This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Liu, Y.-J. Articles by Ohzeki, T. Search for Related Content PubMed PubMed Citation Articles by Liu, Y.-J. Articles by Ohzeki, T. Pubmed/NCBI databases Gene GEO Profiles HomoloGene Protein UniGene Compound via MeSH Substance via MeSH Medline Plus Health Information Diabetes Type 1 Hazardous Substances DB STREPTOZOTOCIN

(Hypertension. 1998;31:885-889.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Gene Expression of 11ß-Hydroxysteroid Dehydrogenase Type 1 and Type 2 in the Kidneys of Insulin-Dependent Diabetic Rats

Yan-Jun Liu; Yuichi Nakagawa; ; Takehiko Ohzeki

From the Department of Pediatrics, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Correspondence to Yan-Jun Liu, Department of Pediatrics, Hamamatsu University School of Medicine, 3600 Handa-Cho, Hamamatsu 431–31, Japan.

Abstract—The presence of 11ß-hydroxysteroid dehydrogenase (11ß-HSD) activity in the kidney has been suggested to be important in the regulation of glucocorticoid-induced disorders of electrolyte balance and the control of blood pressure. To assess the possible effect of 11ß-HSD isoforms in diabetes-related hypertension, we measured the mean systolic blood pressure and the 11ß-HSD activity and mRNA levels for both 11ß-HSD1 and 11ß-HSD2 in the kidney of streptozotocin (STZ)-diabetic female rats. Three weeks after injection of STZ (65 mg/kg), the mean systolic blood pressure of diabetic rats was elevated 13.6% above that of normal rats (P<.01). The renal 11ß-HSD2 activity and level of mRNA expression were significantly decreased in diabetic rats (P<.01). However, the treatment of rats with STZ did not decrease the levels of renal 11ß-HSD1 activity and mRNA expression in diabetic rats. Insulin administered subcutaneously to diabetic rats for 2 weeks completely reversed the decrease in renal 11ß-HSD2 activity and gene expression and prevented the elevation in blood pressure in the diabetic rat. These results indicate that alteration of renal 11ß-HSD2 activity and gene expression may be primarily responsible for the changes in blood pressure of STZ-diabetic rats after early treatment with insulin.

Key Words: 11ß-hydroxysteroid dehydrogenase • streptozotocin • diabetes mellitus • kidney • blood pressure • insulin

This article has been cited by other articles:

				Y. Liu, Y. Nakagawa, Y. Wang, L. Liu, H. Du, W. Wang, X. Ren, K. Lutfy, and T. C Friedman Reduction of hepatic glucocorticoid receptor and hexose-6-phosphate dehydrogenase expression ameliorates diet-induced obesity and insulin resistance in mice J. Mol. Endocrinol., August 1, 2008; 41(2): 53 - 64. [Abstract] [Full Text] [PDF]

				Y. Liu, Y. Nakagawa, Y. Wang, R. Sakurai, P. V. Tripathi, K. Lutfy, and T. C. Friedman Increased Glucocorticoid Receptor and 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Expression in Hepatocytes May Contribute to the Phenotype of Type 2 Diabetes in db/db Mice Diabetes, January 1, 2005; 54(1): 32 - 40. [Abstract] [Full Text] [PDF]

				Y. Liu, Y. Nakagawa, Y. Wang, R. Li, X. Li, T. Ohzeki, and T. C. Friedman Leptin Activation of Corticosterone Production in Hepatocytes May Contribute to the Reversal of Obesity and Hyperglycemia in Leptin-Deficient ob/ob Mice Diabetes, June 1, 2003; 52(6): 1409 - 1416. [Abstract] [Full Text] [PDF]