Editors' ChoicePrenatal Determinants of Adult Obesity

You Are What She Ate

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Science Translational Medicine  21 Apr 2010:
Vol. 2, Issue 28, pp. 28ec63
DOI: 10.1126/scitranslmed.3001164

Childhood obesity is at epidemic levels, and researchers are trying to elucidate the factors that contribute to this problem. A better understanding of the prenatal determinants of postnatal disease could help. One question is how intrauterine growth restriction—that is, being small before birth—can promote obesity in later life. Sutton et al. have set out to investigate this question.

The authors took advantage of a mouse model to examine how limitations on the dietary protein consumed by the mother could alter her offspring’s metabolism. They used C57BL/6 mice because these are most commonly used in diet and obesity studies. Male and female offspring of undernourished (6% protein) and adequately nourished (20% protein with or without 60% high fat) pregnant mice were compared by evaluating insulin resistance and lipid profiles at 8 and 20 weeks after birth. The offspring’s wheel-running activity, food intake, and energy expenditure were also measured at 8 weeks of age. Sutton et al. observed that the pregnant mice exposed to the low-protein diet had offspring with intrauterine growth retardation. These mice grew after birth to catch up to their normal-weight cousins but, in response to a high-fat diet as adults, they gained more weight and had more fat tissue. The prenatally undernourished offspring exhibited increased feeding during the lights-on (normal sleep) period and decreased physical activity during the lights-off (normal wake) period, suggesting that their biological clock was also dysfunctional.

These findings highlight that protein malnutrition during pregnancy increases the offspring’s risk of metabolic and behavioral abnormalities that lead to adult obesity and diabetes—changes that may reflect alterations in the biological clock.

G. M. Sutton et al., Protein malnutrition during pregnancy in C57BL/6J mice results in offspring with altered circadian physiology before obesity. Endocrinology 151, 1385–1386 (2010). [Abstract]

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