Document Detail


Pancreatic islet blood perfusion in the nonobese diabetic mouse: diabetes-prone female mice exhibit a higher blood flow compared with male mice in the prediabetic phase.
MedLine Citation:
PMID:  9681505     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study tested the hypothesis that changes in pancreatic islet blood flow correlate with the difference in diabetes incidence between male and female nonobese diabetic (NOD) mice. The blood flows were determined by a microsphere technique. In animals aged 10 and 14 weeks, the islet blood perfusion was 3-fold higher in female NOD mice compared with that in either age-matched male NOD mice or age- and sex-matched control ICR mice. At 5 weeks of age islet blood flow was similar in all groups. No differences between male and female NOD mice in whole pancreatic, duodenal, ileal, or colonic blood flows were observed at any time point. Administration of a bolus dose of aminoguanidine (a blocker of inducible nitric oxide synthase) to 10-week-old animals selectively and markedly decreased islet blood flow in female NOD mice, whereas islet blood flow in ICR mice and male NOD mice remained unaffected. Aminoguanidine did not affect mean arterial blood pressure or whole pancreatic blood flow in any of the groups. Injection of N(G)-methyl-L-arginine, an unspecific inhibitor of both constitutive and inducible nitric oxide synthase, markedly decreased whole pancreatic and islet blood flow to the same level in both male and female NOD mice. These combined findings suggest that diabetes-prone female NOD mice have an increased islet blood flow, which is mediated by an excessive production of nitric oxide formed by inducible nitric oxide synthase. The islet blood hyperperfusion may augment homing to the pancreatic islets of inflammatory cells and soluble factors involved in beta-cell destruction during the development of insulin-dependent diabetes mellitus in this animal model. The presently observed gender difference in the blood flow response could, therefore, at least partially explain why female NOD mice are more prone to develop hyperglycemia than the males.
Authors:
P O Carlsson; S Sandler; L Jansson
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Endocrinology     Volume:  139     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1998 Aug 
Date Detail:
Created Date:  1998-08-13     Completed Date:  1998-08-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3534-41     Citation Subset:  AIM; IM    
Affiliation:
Department of Medical Cell Biology, Uppsala University, Sweden. per-ola.carlsson@medcellbiol.uu.se
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MeSH Terms
Descriptor/Qualifier:
Aging
Animals
Blood Flow Velocity / drug effects
Blood Glucose / metabolism
Blood Pressure / drug effects
Colon / blood supply
Diabetes Mellitus, Type 1 / pathology,  physiopathology*
Duodenum / blood supply
Enzyme Inhibitors / pharmacology
Female
Guanidines / pharmacology
Ileum / blood supply
Insulin / blood
Islets of Langerhans / blood supply*,  pathology
Male
Mice
Mice, Inbred ICR
Mice, Inbred NOD
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type II
Prediabetic State / physiopathology*
Sex Characteristics*
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Enzyme Inhibitors; 0/Guanidines; 11061-68-0/Insulin; 79-17-4/pimagedine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, mouse

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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