The protein product of the ob gene, called leptin, mainly but not exclusively produced by white adipose tissue, is thought to suppress appetite and regulate energy homeostasis (1,2). Extremely obese individuals have high leptin levels, which is likely to reflect a state of leptin resistance, suggesting that they have reduced sensitivity to its anorectic and metabolic effects (1). Under normal conditions of eating cycles, leptin reflects the proportion of adipose tissue, therefore its concentration rises with increasing adiposity (3). However, there are gender differences in leptin regulation between males and females at the same level of adiposity (4). Women have significantly higher leptin concentrations than men (4) and these gender differences seem to be present already at birth (measured by leptin levels in the umbilical cord plasma), when no remarkable differences in body composition or hormonal values between genders exist (5). Interestingly, pregnant women bearing female foetuses have significantly higher increase in leptin concentration compared to pregnant women bearing males foetuses (6). These evidences indicate a differential resistance to the action of leptin that might have adaptive importance for reproduction.