The effects of prenatal exposure to undernutrition on glucose and insulin metabolism in later life

2006 ◽  
Vol 13 (6) ◽  
pp. 530-535
Author(s):  
Susanne R de Rooij ◽  
Rebecca C Painter ◽  
Tessa J Roseboom
Keyword(s):  
Prenatal Exposure ◽  
Later Life ◽  
Insulin Metabolism

scholarly journals Prenatal exposure to different diets influences programming of glucose and insulin metabolism in dairy ewes

2020 ◽  
Vol 103 (10) ◽  
pp. 8853-8863
Author(s):  
M.F. Lunesu ◽  
A. Ledda ◽  
F. Correddu ◽  
F. Fancello ◽  
A. Marzano ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Insulin Metabolism ◽  
Dairy Ewes

scholarly journals Prenatal Malnutrition-Induced Epigenetic Dysregulation as a Risk Factor for Type 2 Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Alexander Vaiserman ◽  
Oleh Lushchak
Keyword(s):  
Type 2 Diabetes ◽  
Critical Role ◽  
Regulation Of Gene Expression ◽  
Epidemiological Data ◽  
Later Life ◽  
Causal Link ◽  
Related Factors ◽  
Insulin Metabolism ◽  
Prenatal Malnutrition

Type 2 diabetes (T2D) is commonly regarded as a disease originating from lifestyle-related factors and typically occurring after the age of 40. There is, however, consistent experimental and epidemiological data evidencing that the risk for developing T2D may largely depend on conditions early in life. In particular, intrauterine growth restriction (IUGR) induced by poor or unbalanced nutrient intake can impair fetal growth and also cause fetal adipose tissue and pancreatic β-cell dysfunction. On account of these processes, persisting adaptive changes can occur in the glucose-insulin metabolism. These changes can include reduced ability for insulin secretion and insulin resistance, and they may result in an improved capacity to store fat, thereby predisposing to the development of T2D and obesity in adulthood. Accumulating research findings indicate that epigenetic regulation of gene expression plays a critical role in linking prenatal malnutrition to the risk of later-life metabolic disorders including T2D. In animal models of IUGR, changes in both DNA methylation and expression levels of key metabolic genes were repeatedly found which persisted until adulthood. The causal link between epigenetic disturbances during development and the risk for T2D was also confirmed in several human studies. In this review, the conceptual models and empirical data are summarized and discussed regarding the contribution of epigenetic mechanisms in developmental nutritional programming of T2D.

Transgenerational effects of prenatal exposure to the Dutch famine on neonatal adiposity and health in later life

2008 ◽  
Vol 115 (10) ◽  
pp. 1243-1249 ◽  
Author(s):  
RC Painter ◽  
C Osmond ◽  
P Gluckman ◽  
M Hanson ◽  
DIW Phillips ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Later Life ◽  
Transgenerational Effects ◽  
Neonatal Adiposity

The risk of stroke after prenatal exposure to famine

2017 ◽  
Vol 8 (6) ◽  
pp. 658-664 ◽  
Author(s):  
J. Horenblas ◽  
S. R. de Rooij ◽  
T. J. Roseboom
Keyword(s):  
Prenatal Exposure ◽  
Hazard Analysis ◽  
Later Life ◽  
Major Effect ◽  
Late Gestation ◽  
Adult Age ◽  
Fatal Stroke ◽  
Hazard Ratios ◽  
Increased Risk ◽  
Significant Difference

Prenatal exposure to famine is associated with an increased risk of metabolic and cardiovascular diseases in the offspring at adult age. The aim of this study was to assess whether prenatal exposure to undernutrition increases the risk of stroke. This study was performed in the Dutch famine birth cohort, which consist of 2414 members who were born between 1943 and 1947 in the Netherlands. In a subsample of 1177 individuals, interviews were conducted using standardized questionnaires to obtain information about medical history (which included specific questions regarding stroke) and lifestyle. Information on stroke-related mortality was collected by linking the cohort with Statistics Netherlands. A Cox’s proportional hazard analysis was performed to calculate hazard ratios (HRs) comparing the incidence of non-fatal stroke between participants who were exposed, subdivided into early, mid and late gestation, and unexposed to famine prenatally. Three cohort members died of stroke. Of the 1177 subjects who responded to the questionnaires 49 (4.2%) survived a stroke. Unadjusted and adjusted HRs for the risk of non-fatal stroke did not show a significant difference between the unexposed and exposed subjects: HR 1.23 (95% CI 0.53–2.83), HR 1.23 (95% CI 0.53–2.82), HR 1.12 (95% CI 0.46–2.71) for those exposed in late, mid and early gestation, respectively. We were unable to find evidence for a major effect of prenatal exposure to famine on the risk of stroke in later life, although one should be aware that this study was underpowered and the study population too selected and young to identify smaller risks.

