Obesity produces a variety of alterations in the reproductive system and, similarly, manipulations of the hypothalamic-pituitary-gonadal axis produce changes in food intake, body weight and fat distribution. In men, the primary effects of obesity are a weight related reduction testosterone and, with massive overweight, reduction in free testosterone. In females, the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls. One explanation for the relationship of fatness to menarche may be the protein (leptin) which is defective in the obese (oblob) mouse. Leptin is secreted by adipose tissue in proportion to the quantity of fat and may serve as a signal to the hypothalamus that fat stores are adequate to nourish a conceptus to term. In women, parity affects obesity and obesity in turn affects the regularity of the menstrual cycle. In many experimental animals with obesity, particularly the genetic forms obesity, there is complete infertility in the females and marked impairment of reproductive function in the males. In animals with hypothalamic lesions, there is a gender effect on the magnitude of weight gain associated with the sexually dimorphic regions in the medial preoptic area. Castration with removal oestrogen is followed by obesity in female animals and this can be prevented, as can most forms of obesity, by adrenalectomy. The inhibitory effects of oestrogen on food intake may result from suppression of neuropeptide-or galanin peptidergic systems in the arcuate nucleus or medial preoptic area.