Hypothalamic-hypophyseal-gonadal axis in the streptozotocin-induced diabetic male rat

Calvo, Juan; Barañao, J L; Tesone, Marta

doi:10.1016/0022-4731(84)90083-9

Cited by 24 publications

(19 citation statements)

References 21 publications

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“…Loss of ovulation in female rats made diabetic with streptozotocin has been associated with a reduction in, or lack of release of hypo thalamic gonadotropin releasing hormone (GnRH) [4,6]. Other reports have indicated that the cause of reproductive fail ure is the result of the diabetic female rats' inability to respond to GnRH [4,7], Both decreased and unaltered pituitary' release of gonadotropins after GnRH administration have been demonstrated in diabetic rats of both sexes [4,[6][7][8][9][10][11]. Similar disparate data have been reported for basal pituitary and serum gonadotropin levels in insulin-deficient rats [4,[7][8][9][10][11][12].…”

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confidence: 95%

“…Other reports have indicated that the cause of reproductive fail ure is the result of the diabetic female rats' inability to respond to GnRH [4,7], Both decreased and unaltered pituitary' release of gonadotropins after GnRH administration have been demonstrated in diabetic rats of both sexes [4,[6][7][8][9][10][11]. Similar disparate data have been reported for basal pituitary and serum gonadotropin levels in insulin-deficient rats [4,[7][8][9][10][11][12]. These al tered parameters have been largely corrected with insulin ther apy [ 13], Other studies have indicated that reduced ovarian sen sitivity to hormones is the defect responsible for the repro ductive dysfunction in untreated diabetic rats [5,14].…”

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confidence: 99%

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Diabetes-Induced Alterations of Reproductive and Adrenal Function in the Female Rat

Valdés¹,

Elkind‐Hirsch²,

Rogers³

1990

Neuroendocrinology

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Diabetes interferes with reproductive function in laboratory animals. Previous studies in female diabetic rats have not resolved if the reproductive abnormalities observed are at the hypothalamic, pituitary and/or ovarian level. The interaction of the gonadal and adrenal axes has not been studied in the diabetic female rat. The purpose of this study is twofold: first, to determine the level of dysfunction in the hypothalamic-pituitary axis caused by diabetes in the adult female rat controlling for stage of the estrous cycle, and, second, to evaluate basal coricosterone secretion in female diabetic rats. Sixty cycling 40-day-old female rats were randomly assigned to 3 groups; control (n = 32), diabetic (n = 14), and diabetic insulin-replaced animals (n = 14). The level of hyperglycemia in each group was documented by glycosylated hemoglobin levels and biweekly blood glucoses. Three weeks after induction of diabetes, pituitary luteinizing hormone (LH) responsiveness following an i.v. injection of gonadotropin-releasing hormone (GnRH) was assessed in representative diestrous rats from each group. All animals were sacrificed in either diestrus or proestrus for determination of GnRH concentration in the hypothalamus, LH and follicle-stimulating hormone (FSH) content in pituitary and LH, FSH, estradiol and corticosterone in serum. Uterine weight to body weight ratios (a bioassay for estrogen) were also calculated. Hypothalamic GnRH concentration was significantly lower in diabetic versus control diestrous rats. Basal pituitary and serum gonadotropin levels were not different between any groups. GnRH-stimulated serum LH levels were higher in diabetic vs. control and diabetic insulin-treated animals. LH surges occurred in the control and diabetic insulin-replaced but not the diabetic group. Estradiol levels and uterine weight/body weight ratios were high in control and diabetic insulin-replaced animals in proestrus, and low in untreated diabetic animals. Corticosterone levels were significantly lower in diabetic vs. control proestrous animals. The decreased GnRH concentration with normal basal pituitary function suggests that the abnormality in the hypothalamic-pituitary-ovarian axis in diabetes is at the hypothalamic level. Circulating corticosterone levels, which may impact on reproductive function, were not increased in our female diabetic rats as has been previously reported in diabetic male rats.

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confidence: 99%

Diabetes-Induced Alterations of Reproductive and Adrenal Function in the Female Rat

Valdés¹,

Elkind‐Hirsch²,

Rogers³

1990

Neuroendocrinology

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“…Sexual dysfunction is frequently associated with diabetes in men and experimental animals, and it is accepted that infertility is a common complication in diabetic men [2,5,10,16]. Diabetic rats exhibit decreased testicular weight, sperm count, sperm motility and testosterone levels, and increased frequency of abnormal spermatogenesis [6,12,13,17].…”

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confidence: 99%

Streptozotocin-Induced Diabetes Increases Apoptosis through JNK Phosphorylation and Bax Activation in Rat Testes

Koh

2007

J. Vet. Med. Sci.

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ABSTRACT. Diabetic disease is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether streptozotocin-induced diabetes increases apoptotic cell death in rat testes through activation of the JNK and Bax pathway. Diabetes was induced by a single intravenous injection of streptozotocin (40 mg/kg) and testis samples were collected after 3 months. Compared with controls, body weight and testicular weight were lower in the diabetic group, and the apoptotic index in testicular germ cells was significantly increased. Expression of phospho-JNK and Bax was significantly increased in the diabetic group, and the level of activated caspase-3 was also increased, compared to that of controls. Our findings suggest that streptozotocininduced diabetes increases apoptotic cell death in rat testes through phosphorylation of JNK and activation of Bax.

