Literature DB >> 9666343

Reproductive endocrinopathy in acute streptozotocin-induced diabetic male rats. Studies on LHRH.

R W Clough1, S G Kienast, R W Steger.   

Abstract

Streptozotocin-(STZ) treated diabetic male rats have significant reproductive endocrinopathy. To determine the functional responsiveness of luteinizing hormone-releasing hormone (LHRH) neurons in STZ-treated diabetic male rats, stimulated LHRH release was assessed using hypothalami from short-term STZ-treated, STZ-treated insulin-replaced, and control male rats. LHRH release from control, STZ-treated, and STZ-treated, insulin-replaced explants in response to an initial and second 30-min pulse of phenylephrine were not different. A terminal pulse, containing 45 mM KCl, a general secretogogue, also revealed no differences between groups in stimulated LHRH release. Glucose and testosterone levels in the controls and the diabetic rats were significantly different. Cell counts on serial brain sections processed for LHRH immunohistochemistry suggested that the number of LHRH neurons in the preoptic area (POA) and septal areas were not different between control and STZ-treated rats. Thus, the short-term STZ-treated rats of this study were diabetic, and they displayed associated endocrinopathy; however, explants obtained from control and STZ-treated rats exhibited a typical LHRH responsiveness to both phenylephrine and KCl, and appeared similar in LHRH neuron number. Therefore, these findings suggest that reproductive endocrinopathy accompanying short-term STZ-induced diabetes in male rats does not result from deficiency in LHRH neurons per se.

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Year:  1998        PMID: 9666343     DOI: 10.1385/ENDO:8:1:37

Source DB:  PubMed          Journal:  Endocrine        ISSN: 1355-008X            Impact factor:   3.633


  24 in total

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Authors:  R C Kolodny; C B Kahn; H H Goldstein; D M Barnett
Journal:  Diabetes       Date:  1974-04       Impact factor: 9.461

Review 2.  Neural regulation of luteinizing hormone secretion in the rat.

Authors:  S P Kalra; P S Kalra
Journal:  Endocr Rev       Date:  1983       Impact factor: 19.871

3.  Responsiveness of immature versus adult male rat hypothalami to dibutyryl cyclic AMP- and forskolin-induced LHRH release in vitro.

Authors:  D E Hartter; V D Ramirez
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4.  Testosterone replacement fails to reverse the adverse effects of streptozotocin-induced diabetes on sexual behavior in the male rat.

Authors:  R W Steger
Journal:  Pharmacol Biochem Behav       Date:  1990-03       Impact factor: 3.533

5.  Gonadal dysfunction in diabetic men with organic impotence.

Authors:  F T Murray; H U Wyss; R G Thomas; M Spevack; A G Glaros
Journal:  J Clin Endocrinol Metab       Date:  1987-07       Impact factor: 5.958

6.  Involvement of preoptic-anterior hypothalamic GABA neurons in the regulation of pituitary LH and prolactin release.

Authors:  R Lamberts; E Vijayan; M Graf; T Mansky; W Wuttke
Journal:  Exp Brain Res       Date:  1983       Impact factor: 1.972

7.  Functional and morphological changes in mediobasal hypothalamus of streptozocin-induced diabetic rats. In vitro study of LHRH release.

Authors:  G E Bestetti; C E Boujon; M J Reymond; G L Rossi
Journal:  Diabetes       Date:  1989-04       Impact factor: 9.461

8.  Streptozotocin-induced deficits in sex behavior and neuroendocrine function in male rats.

Authors:  R W Steger; A Amador; E Lam; J Rathert; J Weis; M S Smith
Journal:  Endocrinology       Date:  1989-04       Impact factor: 4.736

Review 9.  The sexual problems of diabetic men.

Authors:  C Fairburn
Journal:  Br J Hosp Med       Date:  1981-05

10.  Some effects of experimentally-induced diabetes on pituitary-testicular relationships in rats.

Authors:  B E Howland; E J Zebrowski
Journal:  Horm Metab Res       Date:  1976-11       Impact factor: 2.936

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  3 in total

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2.  In vitro evidence of glucose-induced toxicity in GnRH secreting neurons: high glucose concentrations influence GnRH secretion, impair cell viability, and induce apoptosis in the GT1-1 neuronal cell line.

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Review 3.  Kisspeptin and KISS1R: a critical pathway in the reproductive system.

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