Prenatal exposure to wartime stress – long-term effect on coronary heart disease in later life

2010 ◽  
Vol 43 (7) ◽  
pp. 555-561 ◽  
Author(s):  
Nadja K. Schreier ◽  
Elena V. Moltchanova ◽  
Paul A. Blomstedt ◽  
Eero Kajantie ◽  
Johan G. Eriksson
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Prenatal Exposure ◽  
Later Life ◽  
Term Effect ◽  
Long Term Effect

Effect of Prenatal Exposure to Bisphenols on Newborn Leucocyte Telomere Length: A Prospective Birth Cohort Study in China

2021 ◽  
Author(s):  
Jun Liang ◽  
Yantao Shao ◽  
Dongping Huang ◽  
Chunxiu Yang ◽  
Tao Liu ◽  
...  
Keyword(s):  
Cord Blood ◽  
Telomere Length ◽  
Birth Cohort ◽  
Prenatal Exposure ◽  
Positive Association ◽  
Fold Increase ◽  
Later Life ◽  
Maternal Serum ◽  
Birth Cohort Study ◽  
Bisphenol S

Abstract Telomere length (TL) at birth is related to future diseases and long-term health. Bisphenols exhibit toxic effects and can cross the placenta barrier. However, the effect of prenatal exposure to bisphenols on newborn TL remains unknown. We aimed to explore the effects of prenatal exposure to bisphenols (i.e., bisphenol A (BPA), bisphenol B (BPB), bisphenol F (BPF), bisphenol S (BPS), and tetrabromobisphenol A (TBBPA)) on relative TL in newborns. A total of 801 mother–infant pairs were extracted from the Guangxi Zhuang Birth Cohort (GZBC). The relationships between bisphenol levels in maternal serum and relative TL in cord blood were examined by generalized linear models and restricted cubic spline (RCS) models. After adjusting for confounders, we observed a 3.19% (95% CI: -6.08%, -0.21%) reduction in relative cord blood TL among mothers ≥ 28 years with each 1-fold increase of BPS. However, each 1-fold increase of TBBPA, a 3.31% (95% CI: 0.67%, 6.01%) increased in relative cord blood TL among mothers < 28 years. The adjusted RCS models also revealed similar results (P overall < 0.05, P non-linear > 0.05). This is the first study to show a positive association between serum TBBPA levels and newborn relative TL among younger mothers. However, BPS levels were inversely correlated with TL in fetus born to older mothers. The results suggest fetuses of older pregnant women are more sensitivity to BPS exposure and accelerated aging or BPS-related diseases in later life may stem from early-life exposure.

Prenatal exposure to famine and health in later life

The Lancet ◽  
1998 ◽  
Vol 351 (9112) ◽  
pp. 1361 ◽  
Author(s):  
Kaare Christensen ◽  
James W Vaupel
Keyword(s):  
Prenatal Exposure ◽  
Later Life

Prenatal exposure to the Dutch famine and disease in later life: An overview

2005 ◽  
Vol 20 (3) ◽  
pp. 345-352 ◽  
Author(s):  
Rebecca C. Painter ◽  
Tessa J. Roseboom ◽  
Otto P. Bleker
Keyword(s):  
Prenatal Exposure ◽  
Later Life

Prenatal exposure to famine and health in later life

The Lancet ◽  
1998 ◽  
Vol 351 (9112) ◽  
pp. 1361-1362 ◽  
Author(s):  
John S Yudkin ◽  
Sara Stanner
Keyword(s):  
Prenatal Exposure ◽  
Later Life
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