Long-term cardiovascular risk in relation to birth weight and exposure to maternal diabetes mellitus

Stuart, Andrea; Amer‐Wåhlin, Isis; Persson, Jonas; Källén, Karin

doi:10.1016/j.ijcard.2013.03.032

Cited by 37 publications

(35 citation statements)

References 33 publications

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“…Current study observed that diabetic mother offspring developed glucose intolerance, which is consistent with previous studies reporting increased prevalence of glucose intolerance or diabetes . Interestingly, a registry study demonstrated that the increased risk for cardiovascular disease (defined as consumption of cardiovascular medication) in adult individuals born to diabetic mothers was significantly reduced when the offspring with diabetes were excluded . These evidences suggest that glycemic dysregulation in diabetic mother offspring might contribute to the myocardial ischemic intolerance and increased cardiovascular risk.…”

Section: Discussionsupporting

confidence: 91%

The impaired myocardial ischemic tolerance in adult offspring of diabetic pregnancy is restored by maternal melatonin treatment

Gao

Zhao

Liu

et al. 2016

Journal of Pineal Research

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Diabetic pregnancy, with ever increasing prevalence, adversely affects embryogenesis and increases vasculometabolic disorder risks in adult offspring. However, it remains poorly understood whether maternal diabetes increases the offspring's susceptibility to heart injuries in adulthood. In this study, we observed that cardiac function and structure were comparable between adult offspring born to diabetic mice and their counterparts born to nondiabetic mice at baseline. However, in response to myocardial ischemia/reperfusion (MIR), diabetic mother offspring exhibited augmented infarct size, cardiac dysfunction, and myocardial apoptosis compared with control, in association with exaggerated activation of mitochondria- and endoplasmic reticulum (ER) stress-mediated apoptosis pathways and oxidative stress. Molecular analysis showed that the impaired myocardial ischemic tolerance in diabetic mother offspring was mainly attributable to blunted cardiac insulin receptor substrate (IRS)-1/Akt signaling. Furthermore, the effect of maternal melatonin administration on offspring's response to MIR was determined, and the results indicated that melatonin treatment in diabetic dams during pregnancy significantly improved the tolerance to MIR injury in their offspring, via restoring cardiac IRS-1/Akt signaling. Taken together, these data suggest that maternal diabetes predisposes offspring to augmented MIR injury in adulthood, and maternal melatonin supplementation during diabetic pregnancy may hold promise for improving myocardial ischemic tolerance in the offspring.

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Section: Discussionsupporting

confidence: 91%

The impaired myocardial ischemic tolerance in adult offspring of diabetic pregnancy is restored by maternal melatonin treatment

Gao

Zhao

Liu

et al. 2016

Journal of Pineal Research

View full text Add to dashboard Cite

show abstract

“…A large Danish study of women with DM confirmed that as adults the offspring was at increased risk for CVD (adjusted OR 1.46; 95% CI 1.16–1.83) and for insulin-dependent DM (adjusted OR 4.7; 95% CI 3.9–5.8) compared to offspring of non-diabetic mothers. CVD was associated with FGR rather than macrosomia (OR 1.29; 95% CI 1.24–1.35) (173). Accordingly, undernutrion during pregnancy was linked to decreased glucose tolerance up to age 58 (62) (Table 2).…”

Section: Resultsmentioning

confidence: 99%

Pregnancy: An Underutilized Window of Opportunity to Improve Long-term Maternal and Infant Health—An Appeal for Continuous Family Care and Interdisciplinary Communication

