Abstract
BackgroundPrenatal exposures may have a distinct impact for long-term health, one example being exposure to maternal ‘diabesity’ during pregnancy increasing offspring ‘diabesity’ risk. Malprogramming of the central nervous regulation of body weight, food intake and metabolism has been identified as a critical mechanism. While concrete disrupting factors still remain unclear, growing focus on acquired epigenomic alterations have been proposed. Due to the independent development from the mother, the chicken embryo provides a valuable model to distinctively establish causal factors and mechanisms.AimThe aim of this study was to determine the effects of prenatal hyperglycemia on postnatal hypothalamic gene expression and promoter DNA methylation in the chicken.Methods and FindingsTo temporarily induce high-glucose exposure in chicken embryos, 0.5 ml glucose solution (30 mmol/l) were administered daily via catheter into a vessel of the chorioallantoic egg membrane from days 14 to 17 of incubation. At three weeks of postnatal age, body weight, total body fat, blood glucose, mRNA expression (INSR, LEPR, GLUT1, GLUT3) as well as corresponding promoter DNA methylation were determined in mediobasal hypothalamic brain slices (Nucleus infundibuli hypothalami). Although no significant changes in morphometric and metabolic parameters were detected, strongly decreased mRNA expression occurred in all candidate genes. Surprisingly, however, no relevant alterations were observed in respective promoter methylation.ConclusionPrenatal hyperglycemia induces strong changes in later hypothalamic expression of INSR, LEPR, GLUT1, and GLUT3 mRNA. While the chicken provides an interesting approach for developmental malprogramming, the classical expression regulation via promoter methylation was not observed here. This may be due to alternative/interacting brain mechanisms or the thus far under-explored bird epigenome.
Highlights
Overweight and obesity are continuously increasing in epidemic-like proportions as are the downstream health risks associated with developing diabetes and alterations typical for the Metabolic Syndrome [1, 2]
Body weight was measured at different time points of postnatal development and no significant differences were seen between groups during the entire observational period (Table 2)
No difference was observed in total body fat content at day 21 between the NaCl-treated control group and the prenatally glucose-treated group (Table 2)
Summary
Overweight and obesity are continuously increasing in epidemic-like proportions as are the downstream health risks associated with developing diabetes and alterations typical for the Metabolic Syndrome [1, 2]. Hyperglycemia (e.g. through gestational diabetes) may cause long-lasting malprogramming of the central nervous regulation of body weight, food intake and metabolism, resulting in an increased ‘diabesity’ risk [5, 6]. Because of its nearly ‘unaffected’ embryonic development, independently from the mother, the chicken provides an excellent model for investigations of pre- and perinatal developmental processes [7,8,9]. It allows highly standardized and controlled manipulations of pre- and perinatal environmental factors during distinct time windows of embryonic development. Due to the independent development from the mother, the chicken embryo provides a valuable model to distinctively establish causal factors and mechanisms
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