scholarly journals Early Life Factors and Type 2 Diabetes Mellitus

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Xinli Jiang ◽  
Huijie Ma ◽  
Yan Wang ◽  
Yan Liu
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Early Life ◽  
Animal Experiments ◽  
Adult Life ◽  
Later Life ◽  
Negative Effects ◽  
Early Life Factors

Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.

scholarly journals T2DM: Why Epigenetics?

2011 ◽  
Vol 2011 ◽  
pp. 1-17 ◽  
Author(s):  
Delphine Fradin ◽  
Pierre Bougnères
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Environmental Factors ◽  
Early Life ◽  
Time Dependent ◽  
Phenotypic Traits ◽  
To Come ◽  
Genetic And Environmental Factors

Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder influenced by interactions between genetic and environmental factors. Epigenetics conveys specific environmental influences into phenotypic traits through a variety of mechanisms that are often installed in early life, then persist in differentiated tissues with the power to modulate the expression of many genes, although undergoing time-dependent alterations. There is still no evidence that epigenetics contributes significantly to the causes or transmission of T2DM from one generation to another, thus, to the current environment-driven epidemics, but it has become so likely, as pointed out in this paper, that one can expect an efflorescence of epigenetic knowledge about T2DM in times to come.

Rat maternal diabetes impairs pancreatic β-cell function in the offspring

2007 ◽  
Vol 293 (1) ◽  
pp. E228-E236 ◽  
Author(s):  
Junying Han ◽  
Jianxiang Xu ◽  
Yun Shi Long ◽  
Paul N. Epstein ◽  
Ye Q. Liu
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cell Function ◽  
Adult Life ◽  
Maternal Diabetes ◽  
Metabolic Enzyme ◽  
Β Cell ◽  
Β Cell Function

It has been shown that maternal diabetes increases the risk for obesity, glucose intolerance, and Type 2 diabetes mellitus in the adult life of the offspring. Mechanisms for these effects on the offspring are not well understood, and little information is available to reveal the mechanisms. We studied the effect of maternal diabetes on β-cell function in the offspring of streptozotocin (STZ)-induced diabetic rat mothers (STZ-offspring). STZ-offspring did not become glucose intolerant up to 15 wk of age. At this age, however, insulin secretion was significantly impaired, as measured by in vivo and in vitro studies. Consistent with these changes, islet glucose metabolism and some important glucose metabolic enzyme activities were reduced. No significant changes were found in islet morphological analysis. These data indicate that β-cell function is impaired in adult STZ-offspring; these changes may contribute to the development of type 2 diabetes mellitus in adulthood.

Solanum anguivi Lam. fruit preparations counteract the negative effects of a high-sugar diet on the glucose metabolism in Drosophila melanogaster

2021 ◽  
Author(s):  
Aisha Musaazi Sebunya Nakitto ◽  
Silvia Rudloff ◽  
Christian Borsch ◽  
Anika Wagner
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Drosophila Melanogaster ◽  
Glucose Metabolism ◽  
Negative Effects ◽  
High Sugar ◽  
Underlying Mechanisms

Solanum anguivi Lam. fruits (SALF) are traditionally consumed as a remedy for type 2 diabetes mellitus (T2DM). However, data regarding the potential anti-diabetic effect of SALF and its underlying mechanisms...

scholarly journals TV viewing during childhood and adult type 2 diabetes mellitus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniela Schmid ◽  
Walter C. Willett ◽  
Michele R. Forman ◽  
Ming Ding ◽  
Karin B. Michels
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Early Life ◽  
Health Study ◽  
Adult Women ◽  
Tv Viewing ◽  
Adult Type ◽  
Childhood Physical Activity

AbstractWe examined whether regular television (TV) viewing at ages 3–5 and 5–10 years is related to the incidence of type 2 diabetes mellitus (T2D) in adult women. We used data from 34,512 mother-nurse daughter dyads in the Nurses’ Health Study (NHS) II and the Nurses’ Mothers’ Cohort Study. Mothers of NHS II participants completed a questionnaire on their pregnancy with the nurse and her early life experience. During 391,442 person-years of follow-up from 2001 to 2013, 1515 nurses developed T2D. Increasing levels of TV viewing at 3–5 years of age retrospectively reported by the mothers were related to a greater risk of T2D in adulthood: multivariable-adjusted hazard ratios (HRs) for ≤ 1, 2, and ≥ 3 h/day vs. no TV viewing were 1.11 [95% confidence interval (CI) 0.96–1.28], 1.20 (95% CI 1.02–1.41), and 1.35 (95% CI 1.11–1.65), p trend = 0.002, respectively, after adjustment for early life variables, including childhood physical activity and adiposity. Retrospectively reported TV viewing for ≥ 3 h/day at 5–10 years of age was associated with a 34% greater risk of adult T2D (HR 1.34, 95% CI 1.05–1.70, p trend < 0.001). Additional adjustments for adult variables, including adult TV viewing and current BMI attenuated the effect estimates (≥ 3 h/day TV viewing at 3–5 years: HR 1.22, 95% CI 0.99–1.49, p trend = 0.07; TV viewing at 5–10 years: 1.16, 95% CI 0.91–1.49, p trend = 0.09). The present study suggests that TV viewing during early childhood increases risk of T2D in adult women; adult BMI explains part of this association. Further research is required to confirm this observation and understand the mediating pathways.

scholarly journals Accumulation of Major Life Events in Childhood and Adult Life and Risk of Type 2 Diabetes Mellitus

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0138654 ◽  
Author(s):  
Jolene Masters Pedersen ◽  
Naja Hulvej Rod ◽  
Ingelise Andersen ◽  
Theis Lange ◽  
Gry Poulsen ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Life Events ◽  
Adult Life ◽  
Major Life Events ◽  
Major Life

scholarly journals Early-life Programming of Type 2 Diabetes Mellitus: Understanding the Association between Epigenetics/Genetics and Environmental Factors

2019 ◽  
Vol 20 (6) ◽  
pp. 453-463 ◽  
Author(s):  
Fatma Z. Kadayifci ◽  
Sage Haggard ◽  
Sookyoung Jeon ◽  
Katie Ranard ◽  
Dandan Tao ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Early Life ◽  
Molecular Mechanisms ◽  
Pancreatic Beta Cell ◽  
Public Health Problem ◽  
Increased Risk

Type 2 Diabetes Mellitus is an increasing public health problem that poses a severe social and economic burden affecting both developed and developing countries. Defects in insulin signaling itself are among the earliest indications that an individual is predisposed to the development of insulin resistance and subsequently Type 2 Diabetes Mellitus. To date, however, the underlying molecular mechanisms which result in resistance to the actions of insulin are poorly understood. Furthermore, it has been shown that maternal obesity is associated with an increased risk of obesity and insulin resistance in the offspring. However, the genetic and/or epigenetic modifications within insulin-sensitive tissues such as the liver and skeletal muscle, which contribute to the insulin-resistant phenotype, still remain unknown. More importantly, a lack of in-depth understanding of how the early life environment can have long-lasting effects on health and increased risk of Type 2 Diabetes Mellitus in adulthood poses a major limitation to such efforts. The focus of the current review is thus to discuss recent experimental and human evidence of an epigenetic component associated with components of nutritional programming of Type 2 Diabetes Mellitus, including altered feeding behavior, adipose tissue, and pancreatic beta-cell dysfunction, and transgenerational risk transmission.

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