Document Detail


Tumor necrosis factor activity of pancreatic islets.
MedLine Citation:
PMID:  9277398     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tumor necrosis factor (TNF) is involved in the pathogenesis of acute sepsis-induced organ injury and has been implicated as a mediator of metabolic alterations observed during sepsis. Pancreatic islet cell function may be significantly compromised during sepsis or endotoxemia, and sepsis also increases plasma levels of epinephrine, a modifier of islet insulin secretion. We proposed that islets exposed to bacterial lipopolysaccharide (LPS) produce TNF and that epinephrine attenuates islet secretory activity. We monitored the effects of LPS and epinephrine on TNF and insulin activity of isolated Wistar-Furth rat islets (pancreas digested with collagenase, islets isolated using Ficoll gradients; n = 4 islet populations, each with 632 +/- 11 islets/2.5 ml culture medium). Islets were incubated (37 degrees C, 5% CO2) 3 days. LPS (Escherichia coli, 1 microgram/ml) and epinephrine (14 micrograms/ml) were added to the islets, and incubations were continued for 1-4 h. Glucose (Beckman Glucose Analyzer), insulin (radioimmunoassay), and TNF (L929 cytotoxicity assay) were measured in the islet medium samples at 1- to 4-h time points. In the conditioned medium, glucose decreased (P < 0.05), insulin increased (P < 0.05), and exposure to LPS did not alter these levels [P = not significant (NS)] but did increase TNF activity by 400% (P < 0.05). Epinephrine reduced insulin by 38-43% (P < 0.05) and TNF by 20-25% (P < 0.05) but had no effect on glucose levels (P = NS). We conclude that insulin is secreted from isolated islets and that exposure to LPS acutely increases islet-derived TNF activity, whereas epinephrine modifies TNF and insulin secretion of rat pancreatic islets.
Authors:
S K Leeper-Woodford; B W Tobin
Related Documents :
9788748 - Interference of d-mannoheptulose with d-glucose phosphorylation, metabolism and functio...
8932278 - Dynamics of glucose-induced insulin release from mouse islets transplanted under the ki...
19775318 - Endoscopic gastric submucosal transplantation of islets (endo-sti): technique and initi...
10462138 - Absence of toxicity associated with adenoviral-mediated transfer of the beta-galactosid...
14641268 - The influence of ageing on the insulin signalling system in rat lacrimal and salivary g...
2162348 - Characterization of the (na+ (+) k+)-atpase from 3t3-f442a fibroblasts and adipocytes. ...
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  273     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1997 Aug 
Date Detail:
Created Date:  1997-09-24     Completed Date:  1997-09-24     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  E433-7     Citation Subset:  IM    
Affiliation:
Department of Physiology, Mercer University School of Medicine, Macon, Georgia 31207, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Culture Media / metabolism
Epinephrine / pharmacology
Glucose / metabolism
Insulin / metabolism
Islets of Langerhans / drug effects,  metabolism*
Lipopolysaccharides / pharmacology
Male
Rats
Rats, Inbred WF
Tumor Necrosis Factor-alpha / metabolism*
Grant Support
ID/Acronym/Agency:
HL-52917/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Culture Media; 0/Lipopolysaccharides; 0/Tumor Necrosis Factor-alpha; 11061-68-0/Insulin; 50-99-7/Glucose; 51-43-4/Epinephrine

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


Previous Document:  Relationship of visceral adipose tissue and glucose disposal is independent of sex in black NIDDM su...
Next Document:  Simulation of IGF-I pharmacokinetics after infusion of recombinant IGF-I in human subjects.