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[Interaction between environment and genetic background in type 2 diabetes: lessons from animal models]
Catherine Bernard1, Odile Della Zuana, Alain Ktorza
1Division de recherche sur les maladies métaboliques, Institut de recherches Servier, Suresnes, France. catherine.bernard@fr.netgrs.com
Medecine Sciences : M/S
|September 6, 2013
Summary
Genetic background and environmental factors significantly influence type 2 diabetes (T2D) development in obese individuals. Fetal metabolic environment and diet impact islet cell development, contributing to adult-onset diabetes.
Area of Science:
- Endocrinology
- Genetics
- Metabolic Syndrome
Context:
- The interplay between genetic predisposition and environmental factors in type 2 diabetes (T2D) among obese individuals remains unclear.
- Rodent models are utilized to investigate the impact of prolonged high-fat diets on glycemic control across different genetic backgrounds.
- Prenatal exposure to metabolic stress, such as maternal hypocaloric diets, can alter fetal islet cell development, predisposing offspring to diabetes.
Purpose:
- To elucidate the differential effects of genetic background and environmental factors on T2D development.
- To understand how fetal metabolic derangements contribute to adult-onset diabetes.
- To explore the concept of "nutritional genetics" in the context of T2D.
Summary:
- Rodent studies reveal that genetic background dictates sensitivity to high-fat diets, influencing obesity and diabetes onset.
- Prenatal nutritional insults can lead to altered islet cell development and function, increasing diabetes risk in adulthood.
- Beta-cell dysfunction in response to insulin resistance is a key factor in T2D pathogenesis, highlighting the role of "nutritional genetics".
Impact:
- Provides insights into the complex etiology of type 2 diabetes, integrating genetic and environmental influences.
- Suggests potential targets for early intervention by modifying the prenatal metabolic environment.
- Advances the understanding of "nutritional genetics" and its implications for metabolic disease prevention and treatment.
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