Junctional intercellular communication and the control of growth

The rise, fall, and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weight.

Hunger and satiety are usually discussed from the perspective of the central nervous system. In this paper we instead find the foundation for an understanding of hunger in the basic biochemical and physiological processes of energy metabolism. Such considerations suggest that the stimulus for hunger should be sought among changes that occur in the supply of metabolic fuels rather than in the utilization of specific nutrients or in the levels of fuel reserves. This line of reasoning diverts attention from the brain, which is not usually subject to dramatic fluctuations in its fuel supply, and focuses instead on the intestines, adipose tissue, and liver, the three peripheral organs that are most involved in the production or delivery of metabolic fuels. We propose that the stimulus for hunger derives from information provided to the brain by the liver in the course of normal hepatic function. More specifically, the stimulus for hunger may be associated with an alteration in oxidative metabolism within the liver, with food intake reversing that change. This view of hunger conforms closely to the fundamental features of caloric homeostasis and makes unnecessary such traditional hypothetical constructs as hunger and satiety centers, glucostat, lipostat, and body weight set point.

The physiological psychology of hunger: a physiological perspective.

Juvenile male rats given intracerebroventricular injections of 5,7-dihydroxytryptamine, following treatment with desmethylimipramine, maintained body weight gains of 5 to 6 grams per day into adulthood and grew much larger than control rats. Biochemical analyses of brain tissue obtained 50 to 140 days after the injections revealed 60 to 86% depletions of telencephalic 5-hydroxytryptamine, with catecholamine levels unchanged. Hyperphagia did not develop despite comparable losses of 5-hydroxytryptamine when the pretreatment was withheld, perhaps because substantial depletions of norepinephrine occurred as well.

https://science.sciencemag.org/content/sci/192/4237/385.full.pdf

Hyperphagia and increased growth in rats after intraventricular injection of 5,7-dihydroxytryptamine.

The organization of the ventromedial hypothalamic nucleus.

Bilateral cuts between the ventromedial and lateral hypothalamus in female rats consistently produced hyperphagia. Hyperphagia occurred slightly less reliably when one of the cuts entered the ventromedial hypothalamus and only infrequently if one entered the lateral hypothalamus. The results are consistent with other evidence that suggests that fibers originating medially stop eating by inhibiting cells in the lateral hypothalamus.

https://science.sciencemag.org/content/sci/165/3893/599.full.pdf

L. H. Storlien

Papers

Hyperphagia in Rats with Cuts between the Ventromedial and Lateral Hypothalamus