Studies on the Physiology of Hunger

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Abstract
The gastric motor activity of a man suffering from very severe brain damage has been studied under conditions of negative and positive caloric balance. During a time when he was losing weight vigorous gastric hunger contractions persisted without spontaneous interruption throughout the four-hour periods of study. The intravenous administrations of glucose, fat, and amino acids had no effect upon these contractions but they were promptly abolished by the infusion of small doses of glucagon, the hyperglycemic-glycogenolytic factor of the pancreas. These findings are more readily explained by the glucostatic than by the thermostatic theory of the regulation of food intake. The return of gastric hunger contractions in the presence of markedly increased peripheral utilization of glucose, however, is difficult to explain in terms of the glucostatic theory. When the subject began to gain weight his gastric motor activity reverted toward the normal pattern although gastric hunger contractions were still present a higher percentage of the time than has been found in individuals without brain damage. At this time several previously ineffective agents were able to inhibit gastric motility.

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