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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0424v1 200/1/53    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kirino, Y. Articles by Nakahori, Y. Search for Related Content PubMed PubMed Citation Articles by Kirino, Y. Articles by Nakahori, Y.

Y Kirino, Department of Human Genetics and Public Health, Institute of Health Biosciences, The University of Tokushima Graduate School, Japan, Tokushima, 770-8503, Japan
Y Sato, Department of Human Genetics and Public Health, Institute of Health Biosciences, The University of Tokushima Graduate School, Japan, Tokushima, Japan
T Kamimoto, Department of Clinical Pharmacy, Institute of Health Biosciences, The University of Tokushima Graduate School, Japan, Tokushima, Japan
K Kawazoe, Tokushima, Japan
K Minakuchi, Tokushima, Japan
Y Nakahori, Tokushima, Japan

Correspondence: Yasushi Kirino, Email: kirino{at}clin.med.tokushima-u.ac.jp

Abstract

We examined the roles of dipeptidyl peptidase IV (DPP IV) in the development of diabetes, dyslipidaemia and renal dysfunction induced by streptozotocin (STZ). F344/DuCrlCrlj rats, which lack DPP IV activity, and wild-type rats were treated with STZ. Plasma DPP IV activity and biochemical parameters were measured until 42 days after STZ treatment. At the end of the experiment, renal function and DPP IV expressions of the kidney, liver, pancreas and adipose tissues were determined. Increases in blood glucose, cholesterol and triglycerides were evoked by STZ in both rat strains; however, the onset of hyperglycaemia was delayed in DPP IV-deficient rats as compared to wild-type rats. In contrast, more severe dyslipidaemia was observed in DPP IV-deficient rats than in wild-type rats after STZ treatment. Plasma DPP IV activity increased progressively with time after STZ treatment in wild-type rats. The kidney of wild-type rats showed decreased DPP IV activity with increased DPP IV mRNA after STZ treatment. In addition, kidney weight, serum creatinine and excreted amounts of urinary protein, glucose and DPP IV enzyme were enhanced by STZ. DPP IV-deficient rats showed increased serum creatinine in accordance with decreased creatinine clearance as compared to wild-type rats after STZ treatment. In conclusion, plasma DPP IV activity increased after STZ treatment, positively correlating to blood glucose. DPP IV-deficient rats were resistant to developing diabetes, while susceptible to dyslipidaemia and reduction of glomerular filtration rate by STZ. DPP IV activation may be responsible for hyperglycaemia, lipid metabolism and preservation of renal function.