Developmental programming of type 2 diabetes

Ong, Thomas Prates; Ozanne, Susan E.

doi:10.1097/mco.0000000000000177

Cited by 48 publications

(21 citation statements)

References 48 publications

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“…In many recent studies, compelling evidence was provided that changes in epigenetic regulation of gene expression (heritable alterations in gene function without changes in the nucleotide sequence) is the most plausible mechanism for the link between unfavourable conditions in early development and adverse health outcomes in later life [20]. The main epigenetic mechanisms are DNA methylation and post-translational modifications of histone tails, as well as regulation by non-coding RNAs (microRNAs and long non-coding RNAs) [21].…”

Section: Conceptual Framework For Developmental Nutritional Programentioning

confidence: 99%

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

Vaiserman

2017

Nutrients

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Consistent evidence from both experimental and human studies suggest that inadequate nutrition in early life can contribute to risk of developing metabolic disorders including type 2 diabetes (T2D) in adult life. In human populations, most findings supporting a causative relationship between early-life malnutrition and subsequent risk of T2D were obtained from quasi-experimental studies (‘natural experiments’). Prenatal and/or early postnatal exposures to famine were demonstrated to be associated with higher risk of T2D in many cohorts around the world. Recent studies have highlighted the importance of epigenetic regulation of gene expression as a possible major contributor to the link between the early-life famine exposure and T2D in adulthood. Findings from these studies suggest that prenatal exposure to the famine may result in induction of persistent epigenetic changes that have adaptive significance in postnatal development but can predispose to metabolic disorders including T2D at the late stages of life. In this review, quasi-experimental data on the developmental programming of T2D are summarized and recent research findings on changes in DNA methylation that mediate these effects are discussed.

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Section: Conceptual Framework For Developmental Nutritional Programentioning

confidence: 99%

“…Among them, mechanisms of epigenetic regulation of gene activity seem to play a dominant role [38,39,40]. Inadequate nutritional environment during intrauterine development suppressed transcription of key genes regulating beta-cell development in rats [39].…”

Section: Evidence From Animal Modelsmentioning

confidence: 99%

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

Vaiserman

2017

Nutrients

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“…Heijmans et al [33] had reported that preconception exposure to famine during the Dutch Hunger Winter was associated with lower methylation of the IGF2. And epigenetic dysregulation is associated with several components that contribute to type 2 diabetes risk, including altered feeding behavior, insulin secretion, and insulin action [34]. Moreover, there was animal evidence shows that malnutrition in fetal life might affect appetite, feeding behavior, and adiposity in adulthood [35].…”

Section: Discussionmentioning

confidence: 99%

Exposure to Chinese Famine in Fetal Life and the Risk of Dysglycemiain Adulthood

Zhang

Song

Wang

et al. 2020

IJERPH

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Undernutrition in early life may have a long consequence of type 2 diabetes in adulthood. The current study was aimed to explore the association between famine exposure in fetal life during China’s Great Famine (1959–1961) and dysglycemia in adulthood. The cross-sectional data from 7830 adults from the 2010–2012 China National Nutrition and Health Surveillance was utilized. Participants who were born between 1960 and 1961 were selected as the exposed group, while the participants who were born in 1963 were selected as the unexposed group. Logistic regression was utilized to examine the relationship between fetal famine exposure and dysglycemia in adulthood. The prevalence of type 2 diabetes in the exposed and control group was 6.4% and 5.1%, respectively, and the risk of type 2 diabetes in the exposed group was 1.23 times higher than that of the control group (95%CI, 1.01–1.50; P = 0.042) in adulthood, and 1.40 times in the severely affected area (95%CI, 1.11–1.76; P = 0.004). The fasting plasma glucose of the exposed group was higher than that of the control group, which was only found in the severely affected area (P = 0.014) and females (P = 0.037). The association between famine and impaired fasting glucose was observed only in females (OR 1.31, 95%CI, 1.01–1.70; P = 0.040). Our results suggested that fetal exposure to Chinese famine increased the risk of dysglycemia in adulthood. This association was stronger in the severely affected area and females.

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“…On the other hand, calorie restriction associated with maternal malnutrition has detrimental effects on the offspring. Research has established that low birth weight and maternal malnutrition are associated with insulin resistance in the key organs that control glucose homeostasis, establishing a direct association between maternal undernutrition and altered pancreatic β-cell function with the development of type 2 diabetes mellitus [49]. The possible involvement of deregulation in microRNA expression in the endocrine pancreas has been hypothesized as a mediator of early nutrition in the formation of β-cell mass and the subsequent risk of diabetes mellitus type 2 [50].…”

Section: Nutrition Conditionsmentioning

confidence: 99%

Epigenetics, Maternal Diet and Metabolic Programming

Ramírez‐Alarcón¹,

Sánchez-Agurto²,

Lamperti³

et al. 2019

TOBIOJ

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Background: The maternal environment influences embryonic and fetal life. Nutritional deficits or excesses alter the trajectory of fetus/offspring’s development. The concept of “developmental programming” and “developmental origins of health and disease” consists of the idea that maternal diet may remodel the genome and lead to epigenetic changes. These changes are induced during early life, permanently altering the phenotype in the posterior adult stage, favoring the development of metabolic diseases such as obesity, dyslipidemia, hypertension, hyperinsulinemia, and metabolic syndrome. In this review, it is aimed to overview epigenetics, maternal diet and metabolic programming factors and determine which of these might affect future generations. Scope and Approach: Nutrients interfere with the epigenome by influencing the supply and use of methyl groups through DNA transmethylation and demethylation mechanisms. They also influence the remodeling of chromatin and arginine or lysine residues at the N-terminal tails of histone, thus altering miRNA expression. Fats, proteins, B vitamins and folates act as important cofactors in methylation processes. The metabolism of carbon in the methyl groups of choline, folic acid and methionine to S-Adenosyl Methionine (SAM), acts as methyl donors to methyl DNA, RNA, and proteins. B-complex vitamins are important since they act as coenzymes during this process. Key Findings and Conclusion: Nutrients, during pregnancy, potentially influence susceptibility to diseases in adulthood. Additionally, the deficit or excess of nutrients alter the epigenetic machinery, affecting genes and influencing the genome of the offspring and therefore, predisposing the development of chronic diseases in adults.

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Developmental programming of type 2 diabetes

Cited by 48 publications

References 48 publications

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

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

Exposure to Chinese Famine in Fetal Life and the Risk of Dysglycemiain Adulthood

Epigenetics, Maternal Diet and Metabolic Programming

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