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ESTRADIOL AND LEPTIN OVEREXPRESSION HAVE INDEPENDENT MODES OF ACTION ON DECREASED FOOD INTAKE AND BODY WEIGHT IN MALES RATS

Objective: We recently reported that male compared with female rats are less responsive to long-term central leptin overexpression, as assessed by decreased food intake and delta body weight. Moreover, males were more susceptible to development of leptin resistance than females suggesting that either male hormones mitigate or female hormones exacerbate leptin responses or both. To address the potential role of estradiol, we examined the treatment of leptin with or without estradiol on body weight parameters in male rats. Design and method: To this end, we centrally delivered a viral vector to overexpress ether leptin or green fluorescence protein (GFP) into male rats that were simultaneously treated with either estradiol (25 &mgr;g/kg; S.C., daily) or vehicle in a two x two design. We examined chronic changes in food intake (FI), BW, and body composition over 26 days. Results: BWs in both Leptin-vehicle and GFP-Estradiol were reduced compared with GFP-vehicle but more sustained in Leptin-Estradiol reminiscent of the pattern in females. Changes in FI were unique to each treatment, with a rapid decrease in Leptin-vehicle followed by gradual renormalization typical of leptin-induced leptin resistance. In contrast, the GFP-Estradiol decrease in FI was of lower amplitude (P < 0.001) but sustained over the 26 days (P < 0.003). The Leptin-Estradiol group was mostly additive but with a delay in leptin resistance typical of the pattern observed in female rats. Decreased body fat by TD-NMR was unique to each treatment paralleling FI. Phosphorylation of STAT3 (P-STAT3) was examined at death. No exogenous leptin was administered, thus detected P-STAT3 was due to central overexpressed leptin. P-STAT3 was greater in both leptin groups compared with GFP, but there was no difference between Leptin-vehicle and Leptin-Estradiol. Conclusions: In conclusion, these data suggest that leptin and estradiol both decrease FI and BW, with the pattern of Leptin-Estradiol reminiscent of that observed in females. Furthermore, the estradiol-induced decrease in FI & BW does not involve P-STAT3. These data suggest that estradiol may be one factor in the increased leptin response and the mitigated leptin resistance observed in female rats.