Gonadotropins, testosterone and prolactin in men with abnormal semen findings and an evaluation of the hormone profile

Abramsson, Leif; Duchek, M.

doi:10.1007/bf02549588

Cited by 13 publications

(8 citation statements)

References 21 publications

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“…Meanwhile, although histological evidence suggests severe erosion of testicular interstitium, which was most pronounced in the group co‐exposed to hyperglycaemia and Al, serum T levels was slightly higher, in contrast to significantly lowered serum FSH in all treated groups compared with controls. Such inverse relationship between serum T and FSH had been reported to indicate testicular lesion in human males with azoospermia (Abramsson & Duchek, ). Moreover, although serum LH levels were not assayed in the current study, it is presumed that combined exposure to chronic hyperglycaemia and Al would result in low serum LH as obtained for serum FSH.…”

Section: Discussionmentioning

confidence: 61%

“…Streptozotocin‐induced hyperglycaemia and exposure to oral Al (at 250 ppm) either separately or simultaneously, resulted in lowered serum FSH, and elevated serum oestradiol and testosterone (T) levels compared with the controls. Elevation of serum oestradiol in rats with STZ‐induced hyperglycaemia, Al toxicity or both could be responsible for the reduced serum FSH levels in these animals, as inverse relationship is known to exist between serum FSH and oestradiol (Abramsson & Duchek, ). It is noteworthy that (STZ‐induced) hyperglycaemia had more pronounced suppressing effects on serum FSH than did Al toxicity.…”

Section: Discussionmentioning

confidence: 99%

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Combined effects of chronic hyperglycaemia and oral aluminium intoxication on testicular tissue and some male reproductive parameters in Wistar rats

et al. 2015

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Exposure to either environmental toxicants or chronic hyperglycaemia could impair male reproductive function. However, the extent to which exposure to such toxicants, in the presence of pre-existing metabolic dysfunction, could affect male reproduction is unclear. Streptozotocin-induced diabetic Wistar rats (12 weeks old) were exposed to oral aluminium chloride at 250 ppm for 30 days; followed by evaluation of caudal epididymal sperm count and motility, assay for serum follicle stimulating hormone (FSH), testosterone (T) and oestradiol; and assessment of testicular histology. Moreover, blood glucose was evaluated by the glucose oxidase method. In rats treated with streptozotocin (STZ) or aluminium (Al) alone, erosion of testicular parenchyma and stroma was observed. This effect was most severe in diabetic rats simultaneously exposed to Al; coupled with reduced caudal epididymal sperm count that was least in this (STZ+Al) group (18.75 × 10(6) ml(-1) ) compared with controls (61.25 × 10(6) ml(-1) ; P < 0.05), STZ group or Al group. Moreover, these reproductive perturbations (in the STZ+Al group) were associated with reduced sperm motility and significantly reduced serum FSH (P < 0.05); but elevated serum T and oestradiol (P < 0.05), compared with control. These suggest that diabetes-induced testicular lesion is exacerbated by simultaneous oral Al toxicity in Wistar rats.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Combined effects of chronic hyperglycaemia and oral aluminium intoxication on testicular tissue and some male reproductive parameters in Wistar rats

et al. 2015

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“…In the absence of adequate production of LH or testosterone, spermatogenesis ceases. In addition, if LH andlor testosterone fail to be produced in appropriate, inversely related quantities, spermatogenesis is compromised and potency (the ability to maintain an erection) declines in direct proportion to the deficit involved (Abramasson and Ducheck, 1989;Giagulli and Vermeulen, 1988;Jockenhovel et al, 1989). The concentrations of testosterone within the testes produced by the Leydig cells under LH stimulation are several orders of magnitude higher than in the peripheral circulation, a fact that forms the basis of the development of testosterone-based male contraceptives.…”

Section: Spermatogenesismentioning

confidence: 99%

Reproductive ecology of human males

Leslie

1995

Am. J. Phys. Anthropol.

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Recent demonstrations that female reproductive physiology is highly responsive to environmental factors have led to a growing appreciation of the extent of variation in reproductive function and the adaptive nature of much of that variation. Male reproductive function has received much less attention from anthropologists, whether as an aspect of human variation, as a possible contributor to population variation in fertility, or as the product of selective pressures. Yet, an understanding of male reproductive function, along with that of females, is obviously important for a complete picture of human evolutionary ecology. We review our current understanding of male reproductive function, its response to environmental factors, and implications for male fecundity. Studies among Western populations indicate that male reproductive function is sensitive to environmental stresses, including weight loss, dietary composition, exercise, disease, and psychological stress. Indices of reproductive physiology among males in some non-Western populations are consistent with the notion that chronic environmental stresses can lead to suppression of testicular function. The specific causes of this suppression are not known, nor are the implications, if any, for male fecundity and fertility understood. Further research on males is called for, including the effects of hormonal changes on reproductive behavior and characterization of reproductive function in a wider range of populations. Evolutionary models of the selection pressures underlying male reproductive function should be helpful in focusing these investigations. Despite initial skepticism, recent work in the reproductive ecology of females has demonstrated convincingly that environmental circumstances can have a significant impact on reproductive function (see Ellison [1991, 19941 for a recent comprehensive review). In contrast, the effect of ecological factors on male reproductive function has barely been explored. There is substantial evidence from Western populations (reviewed in the following sections) that testicular function can be suppressed by exercise, weight loss, diet, and psychological stress. Furthermore, testicular function in some anthropological populations is suppressed or truncated compared to that of Western populations (Bentley et al., 1993;KL Campbell, 1994;Christiansen, 1991;Ellison et al., 1989). Yet we remain largely ignorant of the impact of environmental factors on reproductive function among males in non-Western populations.The lack of attention to male reproductive ecology stems from a long-standing orientation toward females in demographic studies of fertility, justified by the observation that women are much more likely than men to be the limiting factor in fertility. In addition, two-sex models of fertility or population replacement were 0 1995 Wiley-Liss, Inc.

