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      Insulin Resistance (HOMA) in Relation to Plasma Cortisol, IGF-I and IGFBP-3

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          Objective: To investigate the possible contribution of plasma cortisol and growth hormone (GH) as reflected by insulin-like growth factor-I (IGF-I)/insulin-like growth factor-binding protein-3 (IGFBP-3) on insulin action in short-statured children. Methods:In this study, insulin resistance (HOMA) was determined in 34 normal short-statured (age 9.4 ± 3.5 years) and in 19 GH-deficient children (age 10.4 ± 2.2 years). HOMA was examined in relation to fasting plasma cortisol, IGF-I, IGFBP-3 and in addition to birthweight and body mass index (BMI). Results: Birthweight was not correlated to insulin resistance. In GH-deficient children, BMI was significantly augmented and was associated with HOMA (p < 0.02). In both groups of patients, fasting plasma cortisol was related to HOMA (normal: r = 0.295, p < 0.05, GH-deficient: r = 0.495, p < 0.02). Only in normal short-statured children IGF-I (r = 0.338, p < 0.03) and IGFBP-3 (r = 0.493, p < 0.002) were associated with insulin resistance. Conclusion: The results indicated that at a young age cortisol contributed to insulin resistance in short-statured children. In normal short-statured children HOMA was associated with IGF-I and IGFBP-3. Possibly GH, a known cause of insulin resistance, contributed to HOMA as IGF-I and IGFBP-3 do not mediate insulin resistance but reflect growth hormone secretion. The results in GH-deficient children supported this conclusion as in the absence of GH insulin resistance was not associated with IGF-I/IGFBP-3.

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          Most cited references 4

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          Genetic versus environmental aetiology of the metabolic syndrome among male and female twins.

           K Kyvik,  H. Beck,  A Vaag (2001)
          The aetiology of the metabolic syndrome including hyperinsulinaemia, glucose intolerance, dyslipidaemia, hypertension and obesity is not known. We studied the relative impact of genetic versus environmental factors for the development of the components in the syndrome among male and female twins. A total of 303 elderly twin pairs participated in the study. We report concordances and heritability estimates of the components by classic twin analysis to assess the proportion of variation attributed to genetic factors. All components correlated significantly. The concordance rates for glucose intolerance, overall obesity and low HDL-cholesterol were significantly higher among monozygotic than dizygotic twins indicating a genetic influence on the development of these phenotypes. The heritability estimates for glucose concentration, BMI and HDL-cholesterol among monozygotic twins confirmed these findings. The heritability estimates for waist-to-hip ratio, fasting insulin and triglycerides, however, were low, indicating a major environmental influence. We found a higher genetic influence on glucose intolerance and systolic blood pressure and a lower genetic influence on low HDL-cholesterol and diastolic blood pressure among male twins compared to female twins. Based on the correlations between the components in the syndrome, we propose a core complex including hyperinsulinaemia, obesity, hypertriglyceridaemia and low HDL-cholesterol with only weak associations to glucose concentrations and blood pressure levels. The study confirms the notion of a multifactorial aetiology of the components including genetic and non-genetic factors. The differences in aetiology between male and female twins indicate an influence of sex on several of the components in the metabolic syndrome.
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            Elevated Plasma Cortisol Concentrations: A Link between Low Birth Weight and the Insulin Resistance Syndrome?

             D Phillips (1998)
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              Childhood size is more strongly related than size at birth to glucose and insulin levels in 10-11-year-old children.

              In adults low birthweight and thinness at birth are associated with increased risk of glucose intolerance and non-insulin-dependent diabetes mellitus. We have examined the relations between size at birth (birthweight, thinness at birth) and levels of plasma glucose and serum insulin in children, and compared them with the effects of childhood size. We performed a school-based survey of 10-11-year-old British children (response rate 64%) with measurements made after an overnight fast. One group of children (n = 591) was studied fasting while the other (n = 547) was studied 30 min after a standard oral glucose load (1.75 g/kg). Serum insulin was measured by a highly specific ELISA method. Birthweight was assessed by maternal recall and thinness at birth using birth records. Neither fasting nor post-load glucose levels showed any consistent relationship with birthweight or ponderal index at birth. After adjustment for childhood height and ponderal index, both fasting and post-load insulin levels fell with increasing birthweight. For each kg increase in birthweight, fasting insulin fell by 16.9% (95% confidence limits 7.1-25.8%, p = 0.001) and post-load insulin by 11.6% (95% confidence limits 3.5-19.1%, p = 0.007). However, the proportional change in insulin level for a 1 SD increase in childhood ponderal index was much greater than that for birthweight (27.2% and -8.8%, respectively, for fasting insulin). We conclude that low birthweight is not related to glucose intolerance at 10-11 years, but may be related to the early development of insulin resistance. However, in contemporary children obesity is a stronger determinant of insulin level and insulin resistance than size at birth.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                28 October 2002
                : 58
                : 5
                : 229-232
                Departments of aPediatrics and bBiometrics and Medical Documentation, University of Ulm, Germany
                66266 Horm Res 2002;58:229–232
                © 2002 S. Karger AG, Basel

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                Page count
                Tables: 2, References: 28, Pages: 4
                Original Paper


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