Glucocorticoid overexposure in neonatal life alters pancreatic beta-cell function in newborn foals.
Abstract: 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 β 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 β 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 (P0.05) 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 β-cell function after ACTH-induced glucocorticoid overexposure during early postnatal life in foals.
Publication Date: 2012-10-16 PubMed ID: 23100584DOI: 10.2527/jas.2012-5475Google Scholar: Lookup
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- Controlled Clinical Trial
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research investigates the impact of excessive glucocorticoids on the function of pancreatic beta cells in newborn foals. The study shows that elevated glucocorticoid levels in the early neonatal period cause changes in insulin secretion responses over time, indicating a potential alteration in adult tissue function due to hormonal imbalances during perinatal development.
Study Rationale and Hypothesis
- The researchers were motivated by prior investigations that linked abnormal performance of adult tissues to excessive glucocorticoids during the perinatal development phase.
- The study hypothesized that variations in glucocorticoid concentration in a foal’s early neonatal life could modify the secretion patterns of pancreatic beta cells.
Methodology
- Newborn foals, born naturally, were administered either saline or long-acting ACTH over a period of 5 days starting from the day after birth. The aim was to keep an internal rise in cortisol levels.
- On the 10th day, the function of pancreatic beta cells was studied using intravenous glucose tolerance, arginine challenge, and tolbutamide challenge.
Findings
- ACTH-treated foals had a lesser increase in plasma insulin in response to exogenous glucose, observed at both 2 and 12 weeks of age.
- There were also developmental changes in the size and biphasic pattern of glucose-stimulated insulin release by 12 weeks.
- The insulin secretion during the early phase was not different between 2 and 12 weeks old foals, but it was significantly more during the later phase at 12 weeks than at 2 weeks.
- Arginine infusion led to a small increase in plasma insulin concentrations, which was the same for both ACTH and saline-treated foals.
- The response of β-cells to tolbutamide was fast and monophasic, and there was no difference in overall insulin secretion at 2 or at 12 weeks. However, post-tolbutamide, the ACTH-treated foals had higher plasma insulin concentrations for a longer duration compared to the saline-treated foals at week 12.
Conclusion
- From this study, it is concluded that overexposure to glucocorticoids triggered by ACTH during early postnatal life in foals alters the function of pancreatic beta cells. This appears to be the first study reporting such a phenomenon.
Cite This Article
APA
Jellyman JK, Allen VL, Holdstock NB, Fowden AL.
(2012).
Glucocorticoid overexposure in neonatal life alters pancreatic beta-cell function in newborn foals.
J Anim Sci, 91(1), 104-110.
https://doi.org/10.2527/jas.2012-5475 Publication
Researcher Affiliations
- Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK. J.K.Jellyman.00@cantab.net
MeSH Terms
- Adrenocorticotropic Hormone / administration & dosage
- Adrenocorticotropic Hormone / toxicity
- Animals
- Animals, Newborn
- Arginine / administration & dosage
- Arginine / pharmacology
- Blood Glucose / drug effects
- Horses / growth & development
- Insulin / blood
- Insulin-Secreting Cells / drug effects
- Tolbutamide / administration & dosage
- Tolbutamide / pharmacology
Citations
This article has been cited 1 times.- Guberman C, Jellyman JK, Han G, Ross MG, Desai M. Maternal high-fat diet programs rat offspring hypertension and activates the adipose renin-angiotensin system. Am J Obstet Gynecol 2013 Sep;209(3):262.e1-8.
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