[Neuroendocrine disturbances in obesity].
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Endocrine System Diseases↗
Biomedical subjects
B Baranowska
Publications and source records attributed to B Baranowska.
Prolactin and LH release in response to vasoactive intestinal peptide (VIP) administration in spontaneously hypertensive and normotensive rats.
UNLABELLED: Vasoactive intestinal peptide (VIP) was injected intravenously at a dose of 10 micrograms in spontaneously hypertensive and normotensive Wistar-Kyoto rats. In order to evaluate the hemodynamic and hormonal effects of this peptide, the mean arterial pressure, heart rate as well as a serum rLH and rPRL levels, the contents of LH-RH in hypothalamus and the content of LH in pituitary tissue were determined. The same procedure was applied in rats receiving placebo. Serum rPRL concentration was measured additionally after combined administration of VIP+dopamine. VIP injection produced a decrease in mean arterial pressure and an increase in heart rate in both spontaneously hypertensive and normotensive rats. Serum rPRL concentration was significantly increased at 10 minutes after injection. The combined therapy (VIP+dopamine) partially inhibited this response. Serum rLH concentration, the content of LH-RH in hypothalamic tissue as well as the content of pituitary LH after VIP injection in spontaneously hypertensive and normotensive rats did not differ from the values obtained for the control group. CONCLUSIONS: 1. VIP injection produced the dramatic hypotensive effects in hypertensive rats; 2. A marked increase in PRL concentration in response to VIP was partially inhibited by dopamine in hypertensive and normotensive rats; 3. VIP injection did not change LH-RH and LH release in both hypertensive and normotensive rats.
Animals↗
Inhibitory effect of bombesin and SMS 201-995 on DNA synthesis in the rat thyroid lobes incubated in vitro.
The effects of 4-h incubation in the presence of bombesin on the incorporation of [3H]-thymidine into DNA of the rat thyroid lobes, collected from animals treated in vivo with a long-acting somatostatin analog (SMS 201-995) or with 0.9% NaCl, were investigated. It was shown that not only in vivo injections of SMS 201-995, but also, unexpectedly, in vitro incubation with bombesin inhibited [3H]-thymidine incorporation. The two examined substances did not reveal any additive action in their inhibitory effects on the thyroid growth.
Animals↗
Effect of bombesin on the structure and function of the rat adrenal cortex.
Intact and dexamethasone-treated adult female Wistar rats were infused (Alzet osmotic minipumps) with bombesin (0.75 micrograms/rat per day) for 7 days. Bombesin depressed body weight and capacity of adrenal homogenate to secrete corticosterone; the latter effect was reflected in intact rats by a drop in serum corticosterone level. Bombesin had no effect on pituitary and serum adrenocorticotropic hormone (ACTH) concentration and serum aldosterone level. In intact animals, infusion of bombesin resulted in lowering of the number of parenchymal cells in adrenal cortex connected with the hypertrophy of glomerulosa and fasciculata cells. Moreover, bombesin lowered basal corticosterone secretion by isolated rat adrenocortical cells; however, neuropeptide applied did not change the response of isolated cells to ACTH stimulation. The data obtained clearly demonstrate inhibitory effect of bombesin on basal corticosterone secretion by the rat adrenal cortex.
Adrenal Cortex↗
A marked decrease of vasoactive intestinal peptide release in obese patients.
The presence of vasoactive intestinal peptide (VIP) in the hypothalamus, anterior pituitary, and hypophyseal portal blood strongly suggests that VIP might be involved in the regulation of pituitary hormone secretion. To elucidate the relationship between VIP and the adrenergic system and its role in the mechanism of disturbed prolactin (PRL) and growth hormone (GH) release in obesity, serum VIP, GH, and PRL concentrations in response to alpha 2-adrenergic receptor agonist-clonidine were measured. Serum VIP levels were dramatically lower in obese as compared with non-obese patients, whereas clonidine did not alter VIP and PRL concentrations in either obese or non-obese patients. However, the response of GH to clonidine injection was blunted in obese patients. These results demonstrate an inhibited release of VIP in obesity. Whether a marked decrease of VIP may play a role in the mechanism of a disturbed release of GH and PRL remains to be explained.
Adult↗
The effect of clonidine on hormone release mediated through activation of opiate receptors.
To elucidate the mechanism of clonidine's effect on hormone release, serum growth hormone (GH), luteinizing hormone (LH), cortisol, and plasma beta-endorphin concentrations were determined after clonidine, naloxone, or the combined therapy of clonidine plus naloxone in six healthy women investigated in the luteal phase of their menstrual cycles. The clonidine injection increased GH levels. Naloxone (0.05, 0.1, and 0.2 mg/kg) decreased serum GH concentrations. Naloxone also increased serum LH, whereas clonidine decreased LH levels. Only the maximal dose of naloxone significantly increased serum cortisol concentrations. Clonidine had opposite effects on cortisol levels. These results demonstrate that combined therapy with clonidine plus naloxone leads to inhibition of the response of GH, LH, and cortisol to clonidine injection.
