Editors' ChoiceDiabetes

Cutting Calories Is Not Always Best

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Science Translational Medicine  17 Nov 2010:
Vol. 2, Issue 58, pp. 58ec178
DOI: 10.1126/scitranslmed.3001910

Impaired function of pancreatic β cells contributes to the development of glucose intolerance and type 2 diabetes. Intrauterine growth restriction due to prenatal malnutrition or an abnormal placenta has been shown to adversely affect β cell development and lead to type 2 diabetes in humans and rats. However, the mechanism underlying this process has not been fully elucidated. Matveyenko et al. propose that reduced formation of pancreatic β cells at birth may promote type 2 diabetes in later life. They sought to investigate this hypothesis in a rat model of intrauterine growth restriction due to prenatal malnutrition.

The investigators examined several aspects of β cell development. They studied early postnatal malnutrition because there is a rapid turnover of β cells during this period. They also compared the effects of prenatal and postnatal malnutrition on β cell formation, proliferation, and cell death. Additionally, they compared the effects of prenatal and postnatal malnutrition on male and female rat offspring, because most nutrient restriction studies have only examined male animals. For prenatal studies, pregnant rats were given a diet that was either 50% calorie-restricted or unrestricted. For postnatal studies, the calorie-restricted or unrestricted diets were maintained during lactation. The authors then analyzed the four groups of rat offspring: control rats exposed to unrestricted diets prenatally and postnatally, rats exposed only to prenatal calorie restriction, rats exposed only to postnatal calorie restriction, and rats exposed to both prenatal and postnatal calorie restriction. They found that prenatal but not postnatal calorie restriction decreased β cell formation and proliferation rate, but not the rate of cell death. Most significantly, the combination of prenatal and postnatal calorie restriction resulted in an 80% reduction in β cell mass compared to control rats. Notably, findings were similar in male and female rat offspring.

This study is a rigorous examination of how pancreatic β cell formation is perturbed by prenatal and postnatal calorie restriction in rats. These findings provide insight into the possible fetal origin of susceptibility to type 2 diabetes and may guide further investigation in humans.

A. V. Matveyenko et al., Differential effects of prenatal and postnatal nutritional environment on β-cell mass development and turnover in male and female rats. Endocrinology, 3 November 2010 (10.1210/en.2010-0978). [Abstract]

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