Effect of transplantation of pancreas on development of hypothalamic obesity

Abstract

HYPOTHALAMIC obesity is a syndrome of hyperphagia and obesity that follows destruction of the ventromedial region of the hypothalamus. This syndrome is associated with loss of normal nocturnal rise in food intake and with several endocrine changes of which increased concentrations of insulin are the most important. It remains to be settled, however, whether the hyperphagia or hyperinsulinaemia is the primary factor in the development of hypothalamic obesity. The aim of the present experiment was to distinguish between these possibilities by freeing the insulin-secreting islets of Langerhans from neural control. This was done by implanting foetal pancreatic tissue under the kidney capsule of diabetic rats. This experiment prevented the characteristic hyperphagia and obesity seen in the control animals with normally innervated pancreatic tissue. Obesity can be produced by several experimental procedures¹. Among the most widely studied is the one due to damage to the ventromedial region of the hypothalamus^2,3. For many years, hypothalamic obesity was ascribed to the destruction of a ‘satiety centre’ which was thought to coincide anatomically with the ventromedial nucleus of the hypothalamus⁴. Ablation of this ‘satiety centre’ was believed to remove the inhibitory influences from a primary feeding centre in the lateral hypothalamus and allow excess feeding. Recent investigations have suggested, however, that this interpretation may be incorrect^5,6, and alternative hypotheses have been proposed. One of these suggests that the increase in food intake and obesity are both secondary to the rise in insulin levels which follow ventromedial hypothalamic (VMH) injury. The present studies were designed to critically examine this hypothesis.