Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence.

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obesity 15 endocrinologydiseases
glucose intolerance 5 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases

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glucose intolerance 11718 expression of genes implicated in various aspects of glucose metabolism such as β-cell dysfunction, glucose intolerance and insulin resistance, have been shown to be critically involved in the pathogenesis of T2D [[25]].
glucose intolerance 13191 characterized by beta-cell failure due to insufficient expansion of beta-cell mass, impaired insulin secretion, glucose intolerance and fasting hyperglycaemia [[34],[35]]. For example, in a study using cross-fostering methodology to
glucose intolerance 25174 siege, however, demonstrated no effect of intrauterine undernutrition during the siege on dyslipidaemia, glucose intolerance , hypertension and the risk of CVD in adulthood [[61],[62]]. Starvation-exposed individuals demonstrated
glucose intolerance 25511 results seem to contradict the thrifty phenotype concept since in utero undernutrition was not related to glucose intolerance in adult persons, although prenatal malnutrition influenced their blood pressure and differ from those
glucose intolerance 32121 from military action as such; the majority died from war-associated starvation [[74]]. The risks of glucose intolerance , hypertension and being overweight 40 years after prenatal exposure to the Biafran Famine have been
metabolic syndrome 34233 non-exposed group, n = 433) [[77]]. The higher risks of hypertension (OR = 1.52), T2D (OR = 1.60), metabolic syndrome (OR = 2.14) and vascular disease (OR = 1.99) were found in exposed individuals.In general, findings
metabolic syndrome 36137 weight in the mid-latitude areas [[95]]. Seasonality of birth has been demonstrated for many aspects of metabolic syndrome , including high systolic blood pressure [[82]], obesity [[83],[84]] and also dyslipidaemia, insulin
obesity 1818 developed and developing. It is caused by insulin resistance resulting from decreased activity and enhanced obesity levels that occur with increasing age. T2D is considered to be adult-onset disease, since it typically
obesity 2141 increasingly diagnosed in younger patients [[1]]. Over the last decades, a rapid increase in the prevalence of obesity arising from high caloric diet intake and sedentary lifestyle is driving a global pandemic of T2D. Currently,
obesity 6720 absorption beyond metabolic capability when energy supplies increase, thereby causing insulin resistance, obesity and T2D in adulthood [[9]]. Among the factors affecting the risk of metabolic dysfunctions, including
obesity 9862 for the key role of DNA methylation and other epigenetic mechanisms in mediating the risk of T2D and obesity has been repeatedly documented over the past years [[22]]. Initial evidence for the role of epigenetic
obesity 9987 repeatedly documented over the past years [[22]]. Initial evidence for the role of epigenetic regulation in obesity and T2D has been mainly provided by studies in animal models. These studies reported changes in epigenetic
obesity 10249 feeding with high-fat diet and by human investigation that demonstrated epigenetic alterations in T2D and obesity candidate genes in obese and/or diabetic persons. More recently, rapid technological advances and price
obesity 15797 mechanisms [[44]]. Catch-up growth following maternal protein restriction also favoured the development of obesity in adult male rat offspring [[45]]. In a mice model, a protein restriction during foetal life followed
obesity 15934 [[45]]. In a mice model, a protein restriction during foetal life followed by catch-up growth led to obesity in adult male mice [[46]]. These changes were associated with increased relative fat mass, hypercholesterolemia,
obesity 18937 phenotypes such as elevated levels of plasma lipids and body mass index (BMI), as well as enhanced risks of obesity and cardiovascular disease (CVD) later in life (for reviews, see refs. [[48],[49],[50]]). Most of these
obesity 25372 individuals demonstrated only evidence for endothelial dysfunction and for a stronger influence of obesity on blood pressure. These results seem to contradict the thrifty phenotype concept since in utero undernutrition
obesity 26540 several more recent studies. Both the increasing incidence and decreasing age of onset of T2D without obesity have been found in women exposed to starvation throughout the Siege of Leningrad during their childhood
obesity 36204 demonstrated for many aspects of metabolic syndrome, including high systolic blood pressure [[82]], obesity [[83],[84]] and also dyslipidaemia, insulin resistance and CVD [[85]]. The seasonal pattern of birth
obesity 40214 However, while genetic factors undoubtedly contribute to an individual susceptibility to development of obesity and T2D, the identified genetic variants can explain only part of the variation [[22],[101]]. Recent
obesity 41263 between poor nutritional intake in utero and impaired glucose regulation, atherogenic lipid profiles and obesity later in life, all known to be risk factors for development of T2D, has been demonstrated [[99],[100],[101],[102]].
obesity 44913 collectivization1932–1933High risk of T2D[[59]]RussiaLeningrad Siege1941–1944Endothelial dysfunction, stronger influence of obesity on blood pressure Increasing incidence of T2D Atherosclerosis, arterial hypertension[[61],[62]] [[64]]

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