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Updated: Jun 8, 2026

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
Published on: February 28, 2013
Developmental programming and diabetes - The human experience and insight from animal models
1King's College London, United Kingdom. lucilla.poston@kcl.ac.uk
Insights
Children born to mothers with diabetes may face higher risks of obesity and diabetes later in life. Maternal factors during pregnancy and early life appear to influence the child's long-term health.
Area of Science:
- Reproductive health
- Pediatric endocrinology
- Metabolic disorders
Background:
- Maternal diabetes, including type 1 DM and type 2 DM, may increase offspring's risk for later-life diabetes and obesity.
- This suggests potential in utero or early postnatal influences on child development.
Purpose of the Study:
- To review existing studies on the hypothesis that maternal diabetes influences offspring's long-term metabolic health.
- To highlight controversies such as confounding factors and maternal BMI influence.
Main Methods:
- Review of existing literature on maternal diabetes and offspring health outcomes.
- Examination of animal models demonstrating effects of maternal hyperglycemia.
- Consideration of prospective study designs.
Main Results:
- Animal studies show maternal hyperglycemia can cause lasting issues in offspring, including pancreatic beta-cell dysfunction, altered insulin signaling, and hypothalamic abnormalities affecting energy regulation and obesity.
- Human studies suggest a correlation between maternal diabetes and offspring susceptibility to metabolic diseases.
Conclusions:
- Maternal diabetes may have transgenerational effects on offspring's susceptibility to diabetes and obesity.
- Further prospective studies, especially those following children from randomized controlled trials (RCTs) of glycemic control in diabetic mothers, are needed to confirm these findings and elucidate mechanisms.
Abstract:
Children born to mothers, rather than to fathers, with type 1 diabetes (type 1 DM) or type 2 diabetes (type 2 DM) may have a greater susceptibility to diabetes and obesity in later life, inferring a role for in utero or early post-natal influences on the developing child. This review summarises the studies contributing to this hypothesis, noting some of the controversies including the potential for residual confounding and the influence of maternal BMI. Animal models demonstrate that maternal hyperglycaemia leads to persistent disorders of offspring pancreatic β cell secretory capacity, abnormal insulin signaling in insulin-sensitive tissues and abnormal development of the hypothalamus, associated with aberrant control of energy regulation and obesity in adult life. Prospective studies, particularly follow-up of children born to diabetic mothers participating in RCTs of improved glycemic control are needed to accurately assess the transgenerational influences of maternal diabetes and to evaluate mechanisms inferred from animal data.
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