REPRODUCTIVE ENDOCRINOPATHY IN ACUTE STREPTOZOTOCIN-INDUCED DIABETIC MALE RATS - STUDIES ON LHRH

Citation
Rw. Clough et al., REPRODUCTIVE ENDOCRINOPATHY IN ACUTE STREPTOZOTOCIN-INDUCED DIABETIC MALE RATS - STUDIES ON LHRH, ENDOCRINE, 8(1), 1998, pp. 37-43
Citations number
27
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
1355008X
Volume
8
Issue
1
Year of publication
1998
Pages
37 - 43
Database
ISI
SICI code
1355-008X(1998)8:1<37:REIASD>2.0.ZU;2-P
Abstract
Streptozotocin-(STZ) treated diabetic male rats have significant repro ductive endocrinopathy. To determine the functional responsiveness of luteinizing hormone-releasing hormone (LHRH) neurons in STZ-treated di abetic male rats, stimulated LHRH release was assessed using hypothala mi from short-term STZ-treated, STZ-treated insulin-replaced, and cont rol male rats. LHRH release from control, STZ-treated, and STZ-treated , insulin-replaced explants in response to an initial and second 30-mi n pulse of phenylephrine were not different. A terminal pulse, contain ing 45 mM KCI, a general secretogogue, also revealed no differences be tween groups in stimulated LHRH release. Glucose and testosterone leve ls in the controls and the diabetic rats were significantly different. Cell counts on serial brain sections processed for LHRH immunohistoch emistry suggested that the number of LHRH neurons in the preoptic area r (POA) and septal areas were not different between control and STZ-tr eated rats. Thus, the short-term STZ-treated rats of this study were d iabetic, and they displayed associated endocrinopathy; however, explan ts obtained from control and STZ-treated rats exhibited a typical LHRH responsiveness to both phenylephrine and KCI, and appeared similar in LHRH neuron number. Therefore, these findings suggest that reproducti ve endocrinopathy accompanying short-term STZ-induced diabetes in male rats does not result from deficiency in LHRH neurons per se.