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Perinatal hyperinsulinism as possible predisposing factor for diabetes mellitus, obesity and enhanced cardiovascular
1Bereich Charité der Humboldt-Universität, Institut für Experimentelle Endokrinologie, Berlin, Germany.
Insights
Maternal metabolic health during pregnancy, including gestational diabetes, influences offspring
Area of Science:
- Metabolic Health
- Developmental Biology
- Epidemiology
Background:
- The intrauterine and neonatal metabolic environment can act as teratogenic determinants for chronic diseases.
- Gestational diabetes and impaired glucose tolerance during pregnancy are linked to increased diabetes susceptibility in offspring.
Purpose of the Study:
- To discuss the role of the intrauterine and neonatal metabolic environment in disease predisposition.
- To explore the mechanisms linking maternal metabolic status to offspring's lifelong health.
- To investigate potential preventative strategies for diabetes, obesity, and cardiovascular diseases.
Main Methods:
- Review of epidemiological, clinical, and experimental findings.
- Analysis of the impact of prenatal and perinatal nutrition on metabolic programming.
- Discussion of fetal/neonatal hyperinsulinism and its effects on hypothalamic regulation.
Main Results:
- Gestational diabetes and impaired glucose tolerance increase offspring's risk for Type I and Type II diabetes.
- Prenatal undernutrition may predispose to Type II diabetes, while perinatal overnutrition may increase Type I diabetes susceptibility.
- Fetal/neonatal hyperinsulinism can lead to malprogramming of metabolic regulatory centers, enhancing lifelong diabetes susceptibility.
Conclusions:
- Epigenetic, maternofetal transmission of acquired metabolic modifications may occur across generations.
- Prevention of gestational diabetes, prenatal undernutrition, and perinatal overnutrition can offer partial prophylaxis.
- Optimizing the maternal metabolic environment is crucial for preventing chronic diseases in offspring.
Abstract:
The importance of the intrauterine and neonatal metabolic environment as possible teratogenic determinants of predispositions to diabetes, obesity and cardiovascular diseases is discussed. Epidemiological, clinical and experimental results suggest that gestational diabetes or even slightly impaired glucose tolerance during pregnancy are important risk factors for the development of an increased Type II- and even Type I diabetes susceptibility in the offspring. In addition, early prenatal undernutrition might also predispose to enhanced risk of Type II diabetes, whereas perinatal overnutrition seems to enhance predominantly Type I diabetes susceptibility. In this context, fetal and/or neonatal hyperinsulinism occurring during a critical period of brain development and leading to permanent malorganization of hypothalamic regulation centres for metabolism and hence to malprogramming of the hypothalamo-pancreatic system, is discussed as a possible reason for lifelong enhanced diabetes susceptibility. In view of epidemiological and experimental findings, an epigenetic maternofetal transmission of such acquired persistent modifications can run over several generations, mediated by gestational hyperglycaemia and fetal or neonatal hyperinsulinism. In conclusion, a partial prophylaxis of diabetes mellitus, obesity and cardiovascular diseases appears to be possible by prevention of gestational diabetes--even mild forms of impaired glucose tolerance during pregnancy--as well as early prenatal undernutrition and perinatal overnutrition.