Role of the Peroxisome Proliferator-Activated Receptors, Adenosine Monophosphate-Activated Kinase, and Adiponectin in the Ovary

Figure 2

Schema illustrating the effects of (a) metformin- or AICAR-induced AMPK activation, (b) adiponectin, and (c) TZDs or PPAR alpha ligands on the rat granulosa cell steroidogenesis. (a) Metformin or AICAR treatment decreases MAPK ERK1/2 phosphorylation and progesterone secretion through AMPK activation [60, 65]. Metformin decreases also oestradiol secretion through an independent AMPK pathway [60]. (b) Adiponectin treatment increases IGF-1-induced IGF-1R 𝛽-subunit tyrosine phosphorylation and MAPK ERK1/2 phosphorylation and progesterone secretion [12]. (c) The PPAR𝛼 ligand, Wy-14 463, inhibits oestradiol secretion whereas TZDs or PGJ2 increases progesterone secretion and inhibits estradiol secretion in eCG-primed immature rats or increases estradiol secretion in gonadotropin-primed immature rat [23, 52]. 3𝛽HSD: 3𝛽-hydroxysteroiddehydrogenase, STAR: Steroidogenic acute regulatory protein, CYP11a1: P450 sidechain cleavage, Adipo R1/2: Adiponectin receptor type I and II, MAPK ERK1/2: Mitogen Activated protein kinase Extracellular Regulated kinase,1/2, PGJ2: prostaglandine J2.