Beta cell adaptation to dexamethasone-induced insulin resistance in rats involves increased glucose responsiveness but not glucose effectiveness
(2001) In Pancreas 22(2). p.148-156- Abstract
- Islet beta cell adaptation to dexamethasone-induced insulin resistance was characterized with respect to glucose-stimulated insulin secretion and islet innervation. Male Sprague-Dawley rats were injected daily with dexamethasone (2 mg/kg for 12 days), which resulted in hyperinsulinemia and hyperglycemia compared with controls (which were injected with sodium chloride). Insulin secretion was characterized in collagenase-isolated islets. Islet innervation was examined by immunocytochemical analysis of tyrosine hydroxylase, neuropeptide Y (sympathetic nerves), and vasoactive intestinal polypeptide (cholinergic nerves). In islets isolated from the insulin-resistant animals, the insulin response to 3.3 or 8.3 mM glucose was three times greater... (More)
- Islet beta cell adaptation to dexamethasone-induced insulin resistance was characterized with respect to glucose-stimulated insulin secretion and islet innervation. Male Sprague-Dawley rats were injected daily with dexamethasone (2 mg/kg for 12 days), which resulted in hyperinsulinemia and hyperglycemia compared with controls (which were injected with sodium chloride). Insulin secretion was characterized in collagenase-isolated islets. Islet innervation was examined by immunocytochemical analysis of tyrosine hydroxylase, neuropeptide Y (sympathetic nerves), and vasoactive intestinal polypeptide (cholinergic nerves). In islets isolated from the insulin-resistant animals, the insulin response to 3.3 or 8.3 mM glucose was three times greater during perifusion compared with controls (p < 0.001). Incubation of islets at 0 to 20 mM glucose revealed a marked leftward shift of the glucose dose-response relation after dexamethasone treatment (potency ratio, 1.78; p < 0.01), with no difference at 0 or 20 mM glucose. Thus, the potency but not the efficacy of glucose was increased. The number of islet nerves did not differ between dexamethasone-treated rats and controls. Dexamethasone-induced insulin resistance leads to adaptively increased glucose responsiveness of the islet beta cells, with increased potency, but not increased efficacy, of glucose to stimulate insulin secretion without any evidence of altered islet innervation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1120374
- author
- Karlsson, Sven ; Ostlund, Björn ; Myrsen-Axcrona, Ulrika ; Sundler, Frank LU and Ahrén, Bo LU
- organization
- publishing date
- 2001
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Islet, Beta Cell, Insulin Secretion, Insulin Resistance, Dexamethasone, Autonomic Nerves, Neuropeptide Y, Vasoactive Intestinal Polypeptide
- in
- Pancreas
- volume
- 22
- issue
- 2
- pages
- 148 - 156
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- pmid:11249069
- scopus:0035111321
- ISSN
- 0885-3177
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medicine (Lund) (013230025), Neuroendocrine Cell Biology (013212008)
- id
- 8165923b-fe36-4123-8194-9f2c70bf60d3 (old id 1120374)
- date added to LUP
- 2016-04-01 11:56:34
- date last changed
- 2024-01-23 00:03:02
@article{8165923b-fe36-4123-8194-9f2c70bf60d3,
abstract = {{Islet beta cell adaptation to dexamethasone-induced insulin resistance was characterized with respect to glucose-stimulated insulin secretion and islet innervation. Male Sprague-Dawley rats were injected daily with dexamethasone (2 mg/kg for 12 days), which resulted in hyperinsulinemia and hyperglycemia compared with controls (which were injected with sodium chloride). Insulin secretion was characterized in collagenase-isolated islets. Islet innervation was examined by immunocytochemical analysis of tyrosine hydroxylase, neuropeptide Y (sympathetic nerves), and vasoactive intestinal polypeptide (cholinergic nerves). In islets isolated from the insulin-resistant animals, the insulin response to 3.3 or 8.3 mM glucose was three times greater during perifusion compared with controls (p < 0.001). Incubation of islets at 0 to 20 mM glucose revealed a marked leftward shift of the glucose dose-response relation after dexamethasone treatment (potency ratio, 1.78; p < 0.01), with no difference at 0 or 20 mM glucose. Thus, the potency but not the efficacy of glucose was increased. The number of islet nerves did not differ between dexamethasone-treated rats and controls. Dexamethasone-induced insulin resistance leads to adaptively increased glucose responsiveness of the islet beta cells, with increased potency, but not increased efficacy, of glucose to stimulate insulin secretion without any evidence of altered islet innervation.}},
author = {{Karlsson, Sven and Ostlund, Björn and Myrsen-Axcrona, Ulrika and Sundler, Frank and Ahrén, Bo}},
issn = {{0885-3177}},
keywords = {{Islet; Beta Cell; Insulin Secretion; Insulin Resistance; Dexamethasone; Autonomic Nerves; Neuropeptide Y; Vasoactive Intestinal Polypeptide}},
language = {{eng}},
number = {{2}},
pages = {{148--156}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{Pancreas}},
title = {{Beta cell adaptation to dexamethasone-induced insulin resistance in rats involves increased glucose responsiveness but not glucose effectiveness}},
volume = {{22}},
year = {{2001}},
}