Abstract
WE report here an experiment which seems to provide definite proof that the hypothalamic feeding mechanism contains glucoreceptors controlling satiety. That such glucoreceptors exist, and are different metabolically from other brain tissue, had been suggested indirectly by studies relating hunger and gastric contractions to the utilization of glucose1 and by work on goldthioglucose. Single injections of this compound cause lesions in the ventromedial area of the hypothalamus2. The action is specific chemically: glucose and not similar metabolites has to be a part of the molecule3. It is specific anatomically: induced weakness of the blood–brain barrier in other cerebral areas does not increase permeability to this compound4. Goldthioglucose destroys cells the axons of which connect the ventromedial area to the lateral area5, and cells at the origin of Schultze's bundle—a structure which links the hypothalamus to the roots of the vagus4. The former gives an anatomical basis for the known physiological relation between the “satiety” area and the “feeding” area, the latter for the physiological role of the ventromedial area in inhibition of gastric contractions by glucagon6 and stimulation of gastric secretion by insulin7. The action of goldthioglucose is blocked by analogues of glucose8 and by alloxan diabetes9, the latter confirming the postulated dependency of the glucoreceptors on insulin. Anand has also shown that the electrical activity of the ventromedial area is increased when the utilization of glucose is increased and vice versa, while the lateral area shows the opposite pattern10.
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GLICK, Z., MAYER, J. Hyperphagia caused by Cerebral Ventricular Infusion of Phloridzin. Nature 219, 1374 (1968). https://doi.org/10.1038/2191374a0
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DOI: https://doi.org/10.1038/2191374a0
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