Effects of bilateral basomedial hypothalamic lesions on feeding, fattiness, and reproductive functions in the White Leghorn hen.

During the last three decades, syndromes caused by bilateral destruction of the basomedial hypothalamus (BMH) were extensively studied in cockerels but not in hens. In the present study bilateral electrolytic lesions in the BMH of White Leghorn (WL) hens produced two main sets of symptoms: (a) Obese, functionally castrated hen (OFC); and (b) Obese, laying hen (OL). Following the placement of the hypothalamic lesion, the OFC hens developed transient hyperphagia, that was followed by hypophagia. Weight gain was accelerated in both periods, and marked obesity developed. These hens had high hematocrit values, and atrophied ovary, oviduct, comb, and adenohypophysis. Plasma estrogen, and total lipids and liver weight were reduced in the OFC hens. In these hens, the lesioned area included the ventromedial hypothalamic nucleus (VMH), the mammillary nuclei, and in some birds also the arcuate nuclei, and the tuberal nucleus. The OL hens manifested transient hyperphagia that subsided into normophagia with the development of obesity. These hens were less obese than the OFC ones and showed normal reproductive traits. The lesioned area in the OL hens was limited to the VMH. Unlike functionally castrated cockerels, where the induced fattiness is accompanied with higher rate of lipogenesis, the OFC hen manifested a unique syndrome: increased fattiness with arrest in estrogen-dependent lipogenesis.