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Glucocorticoid overexposure in neonatal life alters pancreatic beta-cell function in newborn foals.

Studies in humans and animals have linked abnormal programming of adult tissue function to excess glucocorticoids during perinatal development. The current study investigated the hypothesis that physiological variations in glucocorticoid concentrations during early neonatal life of the foal alter th... Full description

Journal Title: Journal of animal science January 2013, Vol.91(1), pp.104-110
Main Author: Jellyman, J K
Other Authors: Allen, V L , Holdstock, N B , Fowden, A L
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1525-3163 ; DOI: 10.2527/jas.2012-5475
Link: http://search.proquest.com/docview/1287887584/?pq-origsite=primo
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title: Glucocorticoid overexposure in neonatal life alters pancreatic beta-cell function in newborn foals.
format: Article
creator:
  • Jellyman, J K
  • Allen, V L
  • Holdstock, N B
  • Fowden, A L
subjects:
  • Adrenocorticotropic Hormone–Administration & Dosage
  • Animals–Toxicity
  • Animals, Newborn–Administration & Dosage
  • Arginine–Pharmacology
  • Blood Glucose–Drug Effects
  • Horses–Growth & Development
  • Insulin–Blood
  • Insulin-Secreting Cells–Drug Effects
  • Tolbutamide–Administration & Dosage
  • Tolbutamide–Pharmacology
  • Blood Glucose
  • Insulin
  • Adrenocorticotropic Hormone
  • Arginine
  • Tolbutamide
ispartof: Journal of animal science, January 2013, Vol.91(1), pp.104-110
description: Studies in humans and animals have linked abnormal programming of adult tissue function to excess glucocorticoids during perinatal development. The current study investigated the hypothesis that physiological variations in glucocorticoid concentrations during early neonatal life of the foal alter the secretory responses of the pancreatic [beta] cells 2 and 12 wk after treatment. Spontaneously delivered foals received either saline or long-acting ACTH for 5 d from 1 d after birth to maintain an endogenous rise in cortisol concentrations. Starting at d 10, pancreatic [beta] cell function was studied using an intravenous (i.v.) glucose tolerance test, an i.v. arginine challenge, and an i.v. tolbutamide challenge. The maximum increment in plasma insulin achieved in response to exogenous glucose was less in ACTH-treated foals at both 2 and 12 wk of age (P < 0.05). By 12 wk of age, developmental changes also occurred in the magnitude and biphasic pattern of glucose-stimulated insulin release. The area under the insulin curve during the early phase of insulin secretion (0 to 30 min) was not different between the 2- and 12-wk-old animals but was significantly greater during the later phase (30 to 120 min) at 12 wk than at 2 wk (P < 0.05). Arginine infusion induced a brief 5 to 15 min increase in plasma concentrations of insulin that was not different in saline- and ACTH-treated foals. The [beta]-cell response to tolbutamide infusion was rapid and monophasic, and there was no difference (P > 0.05) in the area under the insulin curve with treatment at 2 or at 12 wk. However, after tolbutamide, plasma insulin concentrations remained increased for a longer period in the ACTH-treated than in the saline-treated foals at 12 wk of age (P < 0.05). Hence, this is the first study to show altered pancreatic [beta]-cell function after ACTH-induced glucocorticoid overexposure during early postnatal life in foals. Key words: foal, glucocorticoid, insulin
language: eng
source:
identifier: E-ISSN: 1525-3163 ; DOI: 10.2527/jas.2012-5475
fulltext: fulltext
issn:
  • 15253163
  • 1525-3163
url: Link


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titleGlucocorticoid overexposure in neonatal life alters pancreatic beta-cell function in newborn foals.
creatorJellyman, J K ; Allen, V L ; Holdstock, N B ; Fowden, A L
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identifierE-ISSN: 1525-3163 ; DOI: 10.2527/jas.2012-5475
subjectAdrenocorticotropic Hormone–Administration & Dosage ; Animals–Toxicity ; Animals, Newborn–Administration & Dosage ; Arginine–Pharmacology ; Blood Glucose–Drug Effects ; Horses–Growth & Development ; Insulin–Blood ; Insulin-Secreting Cells–Drug Effects ; Tolbutamide–Administration & Dosage ; Tolbutamide–Pharmacology ; Blood Glucose ; Insulin ; Adrenocorticotropic Hormone ; Arginine ; Tolbutamide
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descriptionStudies in humans and animals have linked abnormal programming of adult tissue function to excess glucocorticoids during perinatal development. The current study investigated the hypothesis that physiological variations in glucocorticoid concentrations during early neonatal life of the foal alter the secretory responses of the pancreatic [beta] cells 2 and 12 wk after treatment. Spontaneously delivered foals received either saline or long-acting ACTH for 5 d from 1 d after birth to maintain an endogenous rise in cortisol concentrations. Starting at d 10, pancreatic [beta] cell function was studied using an intravenous (i.v.) glucose tolerance test, an i.v. arginine challenge, and an i.v. tolbutamide challenge. The maximum increment in plasma insulin achieved in response to exogenous glucose was less in ACTH-treated foals at both 2 and 12 wk of age (P < 0.05). By 12 wk of age, developmental changes also occurred in the magnitude and biphasic pattern of glucose-stimulated insulin release. The area under the insulin curve during the early phase of insulin secretion (0 to 30 min) was not different between the 2- and 12-wk-old animals but was significantly greater during the later phase (30 to 120 min) at 12 wk than at 2 wk (P < 0.05). Arginine infusion induced a brief 5 to 15 min increase in plasma concentrations of insulin that was not different in saline- and ACTH-treated foals. The [beta]-cell response to tolbutamide infusion was rapid and monophasic, and there was no difference (P > 0.05) in the area under the insulin curve with treatment at 2 or at 12 wk. However, after tolbutamide, plasma insulin concentrations remained increased for a longer period in the ACTH-treated than in the saline-treated foals at 12 wk of age (P < 0.05). Hence, this is the first study to show altered pancreatic [beta]-cell function after ACTH-induced glucocorticoid overexposure during early postnatal life in foals. Key words: foal, glucocorticoid, insulin
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