Oxidative Stress, Intrauterine Growth Restriction, and Developmental Programming of Type 2 Diabetes

Rashid, Cetewayo S.; Bansal, Amita; Simmons, Rebecca A.

doi:10.1152/physiol.00023.2018

Cited by 58 publications

(48 citation statements)

References 169 publications

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“…[37] Although fetal IUGR and macrosomia are very disparate growth states, both are associated with mitochondrial dysfunction and oxidative stress. [38]…”

Section: Growth Abnormalities and Oxidative Stressmentioning

confidence: 99%

Oxygen radical disease in the newborn, revisited: Oxidative stress and disease in the newborn period

Perez

Robbins

Revhaug

et al. 2019

Free Radical Biology and Medicine

137

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Thirty years ago, there was an emerging appreciation for the significance of oxidative stress in newborn disease. This prompted a renewed interest in the impact of oxygen therapy for the newborn in the delivery room and beyond, especially in premature infants. Today, the complexity of oxidative stress both in normal regulation and pathology is better understood, especially as it relates to neonatal mitochondrial oxidative stress responses to hyperoxia. Mitochondria are recipients of oxidative damage and have a propensity for oxidative self-injury that has been implicated in the pathogenesis of neonatal lung diseases. Similarly, both intrauterine growth restriction (IUGR) and macrosomia are associated with mitochondrial dysfunction and oxidative stress. Additionally, reoxygenation with 100% O2 in a hypoxic-ischemic newborn lamb model increased the production of pro-inflammatory cytokines in the brain. Moreover, the interplay between inflammation and oxidative stress in the newborn is better understood because of animal studies. Transcriptomic analyses have found a number of genes to be differentially expressed in murine models of bronchopulmonary dysplasia (BPD). Epigenetic changes have also been detected both in animal models of BPD and premature infants exposed to oxygen. Antioxidant therapy to prevent newborn disease has not been very successful; however, new therapeutic principles, like melatonin, are under investigation.

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“…[37] Although fetal IUGR and macrosomia are very disparate growth states, both are associated with mitochondrial dysfunction and oxidative stress. [38]…”

Section: Growth Abnormalities and Oxidative Stressmentioning

confidence: 99%

Oxygen radical disease in the newborn, revisited: Oxidative stress and disease in the newborn period

Perez

Robbins

Revhaug

et al. 2019

Free Radical Biology and Medicine

137

View full text Add to dashboard Cite

show abstract

“…The Developmental Origins of Health and Disease Hypothesis posits that environmental stimuli encountered during critical periods of development, including embryonic, fetal and neonatal life, can induce long-lasting changes in the morphology and physiology of the fully developed individual ( Bateson et al, 2004 ; West-Eberhard, 2005 ). Among the mechanisms proposed for the developmental origin of adult disease are unbalanced levels of micro- or macronutrients that cause oxidative stress-related damage to critical biomolecular compounds ( Luo et al, 2006 ; Martin-Gronert and Ozanne, 2012 ; Rashid et al, 2018 ) which, in turn, enter into signaling pathways underlying several chronic degenerative diseases, including cardiovascular diseases (CVD) ( Mansego et al, 2011 ; Sheeran and Pepe, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Maternal Protein Restriction in Two Successive Generations Impairs Mitochondrial Electron Coupling in the Progeny’s Brainstem of Wistar Rats From Both Sexes

