ArticleFEBS open bio2025
Co-overexpression of the caloric restriction-induced mitochondrial factors PGC-1α and MIPEP upregulates Phospho1 expression in adipocytes.
Article in FEBS open bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is a master transcriptional cofactor for mitochondrial biogenesis. Mitochondrial intermediate peptidase (MIPEP), a mitochondrial signal peptidase, plays an important role in the maturation and activation of mitochondrial proteins. Caloric restriction has lifespan-extending effects that are reportedly exerted through induced expression of PGC-1α and MIPEP in white adipose tissue. To evaluate how upregulation of PGC-1α and MIPEP contributes to changes in the cellular characteristics of adipocytes, this study examined the mitochondrial function and differentiation of 3T3-L1 preadipocytes with single overexpression (OE) or double OE of Pgc-1α and Mipep. Compared with single-OE cells, double-OE cells exhibited no significant changes in oxygen consumption rate or mitochondrial morphology, but did show increased mitochondrial DNA levels. White adipocyte cell differentiation was suppressed in both Pgc-1α single-OE cells and double-OE cells. Notably, double-OE cells exhibited increased mRNA levels of phosphoethanolamine/phosphocholine phosphatase 1 (Phospho1), which plays a role in phospholipid metabolism and non-canonical thermogenesis. Phospho1 expression was also increased in white adipose tissue of mice under caloric restriction. In summary, the double OE of Pgc-1α and Mipep induced Phospho1 expression and suppressed adipocyte maturation, with little effect on mitochondrial function. This study provides new insights into the mitochondria-related mechanism of caloric restriction in adipocytes.
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