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      Serum Insulin-Like Growth Factor-I Levels and Potential Risk of Type 2 Diabetes

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          The effects of circulating insulin-like growth factor (IGF)-I on increasing insulin sensitivity are well recognized. IGF-I may have a further important role in maintaining β-cell mass, and lower IGF-I activity could explain links between small size at birth and risk of type 2 diabetes in short, obese adults. In the representative Avon Longitudinal Study of Pregnancy and Childhood birth cohort, whereas insulin sensitivity is related to early postnatal weight gain, insulin secretion is related to IGF-I level and statural growth. Adult studies suggest that lower IGF-I levels at baseline predict increased risk for developing impaired glucose tolerance and type 2 diabetes. A common genetic polymorphism in the IGF1 gene could influence size at birth, postnatal growth and type 2 diabetes risk, but results of studies have been inconsistent. Extrapolation of these data to short children born small for gestational age is complex. Some have evidence of IGF-I and insulin resistance, suggesting inherent defects in IGF-I signalling. These children have poor growth responses to growth hormone (GH) therapy and perhaps the highest type 2 diabetes risk. Where these metabolic abnormalities are less severe, responses to GH therapy are good and diabetes risk may then depend on other genetic factors, indicated by a family history of diabetes or origin from ethnic groups with high diabetes prevalence.

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          Most cited references 12

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          Circulating concentrations of insulin-like growth factor-I and development of glucose intolerance: a prospective observational study.

          Results of experimental and clinical studies suggest that insulin-like growth factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) could be important determinants of glucose homoeostasis. However, experimental models might also reflect compensatory and adaptive metabolic processes. We therefore prospectively examined the associations between circulating concentrations of IGF-I and IGFBP-1 and development of glucose tolerance. Participants in this cohort study were a random sample of 615 normoglycaemic men and women aged 45-65 years. Participants underwent oral glucose tolerance testing based on WHO definitions and criteria in 1990-92 and 1994-96. At the baseline visit, we measured serum concentrations of IGF-I and IGFBP-1, and assessed the relation between these peptides and subsequent glucose intolerance. At 4.5 years of follow-up, 51 (8%) of 615 participants developed impaired glucose tolerance or type-2 diabetes. After adjustment for correlates of IGF-I and risk factors for glucose intolerance, the odds ratio for risk of impaired glucose tolerance or type-2 diabetes for participants with IGF-I concentrations above the median (> or = 152 microg/L) compared with those with concentrations below the median (<152 microg/L) was 0.50 (0.26-0.95). Consistent with this finding, IGF-I also showed a significant inverse association with subsequent 2-h glucose concentrations, which was independent of correlates of IGF-I and risk factors for glucose tolerance (p for linear trend=0.026). We also found that this inverse association was independently modified by IGFBP-1 (p for interaction=0.011). These data show that circulating IGF-I and its interaction with IGFBP-1 could be important determinants of glucose homoeostasis and provide further evidence for the possible protective role of IGF-I against development of glucose intolerance.
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            The Importance of  -Cell Failure in the Development and Progression of Type 2 Diabetes

             S E Kahn (2001)
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              Insulin Resistance Early in Adulthood in Subjects Born with Intrauterine Growth Retardation

               D Jaquet (2000)

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                December 2003
                17 November 2004
                : 60
                : Suppl 3
                : 131-135
                Department of Paediatrics, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
                74514 Horm Res 2003;60(suppl 3):131–135
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 1, References: 38, Pages: 5
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