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Gender differences in the insulin-like growth factor axis response to a glucose load

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Abstract:

Abstract Aims: 

The insulin-like growth factors (IGFs) are thought to contribute to glucose homeostasis. The aim of our study was to examine the response of the IGFs and their binding proteins to an intravenous load of glucose in a cohort of young men and women with normal glucose tolerance. Methods: 

The intravenous glucose tolerance test (IVGTT) was used to quantify insulin sensitivity and insulin secretion in 160 adults aged 20–21 years in Adelaide, Australia. Serum IGF-I, IGF-II, IGF-binding protein (IGFBP)-1 and IGFBP-3 were measured during the IVGTT. Results: 

Women were less insulin sensitive than men with higher fasting insulin (women 55.6 ± 4.4, men 44.1 ± 3.6 pmol L−1, P = 0.001) and first phase insulin secretion (women 3490 ± 286, men 3038 ± 271 pmol L−1 min, P = 0.042). Women showed lower fasting free IGF-I (women 0.29 ± 0.02, men 0.36 ± 0.02 g L−1, P = 0.004) but higher IGFBP-3 (women 46.3 ± 0.53, men 43.3 ± 0.58 mg dL−1, P = 0.001) and higher IGFBP-1 concentrations (women 37.0 ± 2.9, men 24.8 ± 2.3 g L−1, P = 0.012). IGFBP-1 fell by 5 min and remained suppressed. IGFBP-3 and total IGF-I fell until 60 min rising again by 2 h. IGF and IGFBP values were all higher in women. IGFBP-1 showed a negative association with fasting and stimulated insulin concentrations in both genders. First phase insulin secretion however showed positive correlations with IGFBP-3 (r = 0.321, P = 0.004) and IGF-I (r = 0.339 P = 0.002) in men but not women. Conclusion: 

Our data show that IGFBP-1, IGFBP-3 and IGF-I show acute changes following a glucose load and there are marked gender differences in these responses.

Keywords: gender; glucose; insulin; insulin sensitivity; insulin-like growth factor

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1748-1716.2006.01581.x

Affiliations: 1: Department of Endocrinology, Peninsula Medical School, Derriford Hospital, Plymouth, UK 2: Developmental Origins of Health and Disease Division, School of Medicine, University of Southampton, UK 3: Department of Obstetrics and Gynaecology, University of Adelaide, Adelaide, Australia 4: Endocrinology and Metabolic Medicine, Imperial College School of Medicine, London, UK

Publication date: July 1, 2006

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