In female mammals and birds, the role of AMPK has been studied in detail in granulosa cell cultures by using pharmacological agents and adenovirus-mediated expression of dominant negative forms of AMPK (Tosca et al., 2005). However, we reported human studies (about granulosa and thecal cells or human embryonic testis) when it was possible. In this review we report briefly some of the known functions of AMPK in the female and male gonad, and then we describe the potential role of this kinase in the interactions between metabolism and gonadal function. The rats were ORX and treated with vehicle (ORX) or Testosterone (ORX + T). Intracellular fluorescence was measured in the presence or absence of CC (2 µM). D Cardiomyocytes were stimulated with 100 nM testosterone for 24 h and were then incubated with 2-NBDG for 20 min. B ECAR was measured using a Seahorse XF analyzer and values were normalized using the total protein per well. The dysregulation of AMPK signalling has been implicated in several female reproductive disorders, including polycystic ovary syndrome (PCOS), endometriosis, infertility, and reproductive ageing. This signalling pathway is essential for maintaining reproductive homeostasis and influencing steroidogenesis, implantation, and embryonic development. Testosterone and testosterone-BSA stimulated the phosphorylation of AMPK, LKB1, and CaMKII. Glucose uptake was assessed with 2-(3)H deoxyglucose in 3T3-L1 adipocytes. Some mechanisms elucidated are directly linked with mitochondrial function and junctional proteins. These results indicate that high-dose testosterone and testosterone-BSA increase GLUT4-dependent glucose uptake in 3T3-L1 adipocytes by inducing the LKB1/AMPK signaling pathway. Male mice deficient in SIRT1 present with altered germ cell maturation and increased DNA damage in germ cells (Coussens et al., 2008). These results are also observed in Sertoli cells where stimulation with an AMPK activator such as metformin or AICAR has consequences on lactate production and the increase in glucose transport (Galardo et al., 2007). These latter authors have also observed that activation of AMPK induced by dihydrotestosterone (DHT) treatment decreases granulosa cell mitogenesis and consequently could contribute to ovulatory dysfunction observed in hyperandrogenic states (Kayampilly and Menon, 2012). Furthermore, in primary rat Leydig cells, resveratrol, an AMPK agonist impairs human chorionic gonadotropin (hCG)-mediated testosterone production by repressing StAR expression (Svechnikov et al., 2009). The male α1AMPK−∕− have high levels of testosterone that are not due to adrenal disorders or to glucorticoid resistance but to hyperactive Leydig cells (Tartarin et al., 2012a). Metformin reduces follicle-stimulating hormone (FSH) but not forskolin-stimulated aromatase expression and activity in an AMP-activated protein kinase-independent manner in a human granulosa cell line (Rice et al., 2013).
