Association of low birth weight with beta cell function in the adult first degree relatives of non-insulin dependent diabetic subjects.

Cook, J. T. E.; Lévy, Jonathan; Page, R.; Shaw, J. A. G.; Hattersley, Andrew T.; Turner, R. Elaine

doi:10.1136/bmj.306.6873.302

Cited by 78 publications

(52 citation statements)

References 28 publications

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“…Recent research has interlinked the circumstances during intrauterine life, i.e. relative deprivation in utero, and the first year of life, and later occurrence of type 2 diabetes, ischemic heart disease, hypertension and obesity (345)(346)(347)(348)(349). This may be the basis for some of the aberrations becoming apparent during adult life in Turner syndrome.…”

Section: Discussionmentioning

confidence: 99%

Epidemiological, endocrine and metabolic features in Turner syndrome

2004

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Turner syndrome is one of the more common genetic disorders, associated with abnormalities of the X chromosome, and occurring in about 50 per 100 000 liveborn girls. Turner syndrome is usually associated with reduced adult height, gonadal dysgenesis and thus insufficient circulating levels of female sex steroids, and infertility. A number of other signs and symptoms are seen more frequently with the syndrome. Morbidity and mortality are increased. The average intellectual performance is within the normal range. A number of recent studies have provided new insights with respect to epidemiology, cardiology, endocrinology and metabolism. Treatment with GH during childhood and adolescence allows a considerable gain in adult height, although verylong-term consequences of this treatment are not clear. Puberty has to be induced in most cases, and female sex hormone replacement therapy is given during the adult years. The proper dose of hormone replacement therapy (HRT) has not been established, and, likewise, benefits and/or drawbacks from HRT have not been thoroughly evaluated. Since the risk of cardiovascular and endocrinological disease is clearly elevated, proper care during adulthood is emphasized. In summary, Turner syndrome is a condition associated with a number of diseases and conditions which are reviewed in the present paper.

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Section: Discussionmentioning

confidence: 99%

Epidemiological, endocrine and metabolic features in Turner syndrome

2004

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“…Data adjusted for all independent variables in Table 2, and calculated at the mean group values. The hatched areas denote the mean value _+ 2 SD of fasting and 2-h plasma glucose levels in the whole group with reduced beta-cell function at age 43 years, but did not predict the presence of IGT or diabetes [13]. These observations prompted us to re-examine the relationship between birthweight and glucose tolerance and insulin response during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Relation of birthweight to maternal plasma glucose and insulin concentrations during normal pregnancy

et al. 1993

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Summary.Maternal diabetes mellitus is complicated by fetal macrosomia and predisposes the offspring to diabetes, but recent evidence indicates that a low, not high, birthweight is associated with a higher incidence of Type 2 (non-insulin dependent) diabetes in adult life. To clarify the relationships between maternal glucose and insulin levels and birthweight, we measured oral glucose tolerance and neonatal weight in a large group (n = 529) of women during the 26th week of pregnancy. Women with gestational diabetes (n = 17) had more familial diabetes, higher pre-pregnancy body weight, and tended to have large-for-gestational-age babies. In contrast, women with essential hypertension (n = 10) gave birth to significantly (p < 0.01) smaller babies. In the normal group (without gestational diabetes or hypertension, n --503), maternal body weight before pregnancy and at term, maternal height, week of delivery, gender of the newborn, and parity were all significant, independent predictors of birthweight, together explaining 23 % of the variability of neonatal weight. In addition, both fasting (p < 0.006) and 2-h post-glucose (p = 0.03) maternal plasma glucose concentrations were positively associated with birthweight independent of the other physiological determinants, accounting, however, for only 10% of the explained variability. In a subgroup of 134 normal mothers with prepregnancy body mass index of less than 25 kg. m 2, in whom plasma insulin measurements were available, the insulin area-under-curve was inversely related to birthweight (p < 0.02) after simultaneously adjusting for physiological factors and glucose area. When glucose and insulin measurements were combined in the I/G ratio (ratio of insulin to glucose area), this was still inversely related to birthweight. Furthermore, maternal insulinaemia was directly related to blood pressure levels (p <0.001) independently of body weight. We conclude that in normal pregnancy, whereas physiological factors account for most of the explainable variability of infant weight, the influence of the maternal metabolic milieu is dual, positive for glucose levels but negative for insulin concentrations. Maternal hyperinsulinaemia during pregnancy may be one trait linking low birthweight with predisposition to diabetes in adult life.

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“…The idea was encouraged by animal experiments showing impaired ␤-cell function in offspring exposed to a low-protein diet during gestation (26 -33). LBW has been associated with reduced 30-min insulin response after glucose ingestion in young nondiabetic men, relative to glucose and adjusted for BMI (34), and correlated negatively with ␤-cell function in a cohort of normoglycemic or glucose-intolerant first-degree relatives of patients with type 2 diabetes (35). However, a number of studies found no impact of LBW on insulin secretion in humans (6,17,18,36).…”

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confidence: 96%

Early Differential Defects of Insulin Secretion and Action in 19-Year-Old Caucasian Men Who Had Low Birth Weight

et al. 2002

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Several studies have linked low birth weight (LBW) and type 2 diabetes. We investigated hepatic and peripheral insulin action including intracellular glucose metabolism in 40 19-year-old men (20 LBW, 20 matched control subjects), using the hyperinsulinemic-euglycemic clamp technique at two physiological insulin levels (10 and 40 mU/m 2 per min), indirect calorimetry, and [3-3 H]glucose. Insulin secretion was examined during an oral and intravenous glucose tolerance test. Fasting p-glucose was higher in the LBW group (5.6 ؎ 0.1 vs. 5.4 ؎ 0.1; P < 0.05). Basal plasma glycerol concentrations were significantly lower in the LBW group. Insulin-stimulated glycolytic flux was significantly reduced, and suppression of endogenous glucose production was enhanced in the LBW group. Nevertheless, basal and insulin-stimulated rates of whole-body peripheral glucose disposal, glucose oxidation, lipid oxidation, exogenous glucose storage, and nonoxidative glucose metabolism were similar in the two groups. Insulin secretion was reduced by 30% in the LBW group, when expressed relative to insulin sensitivity (disposition index ‫؍‬ insulin secretion ؋ insulin action). We propose that reduced insulin-stimulated glycolysis precedes overt insulin resistance in LBW men. A lower insulin secretion may contribute to impaired glucose tolerance and ultimately lead to diabetes.

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Association of low birth weight with beta cell function in the adult first degree relatives of non-insulin dependent diabetic subjects.

Cited by 78 publications

References 28 publications

Epidemiological, endocrine and metabolic features in Turner syndrome

Epidemiological, endocrine and metabolic features in Turner syndrome

Relation of birthweight to maternal plasma glucose and insulin concentrations during normal pregnancy

Early Differential Defects of Insulin Secretion and Action in 19-Year-Old Caucasian Men Who Had Low Birth Weight

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