Linked Life Data

7796980

Source:http://linkedlifedata.com/resource/pubmed/id/7796980

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-7-31
pubmed:abstractText
The effect of oral vanadate on intestinal sodium-dependent glucose transport and 6-phosphofructo-1-kinase (EC 2.7.1.11) activity was examined in male Sprague-Dawley rats following a 30-day period of non-treated streptozotocin-induced diabetes. Non-treated diabetic rats were hyperglycaemic and demonstrated increased intestinal sodium-dependent glucose transport and Na,K-ATPase activity compared with controls. These increases were associated with a significant decrease in the total activity and activity ratios (activity at 0.5 mmol/l fructose 6-phosphate at pH 7.0/activity at pH 8.0) of intestinal 6-phosphofructo-1-kinase and decreased levels of fructose 2,6-bisphosphate. Supplementation of drinking water with vanadate (0.5 mg/ml) resulted in a rapid decline in blood glucose levels to a slightly hyperglycaemic level. Jejunal glucose transport and Na,K-ATPase activity were normalized after 48 h of vanadate treatment. In contrast, ileal glucose transport was significantly reduced 12 h following beginning vanadate treatment even though Na,K-ATPase activity did not normalize until 36 h later. Km was significantly decreased in both jejunum and ileum by vanadate treatment indicating an increased affinity of the sodium-dependent intestinal glucose transporter for glucose. 6-phosphofructo-1-kinase total activity and susceptibility to ATP inhibition was completely restored after 12 h of vanadate treatment. This increase was associated with a rise in fructose 2,6-bisphosphate levels. Fasting rats for 12 h had no effect on glucose transport or 6-phosphofructo-1-kinase activity, indicating the anorectic effect of vanadate was not responsible for changes in either parameter. In contrast, cycloheximide prevented both the rise in 6-phosphofructo-1-kinase activity and the rise in fructose 2,6-bisphosphate levels, and the subsequent reduction in glucose transport, indicating a requirement for protein synthesis. The removal of vanadate resulted in an immediate return to pre-treatment blood glucose levels. In contrast, intestinal glucose transport and 6-phosphofructo-1-kinase activity remained at treatment levels up until 72 h, indicating that oral vanadate treatment can have prolonged beneficial effects on intestinal function. In conclusion, the treatment of streptozotocin-induced diabetic rats with oral vanadate results in an activation of 6-phosphofructo-1-kinase coupled with a normalization of intestinal sodium-dependent glucose transport. Vanadate may thus have a beneficial effect on intestinal function and may prove useful as oral adjunctive diabetic therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0012-186X
pubmed:author
pubmed:issnType
Print
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
403-12
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:7796980-Analysis of Variance, pubmed-meshheading:7796980-Animals, pubmed-meshheading:7796980-Biological Transport, pubmed-meshheading:7796980-Blood Glucose, pubmed-meshheading:7796980-Cycloheximide, pubmed-meshheading:7796980-Diabetes Mellitus, Experimental, pubmed-meshheading:7796980-Enzyme Activation, pubmed-meshheading:7796980-Glucose, pubmed-meshheading:7796980-Hyperglycemia, pubmed-meshheading:7796980-Ileum, pubmed-meshheading:7796980-Intestinal Absorption, pubmed-meshheading:7796980-Intestinal Mucosa, pubmed-meshheading:7796980-Jejunum, pubmed-meshheading:7796980-Male, pubmed-meshheading:7796980-Microvilli, pubmed-meshheading:7796980-Phosphofructokinase-1, pubmed-meshheading:7796980-Rats, pubmed-meshheading:7796980-Rats, Sprague-Dawley, pubmed-meshheading:7796980-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:7796980-Vanadates
pubmed:year
1995
pubmed:articleTitle
Vanadate treatment rapidly improves glucose transport and activates 6-phosphofructo-1-kinase in diabetic rat intestine.
pubmed:affiliation
Department of Medicine, University of Alberta, Edmonton, Canada.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't