1. Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes.
- Author
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D'Agord Schaan B, Lacchini S, Bertoluci MC, Irigoyen MC, Machado UF, and Schmid H
- Subjects
- Albuminuria urine, Animals, Blood Glucose metabolism, Blotting, Western, Body Weight, Diabetes Mellitus, Experimental urine, Diabetic Nephropathies urine, Glucose Transporter Type 1, Kidney Cortex metabolism, Male, Monosaccharide Transport Proteins urine, Rats, Rats, Wistar, Transforming Growth Factor beta biosynthesis, Diabetes Mellitus, Experimental metabolism, Diabetic Nephropathies metabolism, Monosaccharide Transport Proteins biosynthesis, Transforming Growth Factor beta urine
- Abstract
Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). There was a positive correlation between urinary TGF-beta 1 and plasma glucose levels (r = 0.65, p < 0.05) and albuminuria (r = 0.72, p < 0.05). We concluded that 45 days of diabetes result in incipient diabetic nephropathy and increased cortical GLUT1 protein abundance. We speculate that the higher cortical GLUT1 protein levels in diabetes may amplify the effects of hyperglycemia in determining higher intracellular glucose in mesangial cells, thereby contributing to diabetes-related kidney damage.
- Published
- 2001
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