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Programming of central and peripheral insulin resistance by low birthweight and postnatal catch-up growth in male mice – published online 24/07/2018

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by Lindsey M. Berends, Laura Dearden, Yi Chun L. Tung, Peter Voshol, Denise S. Fernandez-Twinn, Susan E. Ozanne

Low birthweight followed by accelerated postnatal growth is associated with increased risk of type 2 diabetes. It is well established that this is, at least in part, due to programmed peripheral insulin resistance. However, it is unclear if a suboptimal early-life environment also programs central insulin resistance. In this issue, Berends, Dearden et al ( use a mouse model of diet-induced intra-uterine growth restriction (IUGR) followed by accelerated postnatal catch-up growth to show that a suboptimal early-life environment causes insulin to be less effective at signalling to the brain to reduce food intake in later life. Central insulin resistance in IUGR followed by accelerated postnatal growth was shown to be related to altered expression of insulin-signalling components in the brain, as compared with control offspring born to dams fed a control diet. These findings indicate that promoting accelerated growth in offspring born small for gestational age could have negative effects on long-term metabolic health and that central insulin resistance may contribute to this phenomenon. If extrapolated to humans, these findings also suggest that individuals exposed to a suboptimal early-life environment may be less responsive to both lifestyle and pharmaceutical interventions for metabolic improvements in type 2 diabetes

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