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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

TLDR
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.

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The thrifty phenotype hypothesis.

TL;DR: It is proposed that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism.
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In utero programming of chronic disease

TL;DR: This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.
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Glucose tolerance in adults after prenatal exposure to famine.

TL;DR: Prenatal exposure to famine, especially during late gestation, is linked to decreased glucose tolerance in adults, and this effect of famine on glucose tolerance is especially important in people who become obese as adults.
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Fetal programming and adult health.

TL;DR: Although the influences that impair fetal development and programme adult cardiovascular disease remain to be defined, there are strong pointers to the importance of maternal body composition and dietary balance during pregnancy.
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Fetal Origins of Obesity

TL;DR: Low birth weight seems to be associated with later risk for central obesity, which also confers increased cardiovascular risk, and the combination of lower birth weight and higher attained BMI is most strongly associated withLater disease risk.
References
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Journal ArticleDOI

Homeostasis model assessment : insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man

TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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Role of Insulin Resistance in Human Disease

TL;DR: The possibility is raised that resistance to insulin-stimulated glucose uptake and hyperinsulinemia are involved in the etiology and clinical course of three major related diseases— NIDDM, hypertension, and CAD.
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Fetal origins of coronary heart disease

TL;DR: The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease.
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Weight in infancy and death from ischaemic heart disease.

TL;DR: Measurements that promote prenatal and postnatal growth may reduce deaths from ischaemic heart disease and may be especially important in boys who weigh below 7.5 pounds (3.4 kg) at birth.
Journal ArticleDOI

Fetal and infant growth and impaired glucose tolerance at age 64.

TL;DR: Reduced growth in early life is strongly linked with impaired glucose tolerance and non-insulin dependent diabetes and reduced early growth is also related to a raised plasma concentration of 32-33 split proinsulin, which is interpreted as a sign of beta cell dysfunction.
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