Section 6
Chapter 5,191

Dopamine blockade inhibits starvation ketosis in man

Johnston, D.G.; Blesa-Malpica, G.; Burrin, J.M.; Waugh, C.; Cook, D.; Orskov, H.; Alberti, K.G.

Clinical Endocrinology 19(3): 389-396


ISSN/ISBN: 0300-0664
PMID: 6627695
DOI: 10.1111/j.1365-2265.1983.tb00012.x
Accession: 005190818

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The effects of dopamine blockade on the endocrine and metabolic response to starvation were investigated by administration of metoclopramide, 30 mg daily, or placebo to 5 normal subjects fasted for 60 h on 2 occasions. Blood glucose and alanine concentrations fell with starvation and metoclopramide had no further effect. Concentrations of the other gluconeogenic precursors, lactate and pyruvate, were also unaffected by metoclopramide. The rise in circulating ketone body concentrations with fasting was impaired by metoclopramide, significantly from 44 h onwards (blood total ketone body concentration at 60 h 3.42 .+-. 0.94 mmol/l with placebo; 2.08 .+-. 0.67 mmol/l with metoclopramide, P < 0.05). Blood glycerol and plasma non-esterified fatty acids (NEFA) levels rose with starvation, and metoclopramide had no further effect. Serum insulin concentrations remained low with fasting, while circulating glucagon and growth hormone levels rose. Similar changes were noted with both metoclopramide and placebo. Serum prolactin concentrations during starvation were elevated 2- to 4-fold by metoclopramide. The inhibitory effect of dopamine blockade on ketosis thus occurred despite hyperprolactinemia, and did not result from measurable alterations in insulin, glucagon or growth hormone secretion. The data suggest a suggest a stimulatory role for endogenous dopamine on starvation ketonemia in man.

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