Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Anderson, J. E.
Right arrow Articles by Thliveris, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Anderson, J. E.
Right arrow Articles by Thliveris, J. A.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 36, Issue 10 1104-1110, Copyright © 1987 by American Diabetes Association

ARTICLES

Primary hypoandrogenism in experimental diabetes in the Long-Evans rat

JE Anderson, D Jones, SB Penner and JA Thliveris
Department of Anatomy, University of British Columbia, Vancouver, Canada.

The hormonal milieu of the testis was examined in streptozocin-induced diabetic (STZ-D) adult male Wistar and Long-Evans rats. Serum testosterone, creatinine, and urea nitrogen (BUN) levels and blood glucose concentrations were determined in diabetic and control Wistar rats (experiment 1). These parameters plus luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were studied in experiments 2 and 3 with Long-Evans rats in untreated diabetic, control, insulin-treated diabetic, nondiabetic STZ-injected, and semistarved groups. Wistar diabetic rats had significantly decreased serum testosterone and increased blood glucose, BUN, and serum creatinine compared with controls. Several findings in Long-Evans rats suggested the existence of a primary Leydig cell defect in steroidogenesis during untreated diabetes that was completely or partially compensated for by increased pituitary gonadotropin secretion. Serum LH and FSH levels increased in Long-Evans diabetic rats. Serum testosterone was significantly reduced only in experiment 2. These hormonal alterations from control levels were not seen in insulin-treated diabetic animals. Semistarved animals, weight matched to the diabetic group in experiment 2, had significantly decreased serum testosterone and increased FSH levels. In addition, Long-Evans diabetic rat BUN and serum creatinine levels increased much less or were unchanged from control values compared with the increase noted in diabetic Wistar rats. In light of the hypogonadism that complicates clinical uremia, these findings suggest the more apt use of the Long-Evans strain rather than the Wistar strain in the study of STZ-D hypogonadal function.(ABSTRACT TRUNCATED AT 250 WORDS)
Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1987 by the American Diabetes Association.