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Background  Intrauterine environment plays a pivotal role in the origin of fatal diseases such as the metabolic syndrome. Diabetes is associated with low-grade inflammatory state and dysregulated adipokines production. The aim of this study is to investigate the effect of maternal diabetes on adipocytokines (adiponectin, leptin and TNF-α) production in F1 offspring in rats.    Methods  The offspring groups were as follows: F1 offspring of control mothers under control diet (CD) ( CF1-CD ), F1 offspring of control mothers under high caloric diet (HCD) ( CF1-HCD ), F1 offspring of diabetic mothers under CD ( DF1-CD ), and F1 offspring of diabetic mothers under HCD ( DF1-HCD ). Every 5 weeks post-natal, 10 pups of each subgroup were culled to obtain blood samples for biochemical analysis.    Results  The results indicate that DF1-CD and DF1-HCD groups exhibited hyperinsulinemia, dyslipidemia, insulin resistance and impaired glucose homeostasis compared to CF1-CD ( p > 0.05 ). DF1-CD and DF1-HCD groups had high hepatic and muscular depositions of TGs. The significant elevated NEFA level only appeared in offspring of diabetic mothers that was fed HCD. DF1-CD and DF1-HCD groups demonstrated low serum levels of adiponectin, high levels of leptin, and elevated levels of TNF-α compared to CF1-CD ( p > 0.05 ). These results reveal the disturbed metabolic lipid profile of offspring of diabetic mothers and could guide further characterization of the mechanisms involved.    Conclusion  Dysregulated adipocytokines production could be a possible mechanism for the transgenerational transmittance of diabetes, especially following a postnatal diabetogenic environment. Moreover, the exacerbating effects of postnatal HCD on NEFA in rats might be prone to adipcytokine dysregulation. Furthermore, dysregulation of serum adipokines is a prevalent consequence of maternal diabetes and could guide further investigations to predict the development of metabolic disturbances.

Intrauterine diabetic milieu instigates dysregulated adipocytokines production in F1 offspring