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J Diabetes Complications. 2006 Nov-Dec;20(6):380-3.

A motilin agonist, erythromycin, decreases circulating growth hormone levels in normal subjects but not in diabetic subjects.

Author information

1
Division of Diabetes, Digestive and Kidney Diseases, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho Chuo-ku, Kobe 650-0017, Japan. nueno@med.kobe-u.ac.jp <nueno@med.kobe-u.ac.jp>

Abstract

Erythromycin (EM) is a common antibiotic known to be a specific agonist of motilin receptors. We have previously reported that administration of EM improves glycemic control in type 2 diabetes patients. In the present study, we tested the effect of EM on growth hormone (GH) secretion in normal and type 2 diabetic subjects. Erythromycin (300 mg) was administered orally in fasted type 2 diabetic (n=12) and normal (n=10) subjects. Blood samples were obtained before and 2 h after the administration. Blood glucose, plasma insulin, somatostatin (SS), and GH levels were determined. The same fasted groups received intravenous erythromycin infusion (10 mg/kg per hour) for 60 min. Blood samples were collected just prior to the infusion and at 15, 30, 45 and 60 min, and plasma GH and somatostatin levels during the infusion were determined. Oral EM administration increased insulin levels and decreased blood glucose levels. GH levels were significantly decreased, while SS levels did not change in normal subjects. In diabetic subjects, there was an increase in insulin levels, but no change in blood glucose, SS, and GH levels. Intravenous EM infusion resulted in a marked decrease in GH levels, while no change in SS levels occurred in normal subjects. There were no changes in SS and GH levels in diabetic subjects during the infusion. When diabetic subjects were divided into two groups with and without autonomic neuropathy, no changes in GH levels were seen in either group. We conclude that EM decreases GH levels in normal subjects while not changing SS levels. This effect was not observed in type 2 diabetic subjects.

PMID:
17070443
DOI:
10.1016/j.jdiacomp.2005.08.011
[Indexed for MEDLINE]

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