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Tarry-Adkins J.L.,University of Cambridge Metabolic Research Laboratories | Fernandez-Twinn D.S.,University of Cambridge Metabolic Research Laboratories | Madsen R.,University of Cambridge Metabolic Research Laboratories | Chen J.-H.,University of Cambridge Metabolic Research Laboratories | And 4 more authors.
Endocrinology | Year: 2015

Lowbirth weight and rapid postnatal growth increases the risk of developing insulin resistance and type 2 diabetes in later life. However, underlying mechanisms and potential intervention strategies are poorly defined. Here we demonstrate that male Wistar rats exposed to a low-protein diet in utero that had a low birth weight but then underwent postnatal catch-up growth (recuperated offspring) had reductions in the insulin signaling proteins p110-β (13%±6%of controls [P<.001]) and insulin receptor substrate-1 (39%±10% of controls [P<.05]) in adipose tissue. These changes were not accompanied by any change in expression of the corresponding mRNAs, suggesting posttranscriptional regulation. Recuperated animals displayed evidence of a proinflammatory phenotype of their adipose tissue with increased IL-6 (139%±8%[P<.05]) and IL1-β (154%±16% [P < .05]) that may contribute to the insulin signaling protein dysregulation. Postweaning dietary supplementation of recuperated animals with coenzyme Q (CoQ10) (1 mg/kg of body weight per day) prevented the programmed reduction in insulin receptor substrate-1 and p110- and the programmed increased in IL-6. These findings suggest that postweaning CoQ10 supplementation has antiinflammatory properties and can prevent programmed changes in insulin-signaling protein expression. We conclude that CoQ10 supplementation represents an attractive intervention strategy to prevent the development of insulin resistance that results from suboptimal in utero nutrition. © 2015 by the Endocrine Society.

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