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“…Furthermore, considerable controversy exists with regard Received: May 9, 1990 Accepted after revision: November 30, 1990 to the elfect of diabetes on gonadotropin secretion in rats. It has been reported that circulating gonadotropin levels are increased [16], drastically decreased [8,II,15,17], or unchanged [14] in diabetic male rats. Irrespective of the changes in the gonadotro pin secretion, circulating testosterone (T) levels were decreased in experimentally induced diabetic animals [15][16][17] as well as in spontaneously developed diabetic rats [ 18], suggesting a deran gement in the negative feedback action of T at the hypotha lamic-pituitary level.…”

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“…In adult male rats, experimentally induced diabetes reduces gonadal and accessory reproductive organ weights [7][8][9][10][11] and is associated with re duced synthesis of androgens by Leydig cells [4,5]. The pitu itary response to luteinizing hormone releasing hormone (LH-RH) treatment has been shown to be either unaffected [ 12] or decreased [13,14] by diabetes. However, the hypothalamic function in diabetic rats is impaired as evidenced by significant reductions in medial basal hypothalamic (MBH) LH-RH levels [15].…”

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Influence of Diabetes on the Gonadotropin Response to the Negative Feedback Effect of Testosterone and Hypothalamic Neurotransmitter Turnover in Adult Male Rats

Chandrashekar

Steger²,

Bartke³

et al. 1991

Neuroendocrinology

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The influence of diabetes on the gonadotropin response to the negative feedback effect of testosterone (T) and hypothalamic neurotransmitter turnover rates in adult male rats was evaluated. Adult male Sprague-Dawley rats were made diabetic by an intraperitoneal injection of streptozotocin (STZ; 5 mg/100 g body weight) in citrate buffer. Vehicle-injected rats served as controls. On day 9, all rats were bilaterally castrated and treated subcutaneously on alternate days with either peanut oil or T propionate (TP) in peanut oil (100 µg/rat). Plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), and T concentrations were measured by specific radioimmunoassays from blood samples collected on day 1 (before castration) and 2, 4, 6, and 7 days after castration. On day 7 after castration (day 15 after vehicle or STZ treatment), 1 h before autopsy, the rats were injected intraperitoneally with saline or a tyrosine hydroxylase inhibitor, α-methyl-p-tyrosine (25 mg/100 g BW), for the measurements of norepinephrine (NE) and dopamine turnover in median eminence and medial basal hypothalamus (MBH). Circulating FSH, LH, PRL, and Tlevels were significantly lower (FSH and T: p < 0.001; LH and PRL: p < 0.05) in gonad-intact rats treated with STZ than in vehicle-injected animals. The castration-induced increase in plasma LH levels was attenuated in diabetic rats. The suppressive effect of T on LH secretion was significantly greater (p < 0.001) in STZ-treated rats relative to TP-treated nondiabetic controls. Castration in both diabetic and nondiabetic rats increased (p < 0.001) FSH secretion, but these increases were not different until day 6 after castration, when plasma FSH levels in control rats significantly increased (p < 0.01), than in diabetic animals. In STZ-treated rats, the suppressive effect of TP on plasma FSH levels was significantly increased. The NE turnover rates in median eminence and MBH were significantly lower (p < 0.001) in castrated diabetic rats than in castrated controls. The MBH NE turnover was reduced after TP treatment in both subgroups, but the relative decline was much greater (p < 0.01) in diabetic rats. These results clearly indicate that induction of diabetes by STZ treatment reduces gonadotropin and PRL secretion and increases the sensitivity of the hypothalamic-pituitary axis to the negative feedback effect of T on gonadotropin secretion. The effect of diabetes on gonadotropin secretion in the adult male rat is probably due to the suppression of noradrenergic neuronal activity of the hypothalamus.

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Hypothalamic-hypophyseal-gonadal axis in the streptozotocin-induced diabetic male rat

Cited by 24 publications

References 21 publications

Diabetes-Induced Alterations of Reproductive and Adrenal Function in the Female Rat

Diabetes-Induced Alterations of Reproductive and Adrenal Function in the Female Rat

Streptozotocin-Induced Diabetes Increases Apoptosis through JNK Phosphorylation and Bax Activation in Rat Testes

Influence of Diabetes on the Gonadotropin Response to the Negative Feedback Effect of Testosterone and Hypothalamic Neurotransmitter Turnover in Adult Male Rats

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