Disturbances of the Hypothalamo-Hypophysial-Adrenocortical System in the Alloxan Diabetic Rat<sup>*</sup>

L’age, M.; Langholz, J.; Fechner, W.; Salzmann, Harry A

doi:10.1210/endo-95-3-760

Cited by 47 publications

(22 citation statements)

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“…In this experi ment we found significantly lower corticosterone levels in dia betic female rats as compared with control animals in proestrus and no difference compared with diestrus control and insulinreplaced animals. This decrease in CS is in sharp contrast to previous reports of increased CS levels in male STZ-diabetic rats [2,3,25,26,43,44]. The disparity between our findings and other investigators may be explained by known sex differences in basal adrenal function in normal animals and possible sex differences in adrenal function in diabetic animals [45].…”

Section: Discussioncontrasting

confidence: 99%

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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Section: Discussioncontrasting

confidence: 99%

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

Valdés¹,

Elkind‐Hirsch²,

Rogers³

1990

Neuroendocrinology

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“…The effect of experimental diabetes on the pituitary-adrenal axis has been previously tested only 1 month after injection of STZ. An increase in plasma corti costerone levels has been reported in these animals [23][24][25] as well as a disruption in diurnal rythmicity [26]. However, in our study, i.e.…”

Section: Discussioncontrasting

confidence: 75%

Effect of Diabetes on in vivo and in vitro Hypothalamic Somatostatin Release

Joanny¹,

Peyre²,

Steinberg³

et al. 1992

Neuroendocrinology

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In order to better understand the mechanisms underlying the reduction in growth hormone (GH) secretion in diabetic rats, we studied hypothalamic somatostatin secretion both in vivo (into hypophysial portal blood) and in vitro (from hypothalamic fragments) 5,9 and 30 days after induction of diabetes. Experimental diabetes was induced by an intraperitoneal injection of streptozotocin (STZ) at a dose of 65 mg/kg. Basal plasma GH was significantly reduced in diabetic rats at all stages. Somatostatin levels in hypophysial portal blood was unaffected in 5-day STZ-diabetic rats and significantly increased 9 days after STZ administration. Chronic insulin replacement therapy in diabetic animals partly normalized somatostatin levels as well as plasma GH and glucose levels. A good correlation was observed between in vivo and in vitro experiments. Indeed, somatostatin release from hypothalamic fragments did not change 5 days after STZ-induced diabetes and significantly increased 9 and 30 days after STZ administration. The in vitro increase in hypothalamic somatostatin secretion was observed in 10 as well as in 33 mM glucose concentration in the incubation medium. In the same experiment, the in vitro hypothalamic corticotropin-releasing factor secretion was lowered 5 and 9 days after diabetes induction. We conclude that hypothalamic somatostatin release increases in diabetic rats. These changes may contribute to the reduction in GH secretion in these animals. However, since these changes occur after the onset of plasma GH decrease, a factor(s) other(s) than somatostatin may play a causal role in the reduction in GH secretion.

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“…Rats that have been made diabetic by treatment with either alloxan or streptozotocin, or that are chronically exposed to cold, are both hyperresponsive to acute stress and relatively unresponsive to the normal inhibitory effects of dexamethasone [16][17][18] or prednisolone [19] provided 2-6 h prior to acute stress. Thus, the facilitatory effects of chronic stressors on subsequent responses of the adrenocortical system include not only continued or augmented responsiveness to acute stimuli, but also reduced re sponsiveness to feedback inhibition by corticosteroids in all of the temporal domains exhibited by the steroids [20], The mechanism(s) by which central components of the adre nocortical system exhibit facilitatory responses to acute stress and also diminished sensitivity to corticosteroid feedback are unknown.…”

Section: Discussionmentioning

confidence: 99%

Decreased Sensitivity to Glucocorticoid Fast Feedback in Chronically Stressed Rats

1990

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A number of changes in anterior pituitary corticotrophs occur after chronic footshock. These include increased ACTH and β-endorphin content and a loss of glucocorticoid negative feedback on corticotropin-releasing hormone (CRH)-stimulated ACTH and β-endorphin secretion, without changes in sensitivity to ovine CRH examined in vitro [9]. The present studies were undertaken to determine whether the in vitro changes were reflected by similar changes in vivo. We developed a fast feedback paradigm using a 5-min swim stress as challenge, with injection of saline or corticosterone immediately prior to swim. Corticosterone reliably decreased ACTH and β-endorphin responses to swim over the 30-min period studied. This feedback inhibition did not occur in rats that were either exposed to 30 min of chronic footshock for 7 or 14 days or in rats that were treated with corticosterone daily for 14 days in a regimen that has been reported to decrease hippocampal glucocorticoid receptors. By contrast, in rats exposed to the less intense stimulus of 30 min swim for 14 days, the fast feedback action of corticosterone was intact. These results suggest that both fast and delayed feedback corticosterone-inhibitory mechanisms may be blocked by relatively high levels of chronic stress or by chronic treatment with corticosterone, possibly as a consequence of decreased hippocampal glucocorticoid receptor number.

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Disturbances of the Hypothalamo-Hypophysial-Adrenocortical System in the Alloxan Diabetic Rat^*

Cited by 47 publications

References 0 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

Effect of Diabetes on in vivo and in vitro Hypothalamic Somatostatin Release

Decreased Sensitivity to Glucocorticoid Fast Feedback in Chronically Stressed Rats

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Disturbances of the Hypothalamo-Hypophysial-Adrenocortical System in the Alloxan Diabetic Rat*

Cited by 47 publications

References 0 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

Effect of Diabetes on in vivo and in vitro Hypothalamic Somatostatin Release

Decreased Sensitivity to Glucocorticoid Fast Feedback in Chronically Stressed Rats

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Disturbances of the Hypothalamo-Hypophysial-Adrenocortical System in the Alloxan Diabetic Rat^*