Increased basal arterial smooth muscle glucose transport in the Zucker rat

Paul R Standley, Kelly A. Rose, James R. Sowers

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Insulin has recently been reported to stimulate glucose transport in vascular smooth muscle cells (VSMC). This observation suggests a role for this hormone in hypertension associated with insulin resistance. To determine whether VSMC glucose transport abnormalities exist in a state of insulin resistance, we studied basal and insulin-stimulated glucose transport in VSMC derived from Zucker lean (normotensive, insulin sensitive) and obese (hypertensive, insulin resistant) rats. Basal glucose transport, as measured by tracer quantities of [3H]2-deoxyglucose, was 4.2 ± 0.8 and 7.4 ± 0.9 fmol/106 cells/min for lean and obese cells, respectively (P < .05). Kinetic analyses utilizing variable concentrations of unlabeled 2-deoxyglucose in the media revealed that increased transport in the obese rat was due to an increased Vmax of the transporter system: Vmax = 5.9 ± 0.8 and 12.1 ± 1.2 fmol/106 cells/min for lean and obese cells, respectively (P < .05); no changes in Km were noted for the two populations: Km 1.14 ± 0.24 and 0.96 ± 0.10 mmol/L. Insulin (10 μU/mL) increased the Vmax of the transporter in both preparations, but greater stimulation was seen in the lean VSMC: 32 ± 4.8% v 11.5 ± 2.1% (P < .05). Insulin had no effect on the Km of the transporter in either strain. These data suggest that increased basal glucose transport in obese VSMC may predispose the vessel to increased glucose-mediated events, while blunted insulin-stimulated glucose transport in these cells mirrors insulin-resistant glucose disposal in other tissues of the obese rat.

Original languageEnglish (US)
Pages (from-to)48-52
Number of pages5
JournalAmerican Journal of Hypertension
Volume8
Issue number1
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

Zucker Rats
Smooth Muscle
Insulin
Glucose
Vascular Smooth Muscle
Smooth Muscle Myocytes
Deoxyglucose
Insulin Resistance
Hormones
Hypertension

Keywords

  • Glucose
  • muscle cells
  • vascular smooth
  • Zucker rat

ASJC Scopus subject areas

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Increased basal arterial smooth muscle glucose transport in the Zucker rat. / Standley, Paul R; Rose, Kelly A.; Sowers, James R.

In: American Journal of Hypertension, Vol. 8, No. 1, 1995, p. 48-52.

Research output: Contribution to journalArticle

@article{4a29920d0cee4ddfa90cc8a7b85c7df7,
title = "Increased basal arterial smooth muscle glucose transport in the Zucker rat",
abstract = "Insulin has recently been reported to stimulate glucose transport in vascular smooth muscle cells (VSMC). This observation suggests a role for this hormone in hypertension associated with insulin resistance. To determine whether VSMC glucose transport abnormalities exist in a state of insulin resistance, we studied basal and insulin-stimulated glucose transport in VSMC derived from Zucker lean (normotensive, insulin sensitive) and obese (hypertensive, insulin resistant) rats. Basal glucose transport, as measured by tracer quantities of [3H]2-deoxyglucose, was 4.2 ± 0.8 and 7.4 ± 0.9 fmol/106 cells/min for lean and obese cells, respectively (P < .05). Kinetic analyses utilizing variable concentrations of unlabeled 2-deoxyglucose in the media revealed that increased transport in the obese rat was due to an increased Vmax of the transporter system: Vmax = 5.9 ± 0.8 and 12.1 ± 1.2 fmol/106 cells/min for lean and obese cells, respectively (P < .05); no changes in Km were noted for the two populations: Km 1.14 ± 0.24 and 0.96 ± 0.10 mmol/L. Insulin (10 μU/mL) increased the Vmax of the transporter in both preparations, but greater stimulation was seen in the lean VSMC: 32 ± 4.8{\%} v 11.5 ± 2.1{\%} (P < .05). Insulin had no effect on the Km of the transporter in either strain. These data suggest that increased basal glucose transport in obese VSMC may predispose the vessel to increased glucose-mediated events, while blunted insulin-stimulated glucose transport in these cells mirrors insulin-resistant glucose disposal in other tissues of the obese rat.",
keywords = "Glucose, muscle cells, vascular smooth, Zucker rat",
author = "Standley, {Paul R} and Rose, {Kelly A.} and Sowers, {James R.}",
year = "1995",
doi = "10.1016/0895-7061(94)00160-D",
language = "English (US)",
volume = "8",
pages = "48--52",
journal = "American Journal of Hypertension",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "1",

}

TY - JOUR

T1 - Increased basal arterial smooth muscle glucose transport in the Zucker rat

AU - Standley, Paul R

AU - Rose, Kelly A.

