**1. Introduction**

Human reproduction is an energy demanding process which requires the complex interaction of biological molecules and neuroendocrine pathways primarily revolving around the hypothalamic–pituitary–ovarian (HPO) axis [1, 2]. The size of body fat and energy stores and the metabolic state of the individual are two of the key elements which determine the appropriate functioning of human reproduction, including the onset of puberty [1, 3].

In a severely undernourished state, the energy stores of the body are deviated to support the indispensable functions for survival, hence compromising the reproductive ability [4, 5].

It has long been observed that the extreme situations of body fat metabolism, that is, obesity and cachexia are both associated with derangement of female reproductive function including infertility, recurrent pregnancy loss (RPL) and polycystic ovary syndrome (PCOS) [1].

The presumptions on the existence of a missing link between the energy homeostasis of the body and female reproductive health culminated in the year 1994, with the discovery of leptin, an adipose tissue derived hormone that maintains the homeostatic control of the body fat stores [1, 6, 7]. Leptin has now been recognised to control and influence the functioning of the HPO axis also exerting a negative feedback effect on the hypothalamus.
