Horm Metab Res 2011; 43(8): 580-586
DOI: 10.1055/s-0031-1279779
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Growth Hormone, Ghrelin and Peptide YY Secretion after Oral Glucose Administration in Healthy and Obese Women

E. Outeiriño-Blanco1 , J. Garcia-Buela2 , S. Sangiao-Alvarellos3 , 4 , S. Pertega-Diaz5 , T. Martinez-Ramonde1 , F. Cordido1 , 3 , 4
  • 1Department of Endocrinology, University Hospital A Coruña, A Coruña, Spain
  • 2Department of Laboratory, University Hospital A Coruña, A Coruña, Spain
  • 3Department of Investigation, University Hospital A Coruña, A Coruña, Spain
  • 4Department of Medicine, University of A Coruña, A Coruña, Spain
  • 5Clinical Epidemiology and Biostatistics Unit, University Hospital A Coruña, A Coruña, Spain
Further Information

Publication History

received 25.01.2011

accepted 12.05.2011

Publication Date:
10 June 2011 (online)

Abstract

The mechanism of the altered GH secretion in obesity is unclear. There is evidence that oral glucose (OG) administration initially decreases and subsequently stimulates GH secretion. Ghrelin is a peptide that displays strong growth hormone-releasing activity. Its physiological importance on GH regulation is unclear. Our aim was to study fasting GH concentrations and their response to OG administration in relation with ghrelin secretion in obese and healthy women, in order to elucidate the hypothetical participation of ghrelin on post-oral glucose GH secretion. 36 women were included in the study. After an overnight fast, 75 g of oral glucose was administered; glucose, insulin, ghrelin, and PYY1–36 were obtained at baseline and during 300 min. The area under the curve between 0 and 300 min (AUC) of GH μ/l·min) was lower in obese patients than in controls; 262.5±57.5 vs. 534.9±95.6, p=0.01, for obese and controls respectively. GH peak (μg/l) was lower in obese patients than in controls; 3.7±0.7 vs. 7.1±1.0, p=0.012, for obese and controls, respectively. The AUC of total ghrelin (pg/ml·min) was lower in obese patients than in controls; 233 032±12 641 vs. 333 697±29 877, p=0.004, for the obese patients and controls respectively. PYY1–36 was similar in obese and healthy women after OG. There were significant correlations between the different indices of post-oral glucose GH and ghrelin secretion. These data suggest that ghrelin is a physiological regulator of GH in the post-oral glucose state, and the decreased ghrelin secretion could be one of the mechanisms responsible for the altered GH secretion in obesity.

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Correspondence

F. CordidoMD 

Servicio de Endocrinología

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