AU - Sowers, James R.

PY - 1995

Y1 - 1995

N2 - Insulin has recently been reported to stimulate glucose transport in vascular smooth muscle cells (VSMC). This observation suggests a role for this hormone in hypertension associated with insulin resistance. To determine whether VSMC glucose transport abnormalities exist in a state of insulin resistance, we studied basal and insulin-stimulated glucose transport in VSMC derived from Zucker lean (normotensive, insulin sensitive) and obese (hypertensive, insulin resistant) rats. Basal glucose transport, as measured by tracer quantities of [3H]2-deoxyglucose, was 4.2 ± 0.8 and 7.4 ± 0.9 fmol/106 cells/min for lean and obese cells, respectively (P < .05). Kinetic analyses utilizing variable concentrations of unlabeled 2-deoxyglucose in the media revealed that increased transport in the obese rat was due to an increased Vmax of the transporter system: Vmax = 5.9 ± 0.8 and 12.1 ± 1.2 fmol/106 cells/min for lean and obese cells, respectively (P < .05); no changes in Km were noted for the two populations: Km 1.14 ± 0.24 and 0.96 ± 0.10 mmol/L. Insulin (10 μU/mL) increased the Vmax of the transporter in both preparations, but greater stimulation was seen in the lean VSMC: 32 ± 4.8% v 11.5 ± 2.1% (P < .05). Insulin had no effect on the Km of the transporter in either strain. These data suggest that increased basal glucose transport in obese VSMC may predispose the vessel to increased glucose-mediated events, while blunted insulin-stimulated glucose transport in these cells mirrors insulin-resistant glucose disposal in other tissues of the obese rat.

AB - Insulin has recently been reported to stimulate glucose transport in vascular smooth muscle cells (VSMC). This observation suggests a role for this hormone in hypertension associated with insulin resistance. To determine whether VSMC glucose transport abnormalities exist in a state of insulin resistance, we studied basal and insulin-stimulated glucose transport in VSMC derived from Zucker lean (normotensive, insulin sensitive) and obese (hypertensive, insulin resistant) rats. Basal glucose transport, as measured by tracer quantities of [3H]2-deoxyglucose, was 4.2 ± 0.8 and 7.4 ± 0.9 fmol/106 cells/min for lean and obese cells, respectively (P < .05). Kinetic analyses utilizing variable concentrations of unlabeled 2-deoxyglucose in the media revealed that increased transport in the obese rat was due to an increased Vmax of the transporter system: Vmax = 5.9 ± 0.8 and 12.1 ± 1.2 fmol/106 cells/min for lean and obese cells, respectively (P < .05); no changes in Km were noted for the two populations: Km 1.14 ± 0.24 and 0.96 ± 0.10 mmol/L. Insulin (10 μU/mL) increased the Vmax of the transporter in both preparations, but greater stimulation was seen in the lean VSMC: 32 ± 4.8% v 11.5 ± 2.1% (P < .05). Insulin had no effect on the Km of the transporter in either strain. These data suggest that increased basal glucose transport in obese VSMC may predispose the vessel to increased glucose-mediated events, while blunted insulin-stimulated glucose transport in these cells mirrors insulin-resistant glucose disposal in other tissues of the obese rat.

KW - Glucose

KW - muscle cells

KW - vascular smooth

KW - Zucker rat

UR - http://www.scopus.com/inward/record.url?scp=0028967374&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028967374&partnerID=8YFLogxK

U2 - 10.1016/0895-7061(94)00160-D

DO - 10.1016/0895-7061(94)00160-D

M3 - Article

C2 - 7734096

AN - SCOPUS:0028967374

VL - 8

SP - 48

EP - 52

JO - American Journal of Hypertension

JF - American Journal of Hypertension

SN - 0895-7061

IS - 1

ER -