Sexual Disturbances in the Male Diabetic Rat

Foglia, V. G.; Rosner, Jorge M.; Ramos, Mirta Cattaneo de Peralta; Lema, Baltasar

doi:10.1055/s-0028-1095155

Cited by 48 publications

(26 citation statements)

References 4 publications

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“…Some reports in adult rats have suggested a primary testicular disorder as the cause of these alterations [5]. In patients suffering chronic renal failure, an impaired conversion of A to T secondary to low plasma Zn has been reported [13].…”

Section: Discussionmentioning

confidence: 99%

Low Plasma Zinc and Androgen in Insulin-Dependent Diabetes Mellitus

Arreola¹,

Paniagua²,

Herrera

et al. 1986

Archives of Andrology

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Plasma zinc and pituitary and testicular hormone concentrations were measured in two groups of male adolescents. One group comprised insulin-dependent diabetes mellitus patients, aged 14-19 years; the other, as control, included 12 healthy youngsters aged 13-19 years. Plasma concentration of zinc, prolactin, testosterone, and dihydrotestosterone were lower in diabetics than in controls, whereas the ratios of androstenedione and androstenedione to testosterone + dihydrogtestosterone were higher.Plasma FSH and LH were normal. These results suggest a diminished conversion of androstenedione to testosterone and relate zinc with the 17-0-hydroxysteroid dehydrogenase enzyme activity.

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Section: Discussionmentioning

confidence: 99%

Low Plasma Zinc and Androgen in Insulin-Dependent Diabetes Mellitus

Arreola¹,

Paniagua²,

Herrera

et al. 1986

Archives of Andrology

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“…Diabetes-associated reproductive dysfunction has been attributed both to alternations in hypothalamo-pituitary and pituitary gonadal activity. Typically, diabetes in the male rat is associated with a decrease in circulating LH (3,8,26) and testosterone (24, 26) levels which undoubtedly account for the : reported reduction in or absence of spermatogenesis (28, 31) and reduction in accessory sex organ weights (7,9,21). A 5HT mechanism within the POA-AH has been implicated as a major regulatory factor in the control of LH secretion in the male rat (17).…”

Section: Discussionmentioning

confidence: 99%

“…They were unable to determine whether the locus for the androgen nonresponsiveness in these diabetic animals is the pituitary gland or hypothalamus. However, other investigators have reported that pituitary gonadotrophin secretion in STZ-induced diabetic rats responds normally to GnRH stimulation (8,22) suggesting that diabetes adversely affects hypothalamic GnRH dis--' _ 60'i . charge.…”

Section: Discussionmentioning

confidence: 99%

<b>REDUCED HYPOTHALAMIC SEROTONIN SYNTHESIS AND SERUM LUTEINIZING HORMONE LEVELS IN STREPTOZOTOCIN-DIABETIC MALE </b><b>RATS </b>

King¹,

Rohrbach

Miller³

et al. 1987

Biomed. Res.

