Effects of estradiol and tamoxifen on feeding, fattiness, and some endocrine criteria in hypothalamic obese hens.

In White Leghorn hens, basomedial hypothalamic (BMH) lesions result in two syndromes: a) obese, functionally castrated (OFC) hens, in which both the ventromedial hypothalamic nucleus (VMH) and the mammillary nuclei are damaged and plasma estrogen is very low; and b) obese laying (OL) hens, which have normal levels of plasma estrogen and are less obese than the former, and whose lesion is limited to the VMH. In the present study, the involvement of estrogen in regulation of fattiness and energy metabolism was assayed in OFC, OL, and control (CONT) hens. BMH lesions were made at 13 weeks of age. When the typical syndromes reached the static phase, 20 weeks later, CONT, OFC, and OL hens were divided into three subgroups and were injected for 10 weeks on each alternate day, with either 10 mg tamoxifen (TAM)/kg, 2 mg estradiol benzoate (E2)/kg, or the vehicle, corn oil (0.5 ml). E2 raised plasma total lipids and reduced plasma glucose, insulin, and hematocrit in all treated hens, and increased liver weight in OL and OFC, but not in CONT hens. In OFC hens only, E2 reduced food intake (FI) and fattiness. In OL and CONT hens, E2 increased plasma T3, but raised the resting metabolic rate (RMR) only in CONT ones. In OFC hens, E2 reduce plasma T3 and T4 without affecting RMR. E2 reduced comb weight and egg production in CONT and more severely in OL hens. In the latter, E2 diminished ovarian and oviduct weights, whereas in OFC hens it increased the size of the atrophied oviduct. TAM had no visible effect on OFC hens.(ABSTRACT TRUNCATED AT 250 WORDS)