Abstract
Peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α) regulates mitochondrial DNA replication and mitochondrial gene expression by interacting with several transcription factors. White adipose tissue (WAT) mainly comprises adipocytes that store triglycerides as an energy resource and secrete adipokines. The characteristics of WAT vary in response to systemic and chronic metabolic alterations, including obesity or caloric restriction. Despite a small amount of mitochondria in white adipocytes, accumulated evidence suggests that mitochondria are strongly related to adipocyte-specific functions, such as adipogenesis and lipogenesis, as well as oxidative metabolism for energy supply. Therefore, PGC-1α is expected to play an important role in WAT. In this review, we provide an overview of the involvement of mitochondria and PGC-1α with obesity- and caloric restriction-related physiological changes in adipocytes and WAT.
Highlights
Peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1 α (PGC-1α) is a master transcriptional cofactor for mitochondrial biogenesis
In addition to mitochondrial biogenesis, PGC-1α is involved in responses to oxidative stress via induction of sirtuin3 (SIRT3), which is a member of the SIRT family
These findings suggest that downregulation of PGC-1α in White adipose tissue (WAT) is associated with obesity-related disturbance of whole-body metabolism, PGC-1α is endogenously expressed at low levels in WAT [2]
Summary
Adipocytes in WAT contain small and elongated mitochondria in the narrow cytoplasmic space, resulting from a large, unilocular lipid droplet formed by TG [37,38]. 3T3-L1 adipocytes, indicating an association between adipogenesis and mitochondrial biogenesis [44] This is supported by the finding that some mouse models with adipose tissue-specific deletion of mitochondria-related factors show lipoatrophy or lipodystrophy, which represent loss of WAT [45]. Malate is transported into the cytosol and converted into pyruvate by malic enzyme [54] In this process, NADPH, a coenzyme for FA synthesis, is generated [55]. The authors described that this increase is a compensatory reaction for attenuated glucose metabolism due to insulin resistance [59] It remains to be determined whether mitochondria are directly or indirectly associated with insulin sensitivity, mitochondria may participate in lipogenesis via the regulation of insulin signaling in addition to the supply of metabolic intermediates
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