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Eur J Clin Pharmacol. 1984;26(1):23-8.

The metabolic effects of dopamine in man.


The metabolic effects of dopamine have been investigated by its infusion in normal man with and without simultaneous somatostatin administration. Dopamine was infused into overnight fasted men at 1.5 microgram/kg/min (n = 6) and 3.0 micrograms/kg/min (n = 5) for 120 min. Plasma dopamine concentrations at 120 min were 78 +/- 9 nmol/l and 117 +/- 17 nmol/l respectively, associated with a marginal rise in plasma noradrenaline. Dopamine (1.5 microgram/kg/min) induced an early and sustained rise in plasma glucagon (48 +/- 9 pg/ml versus 19 +/- 6 pg/ml in saline controls at 10 min, p less than 0.01) and a transient elevation in serum growth hormone which peaked to 17.7 (range 4.5-71.8) mU/l at 60 min (7.2 (range 0.6-37.7) mU/l with saline, p less than 0.05) but did not alter serum insulin, blood glucose or other metabolite levels. At 3.0 micrograms/kg/min, dopamine in addition provoked mild and transient elevations in blood glucose and serum insulin. Somatostatin (250 micrograms/h) suppressed circulating insulin, glucagon, and growth hormone levels and abolished the small hyperglycaemic effect seen with the higher dopamine dose. Somatostatin alone induced a progressive rise in circulating non-esterified fatty acid and 3-hydroxybutyrate levels reflecting insulin deficiency. This rise in NEFA and 3-hydroxybutyrate was increased by dopamine particularly at the higher dosage (plasma NEFA; somatostatin alone, 1.08 +/- 0.13 mmol/l; somatostatin plus dopamine 3 micrograms/kg/min, 1.44 +/- 0.17 mmol/l at 120 min, p less than 0.01: blood 3-hydroxybutyrate; somatostatin alone, 0.32 +/- 0.04 mmol/l; somatostatin plus dopamine 3 micrograms/kg/min, 0.56 +/- 0.12 mmol/l at 120 min, p less than 0.05). Thus: 1) dopamine at pharmacological dosage has minor effects when other endocrine mechanisms are intact, 2) it enhances lipolysis and ketogenesis during somatostatin-induced insulin deficiency; 3) the hyperglycaemia effect of the higher dopamine dose is probably mediated through stimulated glucagon secretion.

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