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Horm Metab Res 1975; 7(4): 279-283
DOI: 10.1055/s-0028-1093754
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© Georg Thieme Verlag KG Stuttgart · New York

Effect of Cyproheptadine Administration on Insulin Secretion in Acromegalic, Diabetic and Normal Subjects[*]

J. M. Feldman , C. H. Bivens , J. S. Skyler , H. E. Lebovitz
  • Durham Veterans Administration Hospital and Division of Endocrinology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, U.S.A.
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Publikationsdatum:
23. Dezember 2008 (online)

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Abstract

The effect of cyproheptadine (Cypro) and Placebo administration on insulin secretion and glucose utilization following i.v. glucose (IVGTT) was evaluated in 8 normal, 7 diabetic and 8 acromegalic subjects. Five of the diabetic subjects had overt diabetes and two of the diabetic subjects had "chemical" diabetes (oral GTT). One of the acromegalic subjects had overt diabetes, while one had borderline glucose tolerance and six had normal glucose tolerance (oral GTT). Cypro increased insulin secretion in the acromegalic but not in the diabetic or normal subjects. Methysergide (Methy) increased insulin secretion in acromegalic and diabetic subjects but not in normal subjects. Methy and Cypro both increased insulin secretion in the same acromegalic subjects. None of the three groups of subjects had a modification in insulin secretion following Placebo administration. Neither Placebo, Cypro or Methy altered the glucose utilization rate contant (KG). There was no change in insulin half life or tissue sensitivity to insulin from Cypro (normal and acromegalic subjects) or Methy (normal subjects) administration. Despite their increase in insulin secretion in response to serotonin antagonists, acromegalic subjects have normal urinary 5-hydroxyindoleacetic acid excretion and normal serum serotonin concentrations. Their response cannot therefore be attributed to a generalized overproduction of serotonin.

Key words

Acromegaly - Diabetes Mellitus - Insulin Secretion - Cyproheptadine - Methysergide - Serotonin

1 Grant Support:
Supported by the Veterans Administration (2605-1), grants AM-01324, 5T1-AM-5074, K3-AM-17,954, from the National Institute of Arthritis, Metabolic and Digestive Diseases and a grant from the Clinical Research Center Branch Division of Research Facilities and Resources, U.S. Public Health Service (M 01 RR-30).

1 Grant Support:
Supported by the Veterans Administration (2605-1), grants AM-01324, 5T1-AM-5074, K3-AM-17,954, from the National Institute of Arthritis, Metabolic and Digestive Diseases and a grant from the Clinical Research Center Branch Division of Research Facilities and Resources, U.S. Public Health Service (M 01 RR-30).

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