Birth weight and the insulin resistance syndrome: association of low birth weight with truncal obesity and raised plasminogen activator inhibitor-1 but not with abdominal obesity or plasma lipid disturbances

Byberg, Liisa; McKeigue, Paul; Zethelius, Björn; Lithell, Hans

doi:10.1007/s001250050007

Cited by 127 publications

(113 citation statements)

References 38 publications

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“…Having high ponderal index at birth was also beneficial for men. The findings of the present study are in accordance with some earlier studies (Barker et al, 1997;Byberg et al, 2000). Abdominal fat can be estimated as measurements of waist : hip ratio, while the subscapular-totriceps ratio has been used to estimate truncal fat (Haffner et al, 1987;Barker et al, 1997).…”

Section: Figuresupporting

confidence: 91%

“…The skinfold was pinched up in a transverse axis in the dedio-axillar-line. The ratio of subscapular to triceps skinfold was used as an index of truncal fatness (Valdez et al, 1994;Byberg et al, 2000).…”

Section: Collection Of Adult Datamentioning

confidence: 99%

“…Although birth weight has been shown as positively related to adult BMI, studies have shown birth weight to be inversely related to truncal and abdominal fatness in both adolescence and adult life (Law et al, 1992;Valdez et al, 1994;Barker et al, 1997;Byberg et al, 2000). It has therefore been postulated that the tendency to store fat abdominally may be a persistent response to adverse conditions and growth in foetal life (Law et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Association between size at birth, truncal fat and obesity in adult life and its contribution to blood pressure and coronary heart disease; study in a high birth weight population

et al. 2004

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Objective: The aim of the study was to assess the relationship between size at birth and obesity as well as truncal fat, and its contribution to cardiovascular risk in a high birth weight population. Design: Cohort-study with retrospectively collected data on size at birth. Setting: Reykjavik, Iceland. Subjects: A total of 1874 men and 1833 women born in Reykjavik during . Main outcome measures: Size at birth. Adult weight, height and skinfold thickness measurements, systolic and diastolic blood pressure, fatal and nonfatal coronary heart disease (CHD). Results: Birth weight was positively related to adult body mass index (BMI) in both genders (B¼0.3570.14 kg/m 2 , adj. R 2 ¼0.015, P¼0.012 and B¼0.3470.17 kg/m 2 , adj. R 2 ¼0.055, P¼0.043 in men and women, respectively). However, high birth weight was not a risk factor for adult obesity (BMIZ30 kg/m 2 ). In the highest birth weight quartile, the odds ratio (95% CI) for being above the 90th percentile of truncal fat was 0.7 (0.6-1.0, P¼0.021) for men and 0.4 (0.3-0.8, P¼0.002) for women, compared with the lowest birth weight quartile. Truncal fat and BMI were positively related to blood pressure in both genders (Po0.05), but not to CHD. The regression coefficient for the inverse association between birth weight and blood pressure hardly changed when adding truncal fat to the model. Conclusion: In this high birth weight population, high birth weight was related to higher BMI in adulthood without being a risk factor for adult obesity. The inverse association between birth weight and truncal fat in adulthood suggests a role for foetal development in determining adult fat distribution. The inverse relationship of birth weight to blood pressure seems not to be mediated through the same pathway as to truncal fat.

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Section: Figuresupporting

confidence: 91%

Section: Collection Of Adult Datamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association between size at birth, truncal fat and obesity in adult life and its contribution to blood pressure and coronary heart disease; study in a high birth weight population

et al. 2004

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“…Type 2 diabetes mellitus and IGT were defined according to the WHO 1999 criteria using a 75 g OGTT or by the use of oral hypoglycaemic agents. Fasting concentrations of plasma glucose and serum lipids, waist circumference, an electrocardiogram, and supine systolic and diastolic blood pressure were measured under standardised conditions [5].…”

Section: Methodsmentioning

confidence: 99%

Reduced plasma levels of glucagon-like peptide-1 in elderly men are associated with impaired glucose tolerance but not with coronary heart disease

