMed Disclaimer

Figures

Figure 1

Figure 1

Regulation of white fat (A) and brown fat (B) adipogenesis by transcriptional cascades. Black arrows indicate increases of gene expression.

Figure 2

Figure 2

An integrated model of PPARα-regulated ketogenesis. Fasting induces the expression of PPARα and PGC-1α. Activation of PPARα requires de novo synthesis of a PPARα ligand (16:0/18:1 GPC). Together, they induce the expression of fatty acid oxidation genes and FGF21. FGF21 in turn promotes lipolysis in the adipose tissue. The released free fatty acids (FFA) are used as substrates for ketogenesis.

Figure 3

Figure 3

A comparison of the phenotypes among skeletal muscle PPARα transgenic mice, PPARδ transgenic mice, and wild type mice treated with a PPARδ agonist. Mice were fed a high-fat diet. ND, not determined.

Figure 4

Figure 4

A comparison of the cardiac phenotypes of the heart PPAR transgenic mice under a normal diet.

Figure 5

Figure 5

An overview of the physiological and/or pharmacological roles of the PPARs in energy metabolism. Data are summarized from PPAR knockout and ligand studies.

Similar articles

Cited by

References

    1. Reaven GM. The insulin resistance syndrome: definition and dietary approaches to treatment. Annu Rev Nutr. 2005;25:391–406. - PubMed
    1. Stumvoll M, Goldstein BJ, van Haeften TW. Type 2 diabetes: principles of pathogenesis and therapy. Lancet. 2005;365:1333–1346. - PubMed
    1. Savage DB, Petersen KF, Shulman GI. Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiol Rev. 2007;87:507–520. - PMC - PubMed
    1. Schenk S, Saberi M, Olefsky JM. Insulin sensitivity: modulation by nutrients and inflammation. J Clin Invest. 2008;118:2992–3002. - PMC - PubMed
    1. Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest. 2005;115:1111–1119. - PMC - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources