Linked Life Data

7695642

Source:http://linkedlifedata.com/resource/pubmed/id/7695642

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-4-24
pubmed:abstractText
Insulin resistance in the obese (fa/fa) Zucker rat is associated with decreased insulin stimulated glucose transport in skeletal muscle, due primarily to a failure of insulin to stimulate GLUT4 translocation to the plasma membrane from an intracellular pool (1). The thiazolidinedione analog Pioglitazone (PIO) has been shown to improve glucose tolerance in this and other animal models of insulin resistance. The current study was designed to determine whether 7 days of Pioglitazone treatment (20 mg/kg/day by gavage) would improve glucose transport and/or glucose transporter translocation and intrinsic activity in plasma membranes prepared from hindlimb skeletal muscle of obese Zucker (fa/fa) rats. Basal plasma glucose and insulin concentrations in these animals were unchanged by Pioglitazone, while basal plasma triglyceride and nonesterified fatty acid concentrations (NEFA) were reduced by Pioglitazone treatment (501 +/- 88 vs 161 +/- 13 mg/dl, P < 0.0001) and (678 +/- 95 vs 467 +/- 75 microM, P < 0.05) respectively. Pioglitazone had no effect on basal or insulin stimulated glucose influx (Vmax or Km) into plasma membrane vesicles determined under equilibrium exchange conditions compared to controls. Plasma membrane glucose transporter number (R0) (measured by cytochalasin B binding) under basal or insulin stimulated conditions was unchange by Pioglitazone and R0 failed to increase following insulin stimulation in either group. Glucose transporter turnover number (Vmax/R0) increased 2-fold with insulin stimulation compared to basal in both control and Pioglitazone groups, similar to turnover numbers observed in normal rats. These data confirm that impaired glucose transporter translocation in muscle of the Zucker rat is a major factor contributing to its insulin resistance. We conclude that the improved glucose tolerance observed in fa/fa rats following Pioglitazone treatment is not due to an improvement in basal or insulin stimulated skeletal muscle plasma membrane glucose transport or glucose transporter translocation and that Pioglitazone treatment does not affect transporter intrinsic activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
208
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
835-45
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Pioglitazone treatment for 7 days failed to correct the defect in glucose transport and glucose transporter translocation in obese Zucker rat (fa/fa) skeletal muscle plasma membranes.
pubmed:affiliation
Department of Medicine, University of Vermont College of Medicine, Burlington 05404.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't