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Differential effects of diabetes induced by streptozotocin and that develops spontaneously on prostate growth and molecular responses to insulin in BB rats
Author(s) -
Yono Makoto,
Yoshida Masaki,
Ueda Shoichi,
Weiss Robert M,
Latifpour Jamshid
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a434-a
Subject(s) - streptozotocin , medicine , diabetes mellitus , endocrinology , insulin , gene expression , microarray , microarray analysis techniques , gene , biology , biochemistry
We investigated molecular responses to insulin treatment in spontaneous and streptozotocin (STZ)‐induced diabetic rat prostates using microarray and real‐time RT‐PCR. We maintained diabetes prone BB (BBDP/Wor), STZ‐injected diabetes resistant BB (BBDR/Wor) and their age matched control (BBDR/Wor) rats for 32 weeks. Each diabetic group received either sufficient amounts of insulin (euglycemic groups) or suboptimal doses of insulin (hyperglycemic groups). A significant decrease in the weight of ventral prostate was observed in hyperglycemic STZ‐induced diabetic rats which received suboptimal dose of insulin. Microarray analysis revealed that the gene expression profiles of BBDP/Wor and STZ‐induced diabetic rats were distinctly different in each region of the prostate, and that hyperglycemic diabetes in both diabetic rat groups caused differential changes in the expression levels of 856 genes, of which 35 were related to cell growth, proliferation and death. RT‐PCR data verified significant differences in the mRNA expression levels of Igfbp6, Tieg and Clu between euglycemic and hyperglycemic groups, whereas expression levels of these genes in control and euglycemic groups were not significantly different. Our data demonstrate that the diabetes induced by STZ in the BBDR/Wor rats affects prostate growth and the molecular response to insulin differently than that observed in BBDP/Wor rats that develop diabetes spontaneously. Supported by NIH grants DK 38311 and DK 42530.