Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-10-23
pubmed:abstractText
Selenium is a trace element that exerts certain insulin-like actions in vitro. In this study, we evaluated its in vivo effects on the glucose homeostasis of rats made diabetic and insulin-deficient by streptozotocin. Na2SeO4 was administered ad libitum in drinking water and/or food for 10 weeks. The elevated plasma glucose levels (approximately 25 mmol/l) and glucosuria (approximately 85 mmol/day) of untreated rats were decreased by 50 and 80%, respectively, by selenate treatment. The beneficial effect of selenate was also evident during oral and intravenous glucose tolerance tests: the integrated glucose responses were decreased by 40-50% as compared to those in untreated rats. These effects were not due to an increase in plasma insulin levels. Compared to non-diabetic rats, pancreatic insulin reserves were reduced by more than 90% in treated and untreated diabetic rats. The hepatic activities and mRNA levels of two key glycolytic enzymes, glucokinase and L-type pyruvate kinase were blunted in diabetic rats. They increased approximately two- to threefold after selenate treatment, to reach 40-75% of the values in non-diabetic rats. In contrast, elevated activity and mRNA levels of the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase, were reduced by 40-65% after selenate administration. Since selenate induced a moderate decrease in body weight due to an anorexigenic effect, we checked that there was no improvement of glucose homeostasis or hepatic glucose metabolism in an additional group of calorie-restricted diabetic rats, which was weight-matched with the selenate group. In addition, no obvious toxic side-effects on the kidney or liver were observed in the rats receiving selenate. In conclusion, selenate induces a sustained improvement of glucose homeostasis in streptozotocin-diabetic rats by an insulin-like action, which involves partial correction of altered pretranslational regulatory mechanisms in liver metabolism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0012-186X
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-11
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:8720597-Administration, Oral, pubmed-meshheading:8720597-Animals, pubmed-meshheading:8720597-Blood Glucose, pubmed-meshheading:8720597-Blotting, Northern, pubmed-meshheading:8720597-Body Weight, pubmed-meshheading:8720597-DNA Probes, pubmed-meshheading:8720597-Diabetes Mellitus, Experimental, pubmed-meshheading:8720597-Gene Expression, pubmed-meshheading:8720597-Glucokinase, pubmed-meshheading:8720597-Gluconeogenesis, pubmed-meshheading:8720597-Glucose, pubmed-meshheading:8720597-Glucose Tolerance Test, pubmed-meshheading:8720597-Glycolysis, pubmed-meshheading:8720597-Homeostasis, pubmed-meshheading:8720597-Insulin, pubmed-meshheading:8720597-Islets of Langerhans, pubmed-meshheading:8720597-Liver, pubmed-meshheading:8720597-Male, pubmed-meshheading:8720597-Phosphoenolpyruvate Carboxykinase (GTP), pubmed-meshheading:8720597-Pyruvate Kinase, pubmed-meshheading:8720597-Rats, pubmed-meshheading:8720597-Rats, Wistar, pubmed-meshheading:8720597-Selenium, pubmed-meshheading:8720597-Selenium Compounds
pubmed:year
1996
pubmed:articleTitle
Oral selenate improves glucose homeostasis and partly reverses abnormal expression of liver glycolytic and gluconeogenic enzymes in diabetic rats.
pubmed:affiliation
Endocrinology and Metabolism Unit, University of Louvain, Brussels, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't