2017

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Physiologic adaptations during pregnancy unmask a woman’s predisposition to diseases. Complications are increasingly predicted by first-trimester algorithms, amplify a pre-existing maternal phenotype and accelerate risks for chronic diseases in the offspring up to adulthood (Barker hypothesis). Recent evidence suggests that vice versa, pregnancy diseases also indicate maternal and even grandparent’s risks for chronic diseases (reverse Barker hypothesis). Pub-Med and Embase were reviewed for Mesh terms “fetal programming” and “pregnancy complications combined with maternal disease” until January 2017. Studies linking pregnancy complications to future cardiovascular, metabolic, and thrombotic risks for mother and offspring were reviewed. Women with a history of miscarriage, fetal growth restriction, preeclampsia, preterm delivery, obesity, excessive gestational weight gain, gestational diabetes, subfertility, and thrombophilia more frequently demonstrate with echocardiographic abnormalities, higher fasting insulin, deviating lipids or clotting factors and show defective endothelial function. Thrombophilia hints to thrombotic risks in later life. Pregnancy abnormalities correlate with future cardiovascular and metabolic complications and earlier mortality. Conversely, women with a normal pregnancy have lower rates of subsequent diseases than the general female population creating the term: “Pregnancy as a window for future health.” Although the placenta works as a gatekeeper, many pregnancy complications may lead to sickness and earlier death in later life when the child becomes an adult. The epigenetic mechanisms and the mismatch between pre- and postnatal life have created the term “fetal origin of adult disease.” Up to now, the impact of cardiovascular, metabolic, or thrombotic risk profiles has been investigated separately for mother and child. In this manuscript, we strive to illustrate the consequences for both, fetus and mother within a cohesive perspective and thus try to demonstrate the complex interrelationship of genetics and epigenetics for long-term health of societies and future generations. Maternal–fetal medicine specialists should have a key role in the prevention of non-communicable diseases by implementing a framework for patient consultation and interdisciplinary networks. Health-care providers and policy makers should increasingly invest in a stratified primary prevention and follow-up to reduce the increasing number of manifest cardiovascular and metabolic diseases and to prevent waste of health-care resources.

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“…9 Evidence linking excessive fetal growth and a large for gestational age (LGA) birth weight with cardiovascular risk and events is not that well established. [9][10][11][12] Abnormalities in fetal growth are associated with maternal disease and pregnancy disorders, including preeclampsia and diabetes mellitus.…”

Section: See Editorial By Gardiner See Clinical Perspectivementioning

confidence: 99%

Neonatal Arterial Morphology Is Related to Body Size in Abnormal Human Fetal Growth

Olander

Sundholm

Ojala

et al. 2016

Circ: Cardiovascular Imaging

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Background-Restriction in fetal growth is associated with cardiovascular disease in adulthood. It is unclear whether abnormal intrauterine growth influences arterial morphology during the fetal or neonatal stage. The objective was to study the regional arterial morphology with respect to gestational age and abnormal fetal body size. Methods and Results-We studied body anthropometrics and arterial morphology and physiology in 174 neonates born between 31 and 42 weeks of gestation, including neonates with birth weights appropriate, small, and large for age, with very high resolution vascular ultrasound (35-55 MHz). In simple linear regressions, parameters of body size (body weight, body surface area, and organ circumference) and gestational age were statistically significantly associated with common carotid, brachial, femoral arterial parameters (lumen diameter [LD], wall layer thickness [intima-media thickness and intima-media-adventitia thickness], and carotid artery wall stress [CAWS]). Male sex was statistically significantly associated with LD and CAWS. In multiple linear regression models, body size, gestational age, and sex explained a large proportion of the arterial variance (R 2 range, 0.37-0.47 for LD; 0.09-0.35 for intima-media thickness; 0.21-0.41 for intima-media-adventitia thickness; and 0.23 for CAWS; all models P<0.001). Arterial wall layer thickness, LDs, and CAWS were independently and strongly predicted by body size, and no effect of maternal disease was observed when added to the models. Gestational age and male sex were also independently but more weakly associated with arterial LDs and CAWS (P<0.01), but not with arterial wall layers. Conclusions-These results indicate that the intrauterine growth of fetal arterial LD and wall layer thickness are primarily attributed to body growth overall. LD and CAWS show weaker association with gestational age and sex. (Circ Cardiovasc Imaging. 2016;9:e004657.

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Long-term cardiovascular risk in relation to birth weight and exposure to maternal diabetes mellitus

Cited by 37 publications

References 33 publications

The impaired myocardial ischemic tolerance in adult offspring of diabetic pregnancy is restored by maternal melatonin treatment

The impaired myocardial ischemic tolerance in adult offspring of diabetic pregnancy is restored by maternal melatonin treatment

Pregnancy: An Underutilized Window of Opportunity to Improve Long-term Maternal and Infant Health—An Appeal for Continuous Family Care and Interdisciplinary Communication

Neonatal Arterial Morphology Is Related to Body Size in Abnormal Human Fetal Growth

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