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“…GH dose had no effect on the LS mean (Ϯ se) rate of increase of TV (in ml/yr) between the 0.24 and 0.37 mg/kg⅐wk dose groups (3.5 Ϯ 0.3 vs. 3.6 Ϯ 0.3, respectively; P ϭ 0.9). TV of at least 15 ml, the estimated critical volume required for normal adult testicular function (22)(23)(24), was achieved at a median age (in years) of 16.7 (95% CI, 15.5-17.2) in boys receiving 0.24 mg/kg⅐wk GH vs. 15.6 (95% CI, 15.0 -16.2) in boys receiving 0.37 mg/kg⅐wk GH. In boys who were on study throughout puberty, there was no significant difference between the 0.24 and 0.37 mg/kg⅐wk dose groups in final TV (in ml) (17.7 Ϯ 5.0 vs. 16.9 Ϯ 5.4, respectively; P ϭ 0.7).…”

Section: Tsmentioning

confidence: 99%

Effect of Growth Hormone Dose on Bone Maturation and Puberty in Children with Idiopathic Short Stature

Crowe¹,

Rekers-Mombarg²,

Robling³

et al. 2006

The Journal of Clinical Endocrinology & Metabolism

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Context: GH at 0.22 mg/kg⅐wk has been shown to have no effect on pubertal onset or pace, whereas GH at 0.5 mg/kg⅐wk has been shown to advance pubertal onset and bone maturation.Objectives: Our objectives were to determine whether 0.37 mg/kg⅐wk GH advanced pubertal onset, pace, or bone maturation relative to 0.24 mg/kg⅐wk GH; whether 0.37 mg/kg⅐wk GH led to pubertal onset at an inappropriately early age; and whether age at start of GH therapy influenced pubertal onset. Design:We conducted a randomized, open-label study to final height. Patients:We studied children with idiopathic short stature.Intervention: Patients were treated with 0.24 mg/kg⅐wk, 0.24 increasing to 0.37 mg/kg⅐wk, or 0.37 mg/kg⅐wk. Main Outcome Measures:We assessed age at pubertal onset and rates of bone maturation, Tanner stage development, and increase in testicular volume (boys only).Results: For the primary comparison between the 0.24 and 0.37 mg/kg⅐wk dose groups, median ages of pubertal onset (in years) were similar (13.7 vs. 13.5 for boys and 11.7 vs. 11.4 for girls) and were greater than those for the general population for each sex. Age at start of GH therapy did not appear to influence pubertal onset for either sex. Rates of pubertal pace and bone maturation were not significantly different between the 0.24 and 0.37 mg/kg⅐wk dose groups for either sex.Conclusion: GH at 0.37 mg/kg⅐wk does not appear to accelerate pubertal onset, pace, or bone maturation compared with GH at 0.24 mg/kg⅐wk in patients with idiopathic short stature. From a clinical standpoint, our results suggest that the approved dose range of up to 0.37 mg/kg⅐wk GH does not lead to pubertal onset at an inappropriately early age. between GH activity and pubertal timing. Before GH treatment became available, marked delays in pubertal onset were observed in children with isolated GH deficiency (1). Additionally, pubertal delays of 3-7 yr are observed in children with GH insensitivity (2).Randomized controlled studies of recombinant human GH (somatropin) treatment of patients with idiopathic short stature (ISS) have yielded differing results regarding the influence of GH on pubertal onset, pubertal pace, and bone maturation. Although Leschek et al. (3) demonstrated no effect on pubertal onset or pace in boys who began low-dose (0.22 mg/kg⅐wk) GH at a mean age of 12 yr, Kamp et al. (4) demonstrated acceleration of pubertal onset and bone maturation by approximately 1 yr in boys and girls who began high-dose (0.5 mg/kg⅐wk) GH at a mean age of 8 yr. These results suggest that the influence of GH on pubertal timing and bone maturation may be dose-dependent. Thus, based on the current literature, decisions regarding GH dosing are limited by uncertainty as to which doses between 0.22 and 0.5 mg/kg⅐wk might accelerate puberty and bone maturation in patients with ISS.We tested the influence of GH dose on pubertal onset, pubertal pace, and bone maturation during a randomized, open-label study to final height in patients with ISS (mean age, 9.8 yr) randomized to one of three GH dose...

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Gonadotropins, testosterone and prolactin in men with abnormal semen findings and an evaluation of the hormone profile

Cited by 13 publications

References 21 publications

Combined effects of chronic hyperglycaemia and oral aluminium intoxication on testicular tissue and some male reproductive parameters in Wistar rats

Combined effects of chronic hyperglycaemia and oral aluminium intoxication on testicular tissue and some male reproductive parameters in Wistar rats

Reproductive ecology of human males

Effect of Growth Hormone Dose on Bone Maturation and Puberty in Children with Idiopathic Short Stature

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