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Evidence against growth hormone-releasing factor deficiency in children with idiopathic obesity
Insights
Growth hormone releasing factor (GRF) blunts growth hormone (GH) secretion in obese children, similar to GRF-deficient children. This suggests GRF deficiency does not cause decreased GH in obesity.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Hormone Regulation
Background:
- Decreased growth hormone (GH) secretion in human obesity is not well understood.
- Obesity can affect various endocrine functions, including GH regulation.
Purpose of the Study:
- To investigate the role of growth hormone releasing factor (GRF) in the diminished GH secretion observed in obese children.
- To differentiate the mechanisms of GH deficiency in obese children versus those with confirmed GRF deficiency.
Main Methods:
- Administered intravenous GRF to three groups of children: lean, obese, and GRF-deficient.
- Measured plasma GH and prolactin (PRL) levels before and after GRF injection.
- Assessed baseline plasma somatomedin C concentrations.
Main Results:
- Peak plasma GH response to GRF was significantly blunted in both obese and GRF-deficient children compared to lean controls.
- Prolactin (PRL) response to GRF differed: levels increased in GRF-deficient children but remained unchanged in obese and lean children.
- Obese children had high-for-age somatomedin C, while GRF-deficient children had low-for-age levels.
Conclusions:
- GRF deficiency does not explain the reduced GH secretion in obese children.
- Distinct patterns of PRL response and somatomedin C levels suggest different pathophysiological mechanisms in obese versus GRF-deficient children.
Abstract:
The mechanisms whereby growth hormone (GH) secretion is decreased in human obesity remain obscure. We studied the response of plasma GH and prolactin (PRL) to an I.V. dose of 0.5 mcg/kg of growth hormone releasing factor (GRF) in three groups of children: lean (N = 12), obese (N = 15) and GRF-deficient, i.e. children with complete GH deficiency on the basis of conventional provocative testing and evidence of hypothalamic dysfunction on the basis of thyrotropin-releasing hormone testing (N = 7). Mean (+/- SEM) peak plasma GH after GRF was blunted to the same extent in obese and in GRF deficient children (11.1 +/- 2.2 and 8.3 +/- 2.8 ng/ml) as compared to lean control children (34.7 +/- 4.7 ng/ml). The pattern of PRL response to GRF was however different in GRF deficient children, whose high basal PRL levels increased further after GRF injection, and in obese and lean children, who had n alpha acute change in PRL levels after GRF. Baseline plasma somatomedin C concentrations were low for age in GRF deficient children and tended to be high for age in obese children. On the basis of these discrepant patterns of response of PRL to GRF and plasma somatomedin C concentrations, we conclude that GRF deficiency does not account for the decreased GH secretion observed in obese children.