et al. 2009

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Aims/hypothesis Besides the insulinotropic effects of glucagon-like peptide-1 (GLP-1) mimetics, their effects on endothelial dysfunction and myocardial ischaemia are of interest. No previous study has investigated associations between plasma levels of GLP-1 and CHD. Methods We investigated longitudinal relationships of fasting GLP-1 with the dynamic GLP-1 response after OGTT (difference between 60 min OGTT-stimulated and fasting GLP-1 levels ) and CHD in a populationbased cohort of 71-year-old men. In the same cohort, we also cross-sectionally investigated the association between stimulated GLP-1 levels and: (1) cardiovascular risk factors (blood pressure, lipids, urinary albumin, waist circumference and insulin sensitivity index [M/I] assessed by euglycaemic-hyperinsulinaemic clamp); and (2) impaired glucose tolerance (IGT) and type 2 diabetes mellitus.Results During the follow-up period (maximum 13.8 years), of 294 participants with normal glucose tolerance (NGT), 69 experienced a CHD event (13.8 years), as did 42 of 141 with IGT and 32 of 74 with type 2 diabetes mellitus. ΔGLP-1 did not predict CHD (HR 1.0, 95% CI 0.52-2.28). The prevalence of IGT was associated with ΔGLP-1, lowest vs highest quartile (OR 0.3, 95% CI 0.12-0.58), with no such association for type 2 diabetes mellitus (OR 1.0, 95% CI 0.38-2.86). M/I was significantly associated with ΔGLP-1 in the type 2 diabetes mellitus group (r=0.38, p<0.01), but not in the IGT (r=0.11, p=0.28) or NGT (r=0.10, p=0.16) groups. Conclusions/interpretation Impaired GLP-1 secretion is associated with IGT, but not with type 2 diabetes mellitus. This finding in the latter group might be confounded by oral glucose-lowering treatment. GLP-1 does not predict CHD. Although ΔGLP-1 was associated with insulin sensitivity in the type 2 diabetes mellitus group, GLP-1 does not seem to be a predictor of CHD in insulin-resistant patients.

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“…The study was initiated in 1970 when all men born between 1920 and 1924 and residing in Uppsala county, Sweden, were invited to a health survey, in which 2,322 men participated [19]. After 20 years, at around 70 years of age, the men were invited to a reinvestigation, which was performed from August 1991 to May 1995, with 1,221 of the original 2,322 subjects participating [20]. All DNA samples (n=1,142) analysed in this study were collected from the 70-year-old (71±0.6 years) cohort.…”

Section: Methodsmentioning

confidence: 99%

Variants of the TCF7L2 gene are associated with beta cell dysfunction and confer an increased risk of type 2 diabetes mellitus in the ULSAM cohort of Swedish elderly men

et al. 2007

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Aims/hypothesis In a population-based cohort of elderly men with well-defined phenotypes and biochemical markers related to type 2 diabetes mellitus, we analysed two single nucleotide polymorphisms (SNPs), rs7903146 and rs12255372, in the transcription factor 7-like 2 gene (TCF7L2), which are associated with an increased risk of type 2 diabetes mellitus. Materials and methods The 1,142 subjects were from the population-based Uppsala Longitudinal Study of Adult Men cohort study (see http://www.pubcare.uu.se/ULSAM/, last accessed in May 2007). Insulin sensitivity was assessed using a euglycaemic-hyperinsulinaemic clamp; fasting intact and 32-33 split proinsulin, immunoreactive insulin and specific insulin were measured in plasma samples. The SNPs rs7903146 and rs12255372 were genotyped using a fluorescent homogeneous single base extension assay. The SNP genotypes were analysed against diabetes prevalence at age 70 using logistic regression and against quantitative biochemical measures using linear regression analysis. Results We replicated the association with type 2 diabetes mellitus for both SNPs in this cohort of elderly males. The highest significant odds ratio (2.15, 95% CI 1.20-3.85) was found for SNP rs7903146. The odds ratio for SNP rs12255372 was 1.69 (95% CI 1.20-2.39). Both TCF7L2 SNPs were found to be significantly associated with plasma proinsulin when adjusting for insulin sensitivity, both in the whole cohort and when the diabetic subjects were excluded. Analysis for fasting plasma insulin or insulin sensitivity did not give significant results. Conclusions/interpretation The association between the risk alleles of the two SNPs studied and levels of proinsulin in plasma, identified when adjusting for insulin sensitivity using euglycaemic-hyperinsulinaemic clamp measurements in this study, is an important novel finding.

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Birth weight and the insulin resistance syndrome: association of low birth weight with truncal obesity and raised plasminogen activator inhibitor-1 but not with abdominal obesity or plasma lipid disturbances

Cited by 127 publications

References 38 publications

Association between size at birth, truncal fat and obesity in adult life and its contribution to blood pressure and coronary heart disease; study in a high birth weight population

Association between size at birth, truncal fat and obesity in adult life and its contribution to blood pressure and coronary heart disease; study in a high birth weight population

Reduced plasma levels of glucagon-like peptide-1 in elderly men are associated with impaired glucose tolerance but not with coronary heart disease

Variants of the TCF7L2 gene are associated with beta cell dysfunction and confer an increased risk of type 2 diabetes mellitus in the ULSAM cohort of Swedish elderly men

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