The link between Glut-1 and hypertension in diabetic nephropathy

Luigi Gnudi, Leopoldo Raij

Research output: Contribution to journalArticle

Abstract

Nephropathy is a major diabetic microvascular complication; both metabolic and hemodynamic perturbations play critical roles in its occurrence and progression toward end-stage renal disease. Improvements in metabolic and blood pressure control have been shown to confer protection from this diabetic complication. In this article, we review the facilitative glucose transporter Glut-I, its regulation, and its potential role in linking metabolic and hemodynamic perturbations in the pathophysiologic processes that lead to kidney injury in diabetes. We propose that an auto-maintaining mechanism of hemodynamic perturbations and increased tissue angiotensin II may be involved in the initiation and maintenance of a loop in which transforming growth factor β1 and Glut-I upregulation play important roles in the pathophysiology of diabetic-induced kidney lesions. The understanding of the molecular mechanisms that link glomerular hypertension and excessive glucose metabolism may provide insight into new therapeutic strategies for the treatment of diabetic renal disease.

Original languageEnglish
Pages (from-to)79-83
Number of pages5
JournalCurrent Hypertension Reports
Volume8
Issue number1
DOIs
StatePublished - Apr 1 2006
Externally publishedYes

Fingerprint

Diabetic Nephropathies
Hemodynamics
Diabetes Complications
Hypertension
Kidney
Facilitative Glucose Transport Proteins
Transforming Growth Factors
Angiotensin II
Chronic Kidney Failure
Up-Regulation
Maintenance
Blood Pressure
Glucose
Wounds and Injuries
Therapeutics

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

The link between Glut-1 and hypertension in diabetic nephropathy. / Gnudi, Luigi; Raij, Leopoldo.

In: Current Hypertension Reports, Vol. 8, No. 1, 01.04.2006, p. 79-83.

Research output: Contribution to journalArticle

Gnudi, Luigi ; Raij, Leopoldo. / The link between Glut-1 and hypertension in diabetic nephropathy. In: Current Hypertension Reports. 2006 ; Vol. 8, No. 1. pp. 79-83.
@article{702cc50e30b64b9cbe9858613ca02f61,
title = "The link between Glut-1 and hypertension in diabetic nephropathy",
abstract = "Nephropathy is a major diabetic microvascular complication; both metabolic and hemodynamic perturbations play critical roles in its occurrence and progression toward end-stage renal disease. Improvements in metabolic and blood pressure control have been shown to confer protection from this diabetic complication. In this article, we review the facilitative glucose transporter Glut-I, its regulation, and its potential role in linking metabolic and hemodynamic perturbations in the pathophysiologic processes that lead to kidney injury in diabetes. We propose that an auto-maintaining mechanism of hemodynamic perturbations and increased tissue angiotensin II may be involved in the initiation and maintenance of a loop in which transforming growth factor β1 and Glut-I upregulation play important roles in the pathophysiology of diabetic-induced kidney lesions. The understanding of the molecular mechanisms that link glomerular hypertension and excessive glucose metabolism may provide insight into new therapeutic strategies for the treatment of diabetic renal disease.",
author = "Luigi Gnudi and Leopoldo Raij",
year = "2006",
month = "4",
day = "1",
doi = "10.1007/s11906-006-0044-5",
language = "English",
volume = "8",
pages = "79--83",
journal = "Current Hypertension Reports",
issn = "1522-6417",
publisher = "Current Medicine Group",
number = "1",

}

TY - JOUR

T1 - The link between Glut-1 and hypertension in diabetic nephropathy

AU - Gnudi, Luigi

AU - Raij, Leopoldo

PY - 2006/4/1

Y1 - 2006/4/1

N2 - Nephropathy is a major diabetic microvascular complication; both metabolic and hemodynamic perturbations play critical roles in its occurrence and progression toward end-stage renal disease. Improvements in metabolic and blood pressure control have been shown to confer protection from this diabetic complication. In this article, we review the facilitative glucose transporter Glut-I, its regulation, and its potential role in linking metabolic and hemodynamic perturbations in the pathophysiologic processes that lead to kidney injury in diabetes. We propose that an auto-maintaining mechanism of hemodynamic perturbations and increased tissue angiotensin II may be involved in the initiation and maintenance of a loop in which transforming growth factor β1 and Glut-I upregulation play important roles in the pathophysiology of diabetic-induced kidney lesions. The understanding of the molecular mechanisms that link glomerular hypertension and excessive glucose metabolism may provide insight into new therapeutic strategies for the treatment of diabetic renal disease.

AB - Nephropathy is a major diabetic microvascular complication; both metabolic and hemodynamic perturbations play critical roles in its occurrence and progression toward end-stage renal disease. Improvements in metabolic and blood pressure control have been shown to confer protection from this diabetic complication. In this article, we review the facilitative glucose transporter Glut-I, its regulation, and its potential role in linking metabolic and hemodynamic perturbations in the pathophysiologic processes that lead to kidney injury in diabetes. We propose that an auto-maintaining mechanism of hemodynamic perturbations and increased tissue angiotensin II may be involved in the initiation and maintenance of a loop in which transforming growth factor β1 and Glut-I upregulation play important roles in the pathophysiology of diabetic-induced kidney lesions. The understanding of the molecular mechanisms that link glomerular hypertension and excessive glucose metabolism may provide insight into new therapeutic strategies for the treatment of diabetic renal disease.

UR - http://www.scopus.com/inward/record.url?scp=33646067742&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33646067742&partnerID=8YFLogxK

U2 - 10.1007/s11906-006-0044-5

DO - 10.1007/s11906-006-0044-5

M3 - Article

VL - 8

SP - 79

EP - 83

JO - Current Hypertension Reports

JF - Current Hypertension Reports

SN - 1522-6417

IS - 1

ER -