Physiological cardiac hypertrophy activates PPARγ/PGC‐1α axis and up‐regulates perilipin family

Abstract

Peroxisome proliferator‐activated receptor γ (PPARγ) and peroxisome proliferator‐activated receptor gamma coactivator 1‐α (PGC‐1α) are coordinately up‐regulated in hypertrophic cardiomyopathy and cooperate to mediate changes in lipid metabolism and storage that are characteristic of and contribute to common forms of heart disease. Previous results in our laboratory suggest that PPARγ regulates the shift in cardiac metabolism during physiological cardiac hypertrophy. On the other hand, the perilipin family (Plin: 1–5) is involved in the formation of lipid droplets in various tissues, and it has been demonstrated that Plin5 participates protecting the heart during myocardial ischemia and diabetic cardiomyopathy. However, the participation of PPARγ/PGC‐1α and the Plin family in physiologic hypertrophy induced by pregnancy and its reversible process (postpartum) are not well defined. We evaluated PPAR (alpha, delta, gamma) transcriptional activity, and PGC‐1α and Plin family gene expression along with triglyceride content before, during, and after pregnancy in the left ventricle of rat. The activity of PPARγ increased 1.6‐fold during pregnancy, and decreased to basal levels postpartum. Expression of mRNA for PGC‐1α increased 18‐ and 11‐fold during pregnancy and postpartum, respectively. Plin1, Plin2 y Plin5 transcript increased 9‐ to 16‐fold and 2‐ to 11‐fold during pregnancy and postpartum, respectively, while expression of Plin3 did not change and Plin4 was not detected. The results demonstrate that in, pregnancy‐induced, physiological cardiac hypertrophy activates the expression of genes involved in lipid storage suggesting that the shift in cardiac metabolism is mediated by the activation of PPARγ/PGC‐1α.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.