Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-5-1
pubmed:abstractText
Liver cirrhosis is often accompanied by a disturbed carbohydrate metabolism similar to type 2 diabetes. To investigate the severity of the defect in insulin secretion in this form of diabetes, we measured insulin release from isolated pancreatic islets of rats with CCl(4)-phenobarbital-induced liver cirrhosis. Cirrhosis was confirmed by clinical signs, elevated liver enzymes and histology. Fasting venous plasma glucose concentrations were equal in rats with liver cirrhosis and in controls. Plasma insulin and glucagon concentrations were significantly greater (P<0.01) in cirrhotic rats than in control animals. Glucose (16.7 mM)-induced stimulation of insulin release from pancreatic islets revealed a twofold increase in control and cirrhotic rats. Basal and stimulated insulin secretion, however, were significantly lower in cirrhotic animals. The incretin hormone, glucagon-like peptide-1 (GLP-1), has therapeutic potential for the treatment of type 2 diabetes. Therefore, islets from control and cirrhotic animals were incubated with GLP-1 in concentrations from 10(-)(11) to 10(-)(6) M. GLP-1 stimulated insulin release in a concentration-dependent manner. In islets from cirrhotic rats, basal and stimulated insulin secretion was blunted compared with controls. These data show that the hyperinsulinemia observed in liver cirrhosis is not due to an increase of insulin secretion from islets, but could be explained by decreased hepatic clearance of insulin. GLP-1 may ameliorate diabetes in patients with liver cirrhosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-0795
pubmed:author
pubmed:issnType
Print
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10607933-Analysis of Variance, pubmed-meshheading:10607933-Animals, pubmed-meshheading:10607933-Carbon Tetrachloride, pubmed-meshheading:10607933-Culture Techniques, pubmed-meshheading:10607933-Dose-Response Relationship, Drug, pubmed-meshheading:10607933-Glucagon, pubmed-meshheading:10607933-Glucagon-Like Peptide 1, pubmed-meshheading:10607933-Glucose Tolerance Test, pubmed-meshheading:10607933-Insulin, pubmed-meshheading:10607933-Islets of Langerhans, pubmed-meshheading:10607933-Liver Cirrhosis, Experimental, pubmed-meshheading:10607933-Liver Function Tests, pubmed-meshheading:10607933-Male, pubmed-meshheading:10607933-Peptide Fragments, pubmed-meshheading:10607933-Phenobarbital, pubmed-meshheading:10607933-Protein Precursors, pubmed-meshheading:10607933-Rats, pubmed-meshheading:10607933-Rats, Inbred Lew
pubmed:year
2000
pubmed:articleTitle
Insulin secretion defects in liver cirrhosis can be reversed by glucagon-like peptide-1.
pubmed:affiliation
Laboratory of Molecular Gastroenterology and Hepatology, Gastrointestinal Unit, 1st Department of Medicine, Christian-Albrechts-University of Kiel, 24105 Kiel, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't