Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats

Renzo Cordera, Gabrielia Andraghetti, Ralph A. DeFronzo, Luciano Rossetti

Research output: Contribution to journalArticle

Abstract

Liver-purified insulin receptor tyrosine kinase (IRTK) activity was examined in partially pancreatectomized rats following normalization of blood glucose concentration by either phlorizin or vanadate treatment. Chronic moderate hyperglycemia did not modify the IRTK activity, despite the presence of in vivo and in vitro insulin resistance. Oral vanadate administration for 3 weeks normalized glucose tolerance and caused a 2.5-fold increase in basal IRTK activity. In contrast, correction of hyperglycemia with phlorizin, an inhibitor of renal glucose reabsorption, did not change the IRTK activity, although glucose tolerance was returned to normal. The vanadate-induced effect on basal IRTK was due to an increase in Vmax of the enzyme; the Km remained unchanged. The insulin-stimulated IRTK activity was not affected by either vanadate or phlorizin treatment. These results suggest that: 1) partial (90%) pancreatectomy in rats causes insulin resistance in the absence of in vitro alterations in IRTK and 2) correction of chronic hyperglycemia with vanadate, but not with phlorizin, is associated with an increased basal activation of the protein tyrosine kinase in liver insulin receptors.

Original languageEnglish
Pages (from-to)2177-2183
Number of pages7
JournalEndocrinology
Volume126
Issue number4
Publication statusPublished - Apr 1990

Fingerprint

Vanadates
Phlorhizin
Hyperglycemia
Glucose
Therapeutics
Insulin Resistance
TYK2 Kinase
Pancreatectomy
Liver
Insulin Receptor
insulin receptor tyrosine kinase
Protein-Tyrosine Kinases
Oral Administration
Blood Glucose
Insulin
Enzymes

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Cordera, R., Andraghetti, G., DeFronzo, R. A., & Rossetti, L. (1990). Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats. Endocrinology, 126(4), 2177-2183.

Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats. / Cordera, Renzo; Andraghetti, Gabrielia; DeFronzo, Ralph A.; Rossetti, Luciano.

In: Endocrinology, Vol. 126, No. 4, 04.1990, p. 2177-2183.

Research output: Contribution to journalArticle

Cordera, R, Andraghetti, G, DeFronzo, RA & Rossetti, L 1990, 'Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats', Endocrinology, vol. 126, no. 4, pp. 2177-2183.
Cordera, Renzo ; Andraghetti, Gabrielia ; DeFronzo, Ralph A. ; Rossetti, Luciano. / Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats. In: Endocrinology. 1990 ; Vol. 126, No. 4. pp. 2177-2183.
@article{4bfdbcf7b2784a02a7aed5fb78d6de6a,
title = "Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats",
abstract = "Liver-purified insulin receptor tyrosine kinase (IRTK) activity was examined in partially pancreatectomized rats following normalization of blood glucose concentration by either phlorizin or vanadate treatment. Chronic moderate hyperglycemia did not modify the IRTK activity, despite the presence of in vivo and in vitro insulin resistance. Oral vanadate administration for 3 weeks normalized glucose tolerance and caused a 2.5-fold increase in basal IRTK activity. In contrast, correction of hyperglycemia with phlorizin, an inhibitor of renal glucose reabsorption, did not change the IRTK activity, although glucose tolerance was returned to normal. The vanadate-induced effect on basal IRTK was due to an increase in Vmax of the enzyme; the Km remained unchanged. The insulin-stimulated IRTK activity was not affected by either vanadate or phlorizin treatment. These results suggest that: 1) partial (90{\%}) pancreatectomy in rats causes insulin resistance in the absence of in vitro alterations in IRTK and 2) correction of chronic hyperglycemia with vanadate, but not with phlorizin, is associated with an increased basal activation of the protein tyrosine kinase in liver insulin receptors.",
author = "Renzo Cordera and Gabrielia Andraghetti and DeFronzo, {Ralph A.} and Luciano Rossetti",
year = "1990",
month = "4",
language = "English",
volume = "126",
pages = "2177--2183",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The Endocrine Society",
number = "4",

}

TY - JOUR

T1 - Effect of in vivo vanadate treatment on insulin receptor tyrosine kinase activity in partially pancreatectomized diabetic rats

AU - Cordera, Renzo

AU - Andraghetti, Gabrielia

AU - DeFronzo, Ralph A.

AU - Rossetti, Luciano

PY - 1990/4

Y1 - 1990/4

N2 - Liver-purified insulin receptor tyrosine kinase (IRTK) activity was examined in partially pancreatectomized rats following normalization of blood glucose concentration by either phlorizin or vanadate treatment. Chronic moderate hyperglycemia did not modify the IRTK activity, despite the presence of in vivo and in vitro insulin resistance. Oral vanadate administration for 3 weeks normalized glucose tolerance and caused a 2.5-fold increase in basal IRTK activity. In contrast, correction of hyperglycemia with phlorizin, an inhibitor of renal glucose reabsorption, did not change the IRTK activity, although glucose tolerance was returned to normal. The vanadate-induced effect on basal IRTK was due to an increase in Vmax of the enzyme; the Km remained unchanged. The insulin-stimulated IRTK activity was not affected by either vanadate or phlorizin treatment. These results suggest that: 1) partial (90%) pancreatectomy in rats causes insulin resistance in the absence of in vitro alterations in IRTK and 2) correction of chronic hyperglycemia with vanadate, but not with phlorizin, is associated with an increased basal activation of the protein tyrosine kinase in liver insulin receptors.

AB - Liver-purified insulin receptor tyrosine kinase (IRTK) activity was examined in partially pancreatectomized rats following normalization of blood glucose concentration by either phlorizin or vanadate treatment. Chronic moderate hyperglycemia did not modify the IRTK activity, despite the presence of in vivo and in vitro insulin resistance. Oral vanadate administration for 3 weeks normalized glucose tolerance and caused a 2.5-fold increase in basal IRTK activity. In contrast, correction of hyperglycemia with phlorizin, an inhibitor of renal glucose reabsorption, did not change the IRTK activity, although glucose tolerance was returned to normal. The vanadate-induced effect on basal IRTK was due to an increase in Vmax of the enzyme; the Km remained unchanged. The insulin-stimulated IRTK activity was not affected by either vanadate or phlorizin treatment. These results suggest that: 1) partial (90%) pancreatectomy in rats causes insulin resistance in the absence of in vitro alterations in IRTK and 2) correction of chronic hyperglycemia with vanadate, but not with phlorizin, is associated with an increased basal activation of the protein tyrosine kinase in liver insulin receptors.

UR - http://www.scopus.com/inward/record.url?scp=0025342047&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025342047&partnerID=8YFLogxK

M3 - Article

C2 - 2156685

AN - SCOPUS:0025342047

VL - 126

SP - 2177

EP - 2183

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 4

ER -