Abstract

Leptin secreted from white fat acts in the brain to decrease food intake and increase energy expenditure. Although the discovery of leptin promised a powerful way of combating obesity, subsequent research suggested that most obese individuals were actually resistant to the effects of leptin. High circulating levels of leptin are most commonly associated with leptin resistance but evidence is accumulating that sensitivity to leptin differs between sexes and across reproductive states. For example, earlier studies suggest that peripheral administration of leptin is less effective in decreasing food intake in lactating than in cycling rats. Leptin's effects on food intake are believed to be mediated primarily through activation of the JAK/STAT and the resulting phosphorylation of STAT3. In the present study the ability of central leptin injections to induce PSTAT3-ir in the VMH. PVN, and ARC was compared among cycling rats (Cyc) and lactating females on either postpartum day 4 or 16. Results show that in all hypothalamic areas examined there were more PSTAT3 positive cells in rats receiving leptin than those receiving saline. Within the PVN, this response was attenuated in the lactating groups and was most reduced on Day 16 postpartum. These results further support previous findings that there is a reduction in leptin sensitivity that occurs during the lactational period.