title: Dexamethasone and colostrum feeding affect hepatic gluconeogenic enzymes differently in neonatal calves.
abstract: Plasma glucose concentrations in neonates are influenced by colostrum feeding and by glucocorticoids. We have tested whether a high-glucocorticoid status after birth, as well as colostrum feeding, influences glucose metabolism in association with changes of hepatic expression and activities of gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) and pyruvate carboxylase (PC; EC 6.4.1.1) in neonatal calves. Calves (n = 14 per group) were fed either colostrum or a milk-based formula with nutrient and energy contents similar to colostrum. Half the calves in each feeding group were treated with dexamethasone (DEXA; 30 microg/[kg BW x d]). Pre- and postprandial blood samples were taken on d 1, 2, 4, and 5 and liver samples were collected on d 5 of life. Dexamethasone treatment increased (P < or = 0.05) plasma concentrations of glucose, insulin, and glucagon more in colostrum-fed than in formula-fed calves but increased (P < or = 0.05) urea concentrations and decreased (P < or = 0.05) concentrations of NEFA, ACTH, and cortisol independent of colostrum vs. formula feeding. Colostrum feeding increased (P < 0.05) plasma glucose, but decreased (P < 0.05) plasma urea concentrations. Glucagon-to-insulin ratios in DEXA-treated and colostrum-fed calves were decreased (P < 0.05). Dexamethasone treatment decreased hepatic mRNA levels and activities of PC (P < 0.001 and P < 0.10) and activities of PEPCK (P < 0.001) but increased (P < 0.001) the glycogen content. Colostrum feeding increased (P < 0.05) mitochondrial PEPCK mRNA levels and PEPCK activities in calves not treated with DEXA but decreased (P < 0.1) amounts of PC mRNA. In conclusion, increased plasma glucose concentrations after DEXA treatment were not associated with a stimulation of hepatic gluconeogenic enzyme activities; however, colostrum feeding probably raised plasma glucose concentrations because of increased hepatic gluconeogenic activities.
authors.affiliation: Division of Nutrition and Physiology, Institute of Animal Genetics, Nutrition and Housing, Faculty of Veterinary Medicine, University of Berne, CH-3012 Berne, Switzerland. harald.hammon@itz.unibe.ch
authors.forename: H M
authors.initials: HM
authors.lastname: Hammon
authors.forename: S N
authors.initials: SN
authors.lastname: Sauter
authors.forename: M
authors.initials: M
authors.lastname: Reist
authors.forename: Y
authors.initials: Y
authors.lastname: Zbinden
authors.forename: C
authors.initials: C
authors.lastname: Philipona
authors.forename: C
authors.initials: C
authors.lastname: Morel
authors.forename: J W
authors.initials: JW
authors.lastname: Blum
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D000831:Animals, Newborn / Q000097:blood*; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects / Q000378:metabolism; D001806:Blood Urea Nitrogen; D002417:Cattle / Q000097:blood*; D003126:Colostrum; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology*; D004032:Diet; D005526:Food, Formulated; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005934:Glucagon / Q000097:blood; D005938:Glucocorticoids / Q000008:administration & dosage / Q000494:pharmacology*; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D008099:Liver / Q000201:enzymology*; D008112:Liver Glycogen / Q000032:analysis; D008297:Male; D010730:Phosphoenolpyruvate Carboxylase / Q000235:genetics / Q000378:metabolism; D011766:Pyruvate Carboxylase / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D001786:Blood Glucose; D005938:Glucocorticoids; D007328:Insulin; D008112:Liver Glycogen; D012333:RNA, Messenger; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D005934:Glucagon; D010730:Phosphoenolpyruvate Carboxylase; D011766:Pyruvate Carboxylase; D006854:Hydrocortisone