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Modeling intrauterine growth retardation in rodents: Impact on pancreas development and glucose homeostasis
V M Schwitzgebel1, E Somm, P Klee
1Department of Pediatrics, Geneva University Hospitals, Switzerland. Valerie.Schwitzgebel@hcuge.ch
Insights
Adverse fetal environments cause poor fetal growth (IUGR), increasing risks for infant mortality and adult metabolic diseases. This review explores molecular mechanisms behind impaired pancreatic islet development in IUGR models.
Area of Science:
- Developmental biology
- Endocrinology
- Perinatal medicine
Background:
- Adverse fetal environments (e.g., poor nutrition, placental insufficiency, stress) disrupt organ development, leading to intrauterine growth retardation (IUGR).
- IUGR is linked to higher risks of perinatal complications and adult metabolic disorders like obesity, diabetes, and hypertension.
- Experimental IUGR models in rodents reveal reduced beta cell mass and insulin content in the pancreas.
Purpose of the Study:
- To review molecular mechanisms underlying pancreatic islet development in IUGR.
- To understand how fetal insults impact beta cell development and function.
- To provide insights into the consequences of IUGR on long-term health.
Main Methods:
- Review of existing literature on IUGR models and pancreatic islet development.
- Analysis of molecular determinants affecting fetal and postnatal islet growth.
- Examination of rodent models including caloric restriction, protein restriction, glucocorticoid exposure, and placental blood supply restriction.
Main Results:
- IUGR models consistently demonstrate decreased beta cell mass.
- Pancreatic insulin content is significantly lower in experimental IUGR.
- Recent research is elucidating the molecular pathways responsible for beta cell loss in IUGR.
Conclusions:
- Understanding the molecular basis of islet development is crucial for addressing IUGR consequences.
- Fetal adverse environments have lasting impacts on pancreatic beta cell development.
- Further research into these mechanisms can inform strategies to mitigate IUGR-related health risks.
Abstract:
Fetal adverse environment, such as insufficient maternal nutrition, placental insufficiency and stress, alters organ development and leads to poor fetal growth, also called intrauterine growth retardation (IUGR). IUGR is associated with an increased risk of perinatal mortality and morbidity as well as late-onset metabolic diseases, such as obesity, diabetes and hypertension in adulthood. In the rodent model, IUGR can be induced by fetal caloric restriction, fetal protein restriction, by exposure to high levels of glucocorticoids or by restricted placental blood supply. Such experimental IUGR models show a decreased beta cell mass and lower pancreatic insulin content. Recent research has provided an insight into the mechanisms responsible for the loss of beta cells. Here we review models that give further details about the molecular determinants of fetal and postnatal pancreatic islet development that are required to understand the consequences of fetal insults.
