Journal of Clinical Endocrinology & Metabolism, Vol 61, 1152-1157, Copyright © 1985 by Endocrine Society

ARTICLES

Effects of hypopituitarism and growth hormone replacement therapy on the production and utilization of glucose in childhood

PF Bougneres, E Artavia-Loria, P Ferre, JL Chaussain and JC Job

Glucose metabolism during fasting was investigated in 10 children aged 1.5 month-11.5 yr with deficiency of GH with or without other pituitary hormone deficiencies. After 10-16 h of fasting, mean plasma glucose was 56 +/- 4 (SEM) mg/dl, the result of decreased hepatic production of glucose (3.3 +/- 0.3 mg kg-1 min-1) insufficient to match glucose utilization (3.6 +/- 0.4 mg kg-1 min-1). The diminution of plasma glucose and of glucose production was similar whether ACTH deficiency was present (3.2 +/- mg kg-1 min-1) or not (3.5 +/- 0.6 mg kg-1 min-1). These results indicate that the lack of GH was the primary cause of hypoglycemia. Fasting plasma alanine (212 +/- 41 mumol/liter) and lactate (1222 +/- 136 mumol/liter), the main gluconeogenic substrates, were normal and did not correlate with the decrease of hepatic glucose release. Both plasma FFA (552 +/- 35 microM) and beta-hydroxybutyrate (654 +/- 158 microM) were in the low normal range, and neither correlated with the rate of glucose utilization. hGH replacement therapy resulted in a normalization of fasting plasma glucose concentration (78.5 +/- 6 mg/dl, P less than 0.005) and hepatic glucose production (6.1 +/- 1.2 mg kg-1 min-1). No significant changes occurred in the plasma concentrations of gluconeogenic or lipid substrates. These results, together with the known stimulatory effects of GH on carbohydrate-induced insulin secretion and storage of hepatic glycogen, suggest that the changes in glucose production in untreated and GH treated patients reflect the degree of hepatic glycogen replenishment.

This article has been cited by other articles:

				J.-L. Liu, K. T. Coschigano, K. Robertson, M. Lipsett, Y. Guo, J. J. Kopchick, U. Kumar, and Y. L. Liu Disruption of growth hormone receptor gene causes diminished pancreatic islet size and increased insulin sensitivity in mice Am J Physiol Endocrinol Metab, September 1, 2004; 287(3): E405 - E413. [Abstract] [Full Text] [PDF]

				S. Srinivasan, G. D. Ogle, S. P. Garnett, J. N. Briody, J. W. Lee, and C. T. Cowell Features of the Metabolic Syndrome after Childhood Craniopharyngioma J. Clin. Endocrinol. Metab., January 1, 2004; 89(1): 81 - 86. [Abstract] [Full Text] [PDF]

				H. Norrelund, C. Djurhuus, J. O. L. Jorgensen, S. Nielsen, K. S. Nair, O. Schmitz, J. S. Christiansen, and N. Moller Effects of GH on urea, glucose and lipid metabolism, and insulin sensitivity during fasting in GH-deficient patients Am J Physiol Endocrinol Metab, October 1, 2003; 285(4): E737 - E743. [Abstract] [Full Text] [PDF]

				F. P. Dominici and D. Turyn Growth Hormone-Induced Alterations in the Insulin-Signaling System Experimental Biology and Medicine, March 1, 2002; 227(3): 149 - 157. [Abstract] [Full Text] [PDF]

				A. KAMEL, S. NORGREN, A. ELIMAM, P. DANIELSSON, and C. MARCUS Effects of Growth Hormone Treatment in Obese Prepubertal Boys J. Clin. Endocrinol. Metab., April 1, 2000; 85(4): 1412 - 1419. [Abstract] [Full Text]

				L. Ward, J. Paquette, E. Seidman, C. Huot, F. Alvarez, P. Crock, E. Delvin, O. Kämpe, and C. Deal Severe Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy in an Adolescent Girl with a Novel AIRE Mutation: Response to Immunosuppressive Therapy J. Clin. Endocrinol. Metab., March 1, 1999; 84(3): 844 - 852. [Abstract] [Full Text]

				P. Saenger, K. M. Attie, J. DiMartino-Nardi, R. Hintz, L. Frahm, and J. W. Frane Metabolic Consequences of 5-Year Growth Hormone (GH) Therapy in Children Treated with GH for Idiopathic Short Stature J. Clin. Endocrinol. Metab., September 1, 1998; 83(9): 3115 - 3120. [Abstract] [Full Text]