Fertility of the Streptozotocin-Diabetic Male Rat

Gp, Frenkel; Zt, Homonnai; Drasnin, N.; Sofer, A; Kaplan, R.; Pf, Kraicer

doi:10.1111/j.1439-0272.1978.tb01327.x

Cited by 43 publications

(21 citation statements)

References 23 publications

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“…The severity of diabetes and its complications were reflected in the testis metabolome, where, though all diabetic mice exhibited abnormal metabolic profiles, the severity of the abnormality was likely to be exacerbated by low body weight and overall physical well being. As has previously been shown, STZ treatment did not result in sufficient beta-cell destruction for diabetes to develop in all mice (Frenkel et al, 1978). Although there is weak GLUT2 expression in the mouse testis (Kokk et al, 2004), STZ does not appear to influence the testis directly.…”

Section: Metabolomics Of the Stz Diabetic Mouse Testismentioning

confidence: 67%

Metabolic profile changes in the testes of mice with streptozotocin‐induced type 1 diabetes mellitus

et al. 2009

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Contrary to the traditional view, recent studies suggest that diabetes mellitus has an adverse influence on male reproductive function. Our aim was to determine the effect of diabetes on the testicular environment by identifying and then assessing perturbations in small molecule metabolites. Testes were obtained from control and streptozotocin-induced diabetic C57BL/6 mice, 2, 4 and 8 weeks post-treatment. Diabetic status was confirmed by glycated haemoglobin, non-fasting blood glucose, physiological condition and body weight. A novel extraction procedure was utilized to obtain protein free, low-molecular weight, water soluble extracts which were then assessed using (1)H nuclear magnetic resonance spectroscopy. Principal component analysis of the derived profiles was used to classify any variations, and specific metabolites were identified based on their spectral pattern. Characteristic metabolite profiles were identified for control and type 1 diabetic animals with the most distinctive being from mice with the largest physical deterioration and loss of body weight. Eight streptozotocin-treated animals did not develop diabetes and displayed profiles similar to controls. Diabetic mice had decreases in creatine, choline and carnitine and increases in lactate, alanine and myo-inositol. Betaine levels were found to be increased in the majority of diabetic mice but decreased in a few animals with severe loss of body weight and physical condition. The association between perturbations in a number of small molecule metabolites known to be influential in sperm function, with diabetic status and physiological condition, adds further impetus to the proposal that diabetes influences important spermatogenic pathways and mechanisms in a subtle and previously unrecognized manner.

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Section: Metabolomics Of the Stz Diabetic Mouse Testismentioning

confidence: 67%

Metabolic profile changes in the testes of mice with streptozotocin‐induced type 1 diabetes mellitus

et al. 2009

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“…From early in its use as an experimental model of DM, studies have reported on the decreased fertility of the STZ treated male rodent (Frenkel et al. , 1978; Paz et al.…”

Section: Discussionmentioning

confidence: 99%

“…Streptozotocin treatment does not always result in sufficient beta‐cell destruction for diabetes to develop (Frenkel et al. , 1978).…”

Section: Discussionmentioning

confidence: 99%

Differences in mouse models of diabetes mellitus in studies of male reproduction

et al. 2010

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Diabetes Mellitus (DM) has been found to have subtle yet profound effects on the metabolic status of the testis, the expression of numerous spermatogenic genes and is associated with increased numbers of sperm with nuclear DNA damage. The precise mechanism causing these detrimental effects remains unknown. The presence of increased levels of the most prominent member (carboxymethyllysine - CML) of the advanced glycation end product adducts and their receptor (RAGE) in the reproductive tract of DM men has provided a new avenue for research. As there are suspicions that the antibiotic (streptozotocin - STZ) employed to induce DM is also capable of causing oxidative stress and DNA damage, we compared CML and RAGE levels in the reproductive tract and sperm nDNA status of STZ mice with the levels in the Ins(2Akita) mouse to determine which more closely mimics the situation described in the human diabetic. CML was observed in the testes, epididymes and sperm of all animals. Sperm from DM mice showed particularly strong CML immunolocalization in the acrosomal cap, the equatorial region and whenever present, cytoplasmic droplets. Although increased, the level of CML on the sperm of the STZ and Ins(2Akita) DM mice did not reach statistical significance. RAGE was present on the developing acrosome and epididymal sperm of all animals and in discrete regions of the epididymes of the DM models. Only the epididymal sperm of the Ins(2Akita) mice were found to have significantly increased (p < 0.0001) nDNA damage. The Ins(2Akita) mouse therefore appears to more accurately reflect the conditions found in the human and, as such, is a more representative model for the study of diabetes and glycation's influence on male fertility.

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“…The decrease in epithelial-stromal interaction certainly predisposes this gland in diabetic mice to be a prostate disease target. seminal fluid (Frenkel et al 1978;Mcculloch et al 1984). Cagnon et al (2000) and Ribeiro et al (2006) verified atrophied secretory cells, stromal hypertrophy, inflammatory processes, prostatic intraepithelial neoplasia and dilated secretory organelles in the ventral lobe of the prostate in non-obese diabetic mice.…”

Section: Discussionmentioning

confidence: 95%

“…Different experimental studies in the male reproductive system, which exhibited type 1 diabetes mellitus because of either chemical induction or spontaneous development presented retrograde ejaculation (Ellemberg 1980), urinary bladder dysfunction (Buck et al. 1976; Stefan 1996), sexual impotence and decreased spermatozoid number in the seminal fluid (Frenkel et al. 1978; Mcculloch et al.…”

mentioning

confidence: 99%

Dystroglycan patterns on the prostate of non‐obese diabetic mice submitted to glycaemic control

Cagnon

Fávaro

2009

Int J Experimental Path

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Dystroglycan (DG) is an adhesion protein which plays a crucial role in the maintenance of tissue integrity. Diabetes has been pointed out as a disease which causes harmful effects on prostate function. Therefore, the main objective of this work was to verify DG distribution and structure features in diabetic mice with and without glycaemic control and to relate these parameters to prostate pathogenesis. Thirty mice (Nod and BALB/c) were divided into three groups after 20 days of diabetic state: the control group received a 5 ml/kg dose of physiological saline daily for 20 days; the diabetic group had the same treatment as the control group; the diabetic-insulin group received 4-5 IU doses of Neutral Protamine Hagedorn (NPH) insulin daily for 20 days. After 20 days of treatment, all animals were killed and samples from the ventral prostate were processed for immunological and light microscopy analyses. The results showed diminished beta- and alpha-DG receptors in the diabetic group. However, there was a recovery of both beta-and alpha-DG receptor immunolocalization after insulin administration. Epithelial and stromal morphological changes were verified in the diabetic group, which also presented recovery after insulin treatment. Thus, it could be concluded that diabetes disturbed prostate structure integrity and altered the occurrence of alpha and beta-DG receptors, indicating decreased cell-matrix extracellular and cell-basal membrane attachment. However, insulin treatment could partially restore glandular homeostasis. The decrease in epithelial-stromal interaction certainly predisposes this gland in diabetic mice to be a prostate disease target.

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Fertility of the Streptozotocin-Diabetic Male Rat

Cited by 43 publications

References 23 publications

Metabolic profile changes in the testes of mice with streptozotocin‐induced type 1 diabetes mellitus

Metabolic profile changes in the testes of mice with streptozotocin‐induced type 1 diabetes mellitus

Differences in mouse models of diabetes mellitus in studies of male reproduction

Dystroglycan patterns on the prostate of non‐obese diabetic mice submitted to glycaemic control

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