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Infertility is a common sequela to experimentally-induced diabetes mellitus in the male rat as well as to diabetes in the human male. This has been attributed both to alterations in hypothalamo-pituitary and pituitary-testicular activity. In view of the role of serotonin in the hypothalamic regulation of luteinizing hormone secretion, we determined the effects of streptozotocin-induced diabetes on hypothalamic serotonin synthesis relative to circulating levels of luteinizing hormone, folliclestimulating hormone and prolactin in these animals._,Half of a group of adult male Sprague-Dawley rats were injected intraperitoneally with 16 mg-kg" of streptozotocin. The other half were injected with vehicle only. The diabetic group was hyperglycemic throughout the study period (488.7 i21.2 mg-d1""1 in diabetic rats vs. 125.1i39.3 mg-dl""' in control rats). A third group of rats served as semi-starved controls, weight-matched by total calorie restriction diet to diabetic rats. All of the rats were injected intraperitoneally with 200 mg-kg" of NSD-1015 30 min prior to sacrifice. Accumulation of 5-hydroxytryptophan in various hypothalamic areas was then assayed by liquid chromatography with electrochemical detection as a relative index for the rate of serotonin synthesis. Serum radioimmunoassayable luteinizing hormone, follicle-stimulating hormone and prolactin were also assayed in these animals. Our results show a 50% decrease in serotonin synthesis in the preoptic area-anterior hypothalamus and mediobasal hypothalamus-median eminence 16 weeks after streptozotocin treatment. We also found that serotonin synthesis was inhibited 4 weeks after streptozotocin treatment in the preoptic area-anterior hypothalamus, but not in the mediobasal hypothalamus-median eminence, indicating region-specificity in the early hypothalamic response to streptozotocin-induced diabetes. Serum luteinizing hormone levels were decreased both 4 and 16 weeks after streptozotocin treatment. No changes either in hypothalamic serotonin synthesis or in serum luteinizing hormone levels were observed 1 week after streptozotocin treatment. Serum follicle-stimulating hormone and prolactin levels remained unaffected by streptozotocin treatment throughout the study period. The differential effect of diabetes on the gonadotropins may represent further evidence for the hypothesis of differential regulatory mechanisms governing the secretion of these two hormones and further emphasizes the pathophysiologicalspecif1city(i.e., not a generalized metabolic disturbance effect) of diabetes-induced male reproductive neuroendocrinopathy. Our study suggests, at least in part, an explanation for such pathological interaction, namely, diabetic inhibition of a region-specific neurotransmitter system integral to hypothalamic regulation of luteinizing hormone secretion.

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“…Withdrawal of insulin during the middle 12 h of conditioning had no significant effect on the quantities of brain cell nuclear estrogen receptors. These results are in agreement with the hypothesis that decreased cell nuclear binding of estradiol by neural target tissues may contribute to the reproductive dysfunctions of diabetics.Impairments of reproductive function as sociated with diabetes mellitus have been doc umented in human beings [10,23] and labora tory animals of both sexes [9,15]. Female rats, made diabetic by subtotal (95%) pancreatec tomy or by selective destruction of pancreatic /(-cells following alloxan or streptozotocin ad ministration, show a variety of reproductive deficits including delayed sexual maturity [15], altered estrous cycles [4,8,16], diminished…”

mentioning

confidence: 99%

Insulin Withdrawal Impairs Sexual Receptivity and Retention of Brain Cell Nuclear Estrogen Receptors in Diabetic Rats

Li¹,

Gn²

1979

Neuroendocrinology

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Acute withdrawal of exogenous insulin significantly impairs estradiol and progesterone-induced sexual receptivity and retention of brain cell nuclear estrogen receptors in ovariectomized (OVX), streptozotocin-diabetic rats. Insulin withdrawal for 18-24 h of a 24 h estradiol benzoate (EB)-conditioning period resulted in significant reductions in mean lordosis ratings. Omission of insulin for any 12 h period during EB conditioning was without effect on sexual receptivity. 24 h insulin deprivation resulted in a significant reduction of cell nuclear estrogen receptor levels in hypothalamus-preoptic area of rats sacrificed 26 h after EB administration. Withdrawal of insulin during the middle 12 h of conditioning had no significant effect on the quantities of brain cell nuclear estrogen receptors. These results are in agreement with the hypothesis that decreased cell nuclear binding of estradiol by neural target tissues may contribute to the reproductive dysfunctions of diabetics.

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Sexual Disturbances in the Male Diabetic Rat

Cited by 48 publications

References 4 publications

Low Plasma Zinc and Androgen in Insulin-Dependent Diabetes Mellitus

Low Plasma Zinc and Androgen in Insulin-Dependent Diabetes Mellitus

<b>REDUCED HYPOTHALAMIC SEROTONIN SYNTHESIS AND SERUM LUTEINIZING HORMONE LEVELS IN STREPTOZOTOCIN-DIABETIC MALE </b><b>RATS </b>

Insulin Withdrawal Impairs Sexual Receptivity and Retention of Brain Cell Nuclear Estrogen Receptors in Diabetic Rats

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