Research ReportTemporary prenatal hyperglycemia leads to postnatal neuronal 'glucose-resistance' in the chicken hypothalamus

- Effect of prenatal high glucose on later central nervous glucose-sensing in chicken.
- Hypothalamic neuronal glucose sensitivity becomes decreased in juvenile chicken.
- Gene expression of brain glucose transporters (GLUT1, GLUT3) becomes reduced.
- Data speaks for acquired hypothalamic glucose-resistance through prenatal hyperglycemia.

Prenatal exposures may have a distinct impact for long-term health. Exposure to maternal 'diabesity' during pregnancy increases offspring 'diabesity' risk, e.g. by malprogramming the central nervous regulation of body weight, food intake and metabolism. Critical mechanisms and concrete disrupting factors still remain unclear. Due to the independent development, from the mother, the chicken embryo could provide a valuable model to distinctively establish causal factors.Aim of this study was to determine effects of temporary prenatal hyperglycemia on postnatal hypothalamic neuronal glucose sensitivity in the chicken.To induce hyperglycemia in chicken embryos, 0.5 ml glucose solution (concentration 30 mmol/l) were daily administered via catheter into a vessel of the chorioallantoic egg membrane from days 14 to 17 of incubation. On day 21 of postnatal age, body weight, body fat content, blood glucose, neuroelectrophysiological glucose sensitivity as well as glucose transporter expression were determined in hypothalamic brain slices. No significant changes in morphometric and metabolic parameters were observed. However, strongly decreased neuronal glucose sensitivity and glucose transporter expression occurred, indicating prenatally acquired hypothalamic 'glucose-resistance'. In conclusion, temporary late prenatal hyperglycemia induces lasting changes in central glucose sensing. The prenatally glucose-treated chicken provides a valuable new model for investigating early central nervous origins of 'diabesity' and related disorders.