Prevalence of diabetes and obesity in association with prematurity and growth restriction
Gretchen Kopec1, Prem S Shekhawat1, Maroun J Mhanna1
1Department of Pediatrics, MetroHealth Medical Centre, Case Western Reserve University, Cleveland, OH, USA.
Insights
Intrauterine growth restriction (IUGR) can epigenetically alter fetal metabolism, potentially leading to lifelong insulin resistance and metabolic syndrome. Early maternal health interventions may improve long-term population health outcomes.
Area of Science:
- Developmental biology
- Metabolic disorders
- Epigenetics
Background:
- Intrauterine growth restriction (IUGR) occurs when fetuses do not achieve their genetically determined growth potential due to suboptimal intrauterine environments.
- IUGR is linked to epigenetic modifications that can program an infant's metabolism, potentially impacting long-term health.
- The precise association between IUGR/prematurity and later-life metabolic derangements like insulin resistance, obesity, and hypertension is still debated.
Purpose of the Study:
- To explore the link between intrauterine growth restriction and the development of metabolic syndrome.
- To understand the epigenetic mechanisms connecting IUGR to long-term metabolic health.
- To highlight the potential impact of early interventions on population health.
Main Methods:
- Review of existing literature on IUGR, epigenetics, and metabolic syndrome.
- Analysis of studies investigating the long-term health consequences of impaired fetal growth.
- Examination of the role of insulin-like growth factor-1 (IGF-1) in IUGR-related metabolic changes.
Main Results:
- IUGR fetuses experience epigenetic changes affecting metabolism, including altered insulin-like growth factor-1 (IGF-1) levels.
- These epigenetic changes can predispose individuals to insulin resistance, a key component of metabolic syndrome.
- Metabolic syndrome encompasses conditions such as type 2 diabetes, cardiovascular disease, hypertension, dyslipidemia, and inflammation.
Conclusions:
- While the link between IUGR and long-term metabolic syndrome requires further clarification, evidence suggests a significant association.
- Epigenetic programming during fetal development may establish a metabolic vulnerability that persists throughout life.
- Targeting maternal health during pregnancy represents a crucial strategy for preventing future metabolic derangements and ensuring public health.
Abstract:
Intrauterine growth restriction (IUGR) is when fetuses and newborn infants have not reached their true growth potential as genetically defined. Fetuses with IUGR develop in a less than ideal environment that leads to epigenetic changes and marks infants' metabolism for the rest of their lives. Epigenetic changes affect insulin-like growth factor-1 (IGF-1) levels and lead to insulin resistance and ultimately to a metabolic syndrome. The metabolic syndrome is a constellation of illnesses that raise one's risk for type 2 diabetes mellitus, coronary artery disease, and ischemic heart disease, including hypertension, dyslipidemia, central obesity, insulin resistance, and inflammation. The association between IUGR or prematurity and long-term insulin resistance, obesity, hypertension, and metabolic syndrome remains unclear. While studies have shown an association, others have not supported such association. If alteration of intrauterine growth can ultimately lead to the development of metabolic derangements in childhood and adulthood, and if such association is true, then early interventions targeting the health of pregnant women will ensure the health of the population to follow.
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