Programming of Diabetes: Experimental Models
نویسندگان
چکیده
The mechanism by which fetal malnutrition increases the risk for glucose intolerance and type 2 diabetes is not well understood. Besides the insulin resistance that has been proposed to develop as a consequence of the lack of nutrient availability during early life, a primary insult in b-cell development has also been observed. Fetal malnutrition would lead to inappropriate b-cell ontogeny, resulting in a population of b-cells that does not cope adequately with metabolic or oxidative stress later in life. Since, obviously, this hypothesis can not be verified in humans, various animal models have been established. The time course of development is different from one species to another. For instance, humans and guinea-pigs are born more mature than rats or mice. The same is true at the level of the endocrine pancreas. In humans, the initial formation of the endocrine cells in the pancreas occurs at 10 weeks’ gestation (Bouwens et al., 1997). In the guinea-pig, islet formation and remodelling also begin at an early stage of gestation and continue for a longer time after birth. In rodents, the islets develop relatively late in gestation and undergo a remodelling 2 weeks after birth. This means that the critical window for islet development is narrower in rodents than in other species. This could be an advantage for the identification of mechanisms involved when the consequences of nutritional or other experimental manipulations are analysed. However, results from such studies should be viewed with caution until confirmed in other species, before extrapolating them to humans
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