Insulin Resistance and Oxidative Stress in Children Born Small and Large for Gestational Age

Chiavaroli, Valentina; Giannini, Cosimo; D'Adamo, Ebe; Giorgis, Tommaso de; Chiarelli, Francesco; Mohn, Angelika

doi:10.1542/peds.2008-3056

Cited by 98 publications

(79 citation statements)

References 43 publications

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“…A common mechanism for the observed phenotypic outcomes in most of these animal models of developmental programming is oxidative stress and this finding fully recapitulates epidemiological studies in which IUGR children demonstrate increased lipid peroxidation (153)(154)(155) , increased DNA damage (155) and reduced antioxidant enzyme capacity (155) compared with children of a normal birth-weight. Therefore, several animal models of developmental programming have focused upon using antioxidants as a therapeutic intervention in order to reverse the observed phenotypic changes.…”

Section: Developmental Programming Epigenetics and Oxidative Stresssupporting

confidence: 70%

The impact of early nutrition on the ageing trajectory

Tarry-Adkins

Ozanne

2014

Proc. Nutr. Soc.

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Epidemiological studies, including those in identical twins, and in individuals in utero during periods of famine have provided robust evidence of strong correlations between low birthweight and subsequent risk of disease in later life, including type 2 diabetes (T2D), CVD, and metabolic syndrome. These and studies in animal models have suggested that the early environment, especially early nutrition, plays an important role in mediating these associations. The concept of early life programming is therefore widely accepted; however the molecular mechanisms by which early environmental insults can have long-term effects on a cell and consequently the metabolism of an organism in later life, are relatively unclear. So far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification and microRNA) and permanent changes in cellular ageing. Many of the conditions associated with early-life nutrition are also those which have an age-associated aetiology. Recently, a common molecular mechanism in animal models of developmental programming and epidemiological studies has been development of oxidative stress and macromolecule damage, specifically DNA damage and telomere shortening. These are phenotypes common to accelerated cellular ageing. Thus, this review will encompass epidemiological and animal models of developmental programming with specific emphasis on cellular ageing and how these could lead to potential therapeutic interventions and strategies which could combat the burden of common age-associated disease, such as T2D and CVD.

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Section: Developmental Programming Epigenetics and Oxidative Stresssupporting

confidence: 70%

The impact of early nutrition on the ageing trajectory

Tarry-Adkins

Ozanne

2014

Proc. Nutr. Soc.

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“…Fetal hyperinsulinemia, plus a large supply of glucose substrate greatly enhances protein, lipid and glycogen synthesis, thereby promoting growth and adiposity [83,87,88] and may cause ß-cell hyperplasia [88], development of intrauterine IR [89][90][91] and IR during childhood [92]; increased IR and oxidative stress are already present in prepubertal normal-weight, small-forgestational-age (SGA) and LGA infants [92]. In addition, high plasma norepinephrine values were found in infants of diabetic mothers [93].…”

Section: Insulin Action During Pregnancy: Early Onset Of Ir and Cancementioning

confidence: 99%

“…Interestingly, a U-shaped relationship has also been observed between birth weight and IR in utero [89][90][91] and IR in childhood [92,100].…”

Section: Birth Weight and Stem Cells-a Link To (Childhood) Cancer?mentioning

confidence: 99%

Significant Dietary Changes during Human Evolution and the Development of Cancer: From Cells in Trouble to Cells Causing Trouble

Köpp¹

2017

J Carcinog Mutagen

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In all western societies, mortality rates from cancer are high and even increasing. In striking contrast, cancer rates are very rare and even non-existent in primitive cultures, like hunter-gatherer (HG) populations. HGs are free of disease as long as they adhere to their traditional low-insulinemic "Paleolithic" nutrition. With acculturation and transition to current high-carbohydrate/high-insulinemic "Western" diets (HCHIDs), cancer develops in high rates. This paper follows the question of how significant nutritional changes, brought about by the Agricultural revolution, may cause development of cancer. The evidence presented shows that the switch from a Paleolithic to a Western nutrition has brought about significant metabolic perturbations, like an abnormally increased activation of the insulinlike growth factor system, the sympathetic nervous system and the renin-angiotensin-system, an increased expression of HIF-1α and other more, all of which are deeply involved in cancer development through promotion of proliferation, angiogenesis, inflammation, macrophage infiltration, metastasis and inhibition of apoptosis.In addition, HCHIDs generate oxidative stress which may cause mitochondrial damage and genomic instability, and may interfere with normal stem cell development. Faulty redox signaling is suggested to play a significant role in cancer development: hydrogen peroxide, generated at low concentrations, represents an important chemical mediator in the regulation of various cellular signal transduction processes, including stem cell development. Oxidative stress may be sensed by cells as redox signaling. Faulty "redox signaling" is proposed to affect normal stem cell development by sustained activation of uncoupling protein 2, leading to inhibition of differentiation ("maturation arrest"), sustained uncontrolled proliferation, and glycolysis with high expression of hexokinase II, typical features of cancer. In summary, an abnormal diet-related activation of various metabolic systems, together with faulty redox signaling, is suggested to play a pivotal role in cancer development.

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“…У детей 8-13 лет, рожденных с низкой массой, продемонстрирован по-вышенный уровень окисления липидов и более вы-сокие цифры артериального давления по сравнению с детьми, рожденными с нормальной массой тела [67,68]. При этом у детей с низкой массой при ро-ждении уровень антиоксидантных соединений (супе-роксиддисмутазы, каталазы, глутатионпероксидазы) в крови выше.…”

Section: роль оксидативного стресса как эпигенетического фактораunclassified

“…При этом у детей с низкой массой при ро-ждении уровень антиоксидантных соединений (супе-роксиддисмутазы, каталазы, глутатионпероксидазы) в крови выше. Это свидетельствует о том, что их ор-ганизм подвергается существенному оксидативному стрессу [68]. Уровень пероксидации липидов повы-шен в плаценте женщин с преэклампсией, а также в крови женщин, у плодов которых имелся синдром задержки развития [69,70].…”

Section: роль оксидативного стресса как эпигенетического фактораunclassified

Perinatal programming and cardiomyocyte aging

Ковтун¹,

Цывьян²,

Соловьева³

2017

Ross. vestn. perinatol. pediatr.

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Insulin Resistance and Oxidative Stress in Children Born Small and Large for Gestational Age

Abstract: Increased IR and oxidative stress are already present in prepubertal normal-weight SGA and LGA children with a continuous alteration in relation to obesity, suggesting that BW and adiposity represent 2 independent risk factors for degenerative diseases.

Cited by 98 publications

References 43 publications

The impact of early nutrition on the ageing trajectory

The impact of early nutrition on the ageing trajectory

Significant Dietary Changes during Human Evolution and the Development of Cancer: From Cells in Trouble to Cells Causing Trouble

Perinatal programming and cardiomyocyte aging

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