PPARs as Metabolic Regulators in the Liver: Lessons from Liver-Specific PPAR-Null Mice

Yaping Wang; Takero Nakajima; Frank J Gonzalez; Naoki Tanaka

doi:10.3390/ijms21062061

PPARs as Metabolic Regulators in the Liver: Lessons from Liver-Specific PPAR-Null Mice

Int J Mol Sci. 2020 Mar 17;21(6):2061. doi: 10.3390/ijms21062061.

Authors

Yaping Wang¹, Takero Nakajima¹, Frank J Gonzalez², Naoki Tanaka^{1

3}

Affiliations

¹ Department of Metabolic Regulation, Shinshu University School of Medicine, Matsumoto, Nagano 390-8621, Japan.
² Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
³ Research Center for Social Systems, Shinshu University, Matsumoto, Nagano 390-8621, Japan.

Abstract

Peroxisome proliferator-activated receptor (PPAR) α, β/δ, and γ modulate lipid homeostasis. PPARα regulates lipid metabolism in the liver, the organ that largely controls whole-body nutrient/energy homeostasis, and its abnormalities may lead to hepatic steatosis, steatohepatitis, steatofibrosis, and liver cancer. PPARβ/δ promotes fatty acid β-oxidation largely in extrahepatic organs, and PPARγ stores triacylglycerol in adipocytes. Investigations using liver-specific PPAR-disrupted mice have revealed major but distinct contributions of the three PPARs in the liver. This review summarizes the findings of liver-specific PPAR-null mice and discusses the role of PPARs in the liver.

Keywords: NAFLD; NASH; PPAR; insulin resistance; liver fibrosis.

Publication types

Review

MeSH terms

Animals
Energy Metabolism*
Gene Expression Regulation*
Homeostasis
Humans
Lipid Metabolism
Liver / metabolism*
Mice
Mice, Knockout
Multigene Family
Organ Specificity / genetics
Peroxisome Proliferator-Activated Receptors / genetics*
Peroxisome Proliferator-Activated Receptors / metabolism*
Protein Isoforms
Signal Transduction

Substances

Peroxisome Proliferator-Activated Receptors
Protein Isoforms