title: Temporary prenatal hyperglycemia leads to postnatal neuronal 'glucose-resistance' in the chicken hypothalamus.
abstract: 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.
authors.affiliation: Humboldt-University of Berlin, Institute of Biology, Berlin, Germany.
authors.forename: Barbara
authors.initials: B
authors.lastname: Tzschentke
authors.affiliation: Humboldt-University of Berlin, Institute of Biology, Berlin, Germany.
authors.forename: Semjon
authors.initials: S
authors.lastname: Bogatyrev
authors.affiliation: Clinic of Obstetrics, Division of 'Experimental Obstetrics', Charité - University Medicine Berlin, Campus Virchow-Klinikum, Berlin, Germany.
authors.forename: Karen
authors.initials: K
authors.lastname: Schellong
authors.affiliation: Clinic of Obstetrics, Division of 'Experimental Obstetrics', Charité - University Medicine Berlin, Campus Virchow-Klinikum, Berlin, Germany.
authors.forename: Rebecca C
authors.initials: RC
authors.lastname: Rancourt
authors.affiliation: Clinic of Obstetrics, Division of 'Experimental Obstetrics', Charité - University Medicine Berlin, Campus Virchow-Klinikum, Berlin, Germany. Electronic address: andreas.plagemann@charite.de.
authors.forename: Andreas
authors.initials: A
authors.lastname: Plagemann
mesh_terms: D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose; D001823:Body Composition / Q000502:physiology; D001835:Body Weight; D002642:Chick Embryo; D002645:Chickens; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D005947:Glucose / Q000009:adverse effects / Q000378:metabolism; D051272:Glucose Transporter Type 1 / Q000235:genetics / Q000378:metabolism; D051274:Glucose Transporter Type 3 / Q000235:genetics / Q000378:metabolism; D006943:Hyperglycemia / Q000473:pathology*; D007031:Hypothalamus / Q000254:growth & development / Q000378:metabolism*; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000473:pathology*; D018709:Statistics, Nonparametric
chemical_list: D001786:Blood Glucose; D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; D005947:Glucose
keywords: Chicken embryo; Fetal programming; Glucose transporter expression; Hypothalamus; Neuronal glucose sensitivity