Horm Metab Res 2013; 45(11): 840-843
DOI: 10.1055/s-0033-1354381
Immediate Interest
© Georg Thieme Verlag KG Stuttgart · New York

Changes in Renal Glucose Transporters in an Animal Model of Metabolic Syndrome

A. M. Lehnen
1   Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia, Rio Grande do Sul, Brazil
2   Serviço de Endocrinologia, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Brazil
,
N. M. Leguisamo
1   Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia, Rio Grande do Sul, Brazil
,
L. D. Dias
1   Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia, Rio Grande do Sul, Brazil
,
G. H. Pinto
1   Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia, Rio Grande do Sul, Brazil
,
N. M. Okamoto
3   Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
,
U. F. Machado
3   Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
,
B. D. Schaan
1   Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia, Rio Grande do Sul, Brazil
2   Serviço de Endocrinologia, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Brazil
› Author Affiliations
Further Information

Publication History

received 04 April 2013

accepted 12 August 2013

Publication Date:
23 September 2013 (online)

Abstract

Considering the similarity between structural, hemodynamic, and functional changes of obesity-related renal disease and diabetic nephropathy, we hypothesized that renal glucose transporter changes occur in obesity as in diabetes. The aim of the work was to evaluate GLUT1 and GLUT2 in kidneys of an animal model of metabolic syndrome. Neonate spontaneously hypertensive rats (SHR), n=15/group, were treated with monosodium glutamate (5 mg/g) (MetS) for 9 days and compared with saline-treated Wistar-Kyoto (C) and SHR (H) rats. Lee index, systolic arterial pressure (SAP), glycemia, insulin resistance, triglycerides, and HDL cholesterol were evaluated at 3 and 6 months. Medullar GLUT1 and cortical GLUT2 were analyzed by Western blot. MetS vs. C and H rats had the highest Lee index (p<0.001) and insulin resistance (3-months C: 4.3±0.7, H: 3.9±0.9, MetS: 2.7±0.6; 6-months C: 4.2±0.6, H: 3.8±0.5, MetS: 2.4±0.6% · min−1, p<0.001), similar glycemia, and the lowest HDL-cholesterol at 6-months (p<0.001). In the MetS and H rats, SAP was higher vs. C at 3-months (p<0.001) and 6-months (C: 151±15, H: 190±11, MetS: 185±13 mm Hg, p<0.001) of age. GLUT1 was ̴ 13× lower (p<0.001) at 3-months, reestablishing its content at 6-months in MetS group, while GLUT2 was 2× higher (p<0.001) in this group at 6-months of age. Renal GLUT1 and GLUT2 are modulated in kidney of rats with metabolic syndrome, where obesity, insulin resistance and hypertension coexist, despite normoglycemia. Like in diabetes, cortical GLUT2 overexpression may contribute to the development of kidney disease.

 
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