Endocrine Abstracts

The results concerning the role of leptin in mediating effect of food restriction on ovarian functions, in controlling these functions, as well as the endocrine and intracellular mechanisms of leptin action are reviewed.

In our experiments, food restriction resulted in a reduction in rabbit and chicken plasma leptin, GH, IGF1 and gonadal steroid hormone levels and ovulation rate. Malnutrition (serum deprivation) inhibited hormone release and the expression of proliferation- and apoptosis-related substances (PCNA, cyclin B1, bax, bcl-2, ASK-1, MAP kinase, protein kinase A, CDC2 kinase, transcription factors p53, CREB1, STAT-1 and NFkB) and promoted the accumulation of heat shock proteins mRNA in cultured rabbit, human, porcine and chicken ovarian cells. Administration of leptin or IGF1 both in vivo and in vitro altered hormone release and the expression of these proliferation- and apoptosis-related substances, oocyte maturation, response of ovarian cells to gonadotropin and other hormones, and prevented effect of malnutrition. Immunoneutralisation of IGF-I reversed the effects of leptin on the secretory activity of human granulosa cells. Inhibitors of protein kinases PKA, MAPK and CDC2, as well as the transfection of ovarian cells with cDNA constructs encoding ASK-1, p53, STAT-1 and CREB-1 were able to affect ovarian functions listed above, as well as to promote or prevent effects of leptin and IGF1.

The present data suggest that leptin/IGF1 axis plays an important role in control of ovarian functions in mammals and birds. It is proposed, that food restriction can control reproductive functions via changes in leptin output, which in turn, through IGF1, protein kinases, transcription factors and heat shock proteins, can affect ovarian cell proliferation, apoptosis, secretory activity, response to hormonal stimulators and fecundity.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.