Food intake and leptin during pregnancy and lactation.

Successful reproduction requires the accumulation of energy reserves. Although acute and chronic food deprivation disrupts reproduction, surprisingly, an over-abundance of energy reserves can also result in infertility. The infertility of obese, ob/ob mice can be reversed by the reintroduction of leptin, the protein product of the ob gene. In rats, energy reserves are increased during pregnancy by far accumulation and during lactation by hyperphagia. We have therefore investigated the interactions of leptin and food intake during late pregnancy and lactation in rats. Cycling rats consume their daily food intake during the dark phase and this is accompanied by a subsequent increase in plasma leptin concentration compared to light levels. During late pregnancy, rats increase their food intake during the dark phase and this is accompanied by a nocturnal increase in plasma leptin level. However, the nocturnal increase is not seen on the day prior to parturition, and is absent throughout lactation. Surprisingly, despite the massive increase in food intake during lactation plasma leptin levels continue to fall, suggesting that leptin release in response to food intake is suppressed during lactation. Furthermore, central leptin administration is less effective in reducing food intake in late pregnant and early lactating rats compared to cycling rats which suggests that these rats are insensitive to leptin. This may result from downregulation of brain leptin receptors. Decreased leptin production and action during late pregnancy and lactation will result in a decreased satiety effect, with up-regulation of orexigenic factors that produce hyperphagia, so allowing adequate energy intake for successful rearing of offspring.