et al. 2019

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Maternal protein deficiency during the critical development period of the progeny disturbs mitochondrial metabolism in the brainstem, which increases the risk of developing cardiovascular diseases in the first-generation (F1) offspring, but is unknown if this effect persists in the second-generation (F2) offspring. The study tested whether mitochondrial health and oxidative balance will be restored in F2 rats. Male and female rats were divided into six groups according to the diet fed to their mothers throughout gestation and lactation periods. These groups were: (1) normoprotein (NP) and (2) low-protein (LP) rats of the first filial generation (F1-NP and F1-LP, respectively) and (3) NP and (4) LP rats of the second filial generation (F2-NP and F2-LP, respectively). After weaning, all groups received commercial chow and a portion of each group was sacrificed on the 30th day of life for determination of mitochondrial and oxidative parameters. The remaining portion of the F1 group was mated at adulthood and fed an NP or LP diet during the periods of gestation and lactation, to produce progeny belonging to (5) F2R-NP and (6) F2R-LP group, respectively. Our results demonstrated that male F1-LP rats suffered mitochondrial impairment associated with an 89% higher production of reactive species (RS) and 137% higher oxidative stress biomarkers, but that the oxidative stress was blunted in female F1-LP animals despite the antioxidant impairment. In the second generation following F0 malnutrition, brainstem antioxidant defenses were restored in the F2-LP group of both sexes. However, F2R-LP offspring, exposed to LP in the diets of the two preceding generations displayed a RS overproduction with a concomitant decrease in mitochondrial bioenergetics. Our findings demonstrate that nutritional stress during the reproductive life of the mother can negatively affect mitochondrial metabolism and oxidative balance in the brainstem of F1 progeny, but that restoration of a normal diet during the reproductive life of those individuals leads toward a mitochondrial recovery in their own (F2) progeny. Otherwise, if protein deprivation is continued from the F0 generation and into the F1 generation, the F2 progeny will exhibit no recovery, but instead will remain vulnerable to further oxidative damage.

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“…25 Numerous studies have shown that embryonic retardation can lead to abnormal pancreatic development and increase the possibility of T2DM through epigenetics mechanisms. 7 To investigate the relationship between IUGR and T2DM, we constructed the IUGR model using a low-protein diet. The body weights of these mice after birth were found to be significantly lower than that of normal newborn mice.…”

Section: Discussionmentioning

confidence: 99%

“…Insufficient nutrient supply in the foetal period leads to poor development of the embryo in the uterus, which can cause irreversible damage to the development of islet cells in the early stage of the embryo, and lead to abnormal glucose tolerance and even T2DM in adulthood. 7 With the rapid development of genomics, studies have found that noncoding RNAs play important roles in growth and development, Yihui Li and Chengting Dai contributed equally to this study. disease occurrence and other processes.…”

Section: Introductionmentioning

confidence: 99%

The mechanisms of lncRNA Tug1 in islet dysfunction in a mouse model of intrauterine growth retardation

Dai

Yuan

et al. 2020

Cell Biochemistry & Function

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Taurine upregulated gene 1 (Tug1) is a novel lncRNA that participates in growth, and the abnormal expression of Tug1 related to mouse islet cell dysfunction. A recent study revealed that intrauterine growth retardation (IUGR) related to the pathogenesis of diabetes. Here, we aimed to explore the role and mechanism of Tug1 in IUGRmediated islet dysfunction. We observed that newborn IUGR mice had lower body and pancreas weight and smaller islets than newborn control mice. After IUGR mice were given a normal diet, they showed catch-up growth and abnormal glucose tolerance; however, the pancreas/body weight ratio remained low. Blood glucose, serum insulin and related gene expression showed mild recovery after overexpression of Tug1 in IUGR mice. Furthermore, Tug1 was enriched in the nuclei of MIN6 cells. Using RIP and CHIP analyses we found that Tug1 could regulate Hes1 expression by binding to EZH2 to affect insulin synthesis in MIN6 cells. These findings indicate that lncRNA Tug1 could regulate the expression of Hes1 via EZH2-driven H3K27 methylation and affect insulin production.

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Oxidative Stress, Intrauterine Growth Restriction, and Developmental Programming of Type 2 Diabetes

Cited by 58 publications

References 169 publications

Oxygen radical disease in the newborn, revisited: Oxidative stress and disease in the newborn period

Oxygen radical disease in the newborn, revisited: Oxidative stress and disease in the newborn period

Maternal Protein Restriction in Two Successive Generations Impairs Mitochondrial Electron Coupling in the Progeny’s Brainstem of Wistar Rats From Both Sexes

The mechanisms of lncRNA Tug1 in islet dysfunction in a mouse model of intrauterine growth retardation

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