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Beta cell adaptation to dexamethasone-induced insulin resistance in rats involves increased glucose responsiveness but not glucose effectiveness

Karlsson, Sven; Ostlund, Björn; Myrsen-Axcrona, Ulrika; Sundler, Frank LU and Ahrén, Bo LU (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)
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author
organization
publishing date
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
id
8165923b-fe36-4123-8194-9f2c70bf60d3 (old id 1120374)
date added to LUP
2008-07-01 11:30:17
date last changed
2018-01-07 05:34:55
@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 &lt; 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 &lt; 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},
  keyword      = {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},
}