Knockdown of regulatory associated protein of TOR (raptor) in hypothalamus-stimulated folliculogenesis and induced ovarian cysts.

Context: Mammalian target of rapamycin complex 1 (mTORC1) is an essential sensor that regulates fundamental biological processes like cell growth, proliferation and energy metabolism. The treatment of disease by sirolimus, a mTORC1 inhibitor, causes adverse effects, such as female fertility disorders.

Aims: The objective of the study was to decipher the reproductive consequences of a downregulation of mTORC1 in the hypothalamus.

Effect of metformin on the fertilizing ability of mouse spermatozoa.

Numerous antioxidants have been added to cryopreservation media with varied success. The biguanide, metformin, commonly used for the treatment of type II diabetes, possesses properties impacting metabolism control that have not been yet assessed in cryopreservation protocols. The aim of this experiment was to; (i) determine the effect of metformin on fresh spermatozoa properties; and (ii) to assess positive or negative effects of metformin in post-thaw function and fertilizing capacity of mouse spermatozoa when used in cryopreservation media.

[mTORC1 and sirolimus: a link with fertility].

mTOR (mammalian target of rapamycin), a protein kinase highly conserved, is the catalytic subunit of two complexes, mTORC1 and mTORC2. These complexes are regulated by amino acids availability, by insulin and growth factors signaling pathways. Thus, mTORC1 and mTORC2 complexes are essential sensors of the cellular nutrient and energy levels in living organisms.

Inactivation of AMPKα1 induces asthenozoospermia and alters spermatozoa morphology.

AMP-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, is present in metabolic tissues (muscle and liver) and has been identified as a modulator of the female reproductive functions. However, its function in the testis has not yet been clearly defined. We have investigated the potential role of AMPK in male reproduction by using transgenic mice lacking the activity of AMPK catalytic subunit α1 gene [α1AMPK knockout (KO)].