Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 26 P166

ECE2011 Poster Presentations Neuroendocrinology (36 abstracts)

Evaluation of insulin secretion and sensitivity and lipid profile in GH deficient children before and at the end of rhGH therapy

F Prodam 1, , S Savastio 2 , S Bellone 2 , C Balossini 2 , R Ricotti 2 , G Genoni 2 , G Aimaretti 1 & G Bona 2


1Department of Clinical and Experimental Medicine, Endocrinology, University of Piemonte Orientale, Novara, Italy; 2Division of Pediatrics, Department of Medical Science, University of Piemonte Orientale, Novara, Italy.


Introduction: A rise in serum insulin levels during GH therapy is reported. Insulin resistance is a risk factor for type 2 diabetes, atherosclerosis, dyslipidemia, and hypertension. Few data describe insulin secretion and lipids after the end of GH therapy.

Subjects and methods: Aim of our study was to evaluate changes in insulin secretion, sensitivity and lipid profile in children with isolated GHD longitudinally followed during rhGH treatment. We measured lipid profile, glucose and insulin levels at fasting and after an oral glucose tolerance test (OGTT) in 24 GHD children at 4 times: i) before starting of GH therapy (BT); ii) during the last year of therapy (T1); iii) 6 months (T6) and iv) 12 months (T12) after stopped therapy. They were compared at T12 with 28 healthy puberty matched subjects.

Results: No subjects showed dysglycemia or hypertension. Basal glucose levels were lower at BT but similar among the last 3 times. Fasting insulin, insulin and glucose levels at each point after OGTT were progressively lower at T6 and T12 compared to T1 (P<0.02). HOMA-IR index was higher, and Matsuda and QUICKI indexes were lower at T1 respect to T6 and T12 (P<0.02) without returning to the BT prepubertal levels. A compensatory insulin secretion was recorded at T1 as HOMA-B and insulinogenic index both of which progressively decreased at T6 and T12 respect to T1 (P<0.04) returning to BT levels. The disposition index was unchanged from BT to T12. HDL-cholesterol decreased after stopped therapy (P<0.04). All the parameters were similar to controls at T12.

Conclusions: Insulin sensitivity decreased during rhGH therapy without the onset of dysglycemia and was associated with a compensatory insulin secretion after OGTT and without changes of the disposition index. Insulin and glucose secretion progressively restored after stopping treatment being similar to controls in the next 12 months.

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