AQP1 expression in the proximal tubule of diabetic rat kidney
Erika A. Seyahian,
Leornardo Cacciagiu,
Alicia E. Damiano,
Elsa Zotta
Affiliations
Erika A. Seyahian
Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO)- CONICET- Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina; Cátedra de Fisiopatología, Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina
Leornardo Cacciagiu
Hospital Cesar Milstein - Laboratorio Central- Sección Química Clínica, Buenos Aires, Argentina
Alicia E. Damiano
Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO)- CONICET- Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina; Cátedra de Biología Celular y Molecular, Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina
Elsa Zotta
Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO)- CONICET- Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina; Cátedra de Fisiopatología, Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina; Corresponding author.
Polyuria is a hallmark symptom and the first clinical manifestation of diabetes mellitus (DM). The glucose that remains in renal tubules was proposed to produce an osmotic effect resulting in polyuria. Although water is reabsorbed in proximal tubules through an aquaporin-1 (AQP1) dependent mechanism, AQP1 role in the genesis of polyuria is unknown. AQP1 expression was studied in a rat model of Type-1 DM at 15-days and 5-months of evolution. A different AQP1 expression pattern was found in both experimental groups, with no changes in AQP1 localization, suggesting that changes in AQP1 may be involved in the development of polyuria.