Adult↗
Are disturbances in opioid and adrenergic systems involved in the hormonal dysfunction of anorexia nervosa?
Opioid peptides and catecholamines play an important role in the control of appetite, behaviour and hormonal secretion. To evaluate the role of the opioid and adrenergic systems in the hormonal dysfunction of anorexia nervosa (AN), we investigated the effects of naloxone and clonidine on serum GH, LH, FSH, beta-endorphin, TSH, prolactin and cortisol concentrations in 35 women with AN. Basal plasma beta-endorphin concentrations were significantly lower than those in healthy controls. The response of beta-endorphin to clonidine in the AN patients was increased, whereas the response of beta-endorphin to naloxone was decreased. Basal serum cortisol concentrations were significantly higher in the AN patients than that in the controls. There was a significant increase in the cortisol response to naloxone in the controls but a lack of cortisol response to naloxone in the patients with AN. Naloxone produced a significant increase in LH release in the controls during the luteal phase of the menstrual cycle, as well as in the majority of AN patients. Clonidine caused a diminution of LH in the controls and did not alter LH in the patients. After clonidine injection, a significant increase in GH release was observed in both groups of subjects. If these disturbances persist after normalization of body weight, it might suggest that altered opioid and adrenergic activity is an aetiological factor in the pathogenesis of anorexia nervosa.
Adult↗
An enhanced diuresis and natriuresis in response to clonidine in spontaneously hypertensive rats.
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Animals↗
Clonidine stimulates atrial natriuretic factor (ANF) release in water-deprived rats.
To determine the effect of clonidine, an alpha 2-adrenergic agonist, on atrial natriuretic factor (ANF) release during water deprivation, plasma immunoreactive ANF (IR-ANF) arginine vasopressin, diuresis and natriuresis were measured in rats which had been deprived of water for 24 and 48 hr after intravenous (IV) administration of 50 micrograms clonidine. In normally-hydrated rats clonidine produced a marked elevation of plasma IR-ANF from 40.5 +/- 4.6 pg/ml to 1064 +/- 22 pg/ml (mean +/- SEM) and sodium excretion from 73.3 +/- 6.8 microEq to 723.4 +/- 62.3 microEq. Clonidine evoked an increase in plasma IR-ANF from 16.6 +/- 5.9 pg/ml to 229.5 +/- 60 pg/ml (mean +/- SEM) after 24 hr water deprivation and from 13.6 +/- 7.4 pg/ml to 104.8 +/- 21 pg/ml (mean +/- SEM) after 48 hr water deprivation. Clonidine did not induce any significant changes in vasopressin levels. During 24 hr and 48 hr water deprivation vasopressin rose from 3.1 +/- 0.3 pg/ml to 7.3 +/- 1.3 pg/ml and 8.4 +/- 0.6 pg/ml (mean +/- SEM), respectively. In normally-hydrated rats clonidine produced a marked diuresis and natriuresis. These effects and urinary cGMP excretion were significantly inhibited by anti-ANF antibodies. Clonidine caused a significant increase in urine output in 24 hr water-deprived rats but the response was markedly lower than that seen in normally-hydrated rats. In conclusion, clonidine stimulates ANF release both in normally-hydrated and water-deprived rats. The diuretic effect of clonidine appears to be related to ANF release but not to inhibition of vasopressin.
Animals↗
Opposite effects of neuropeptide Y (NPY) and polypeptide YY (PYY) on plasma immunoreactive atrial natriuretic factor (IR-ANF) in rats.
Female Sprague-Dawley rats were administered NPY and PYY in doses of 0.1, 2.5 or 5, and 10 micrograms in order to determine whether the natriuretic action is the result of increased ANF secretion. NPY injection increased significantly IR-ANF while PYY decreased IR-ANF in the dose-response manner in normally-hydrated rats as well as in water-loaded rats. Opposite effects on plasma IR-ANF were exerted by NPY and PYY, indicating that an increase of ANF release may be responsible for NPY-induced natriuresis.
Animals↗
Plasma immunoreactive atrial natriuretic factor is inhibited by selective blockade of alpha 2-adrenergic receptors in conscious Sprague-Dawley rats.
Effects of alpha 2-adrenergic receptors and calcium channel blockade on basal and clonidine-stimulated immunoreactive atrial natriuretic factor (IR-ANF) in conscious Sprague-Dawley rats were evaluated. Clonidine was injected intravenously (i.v.) in a dose of 50 micrograms. Yohimbine and verapamil were used as a pretreatment, with clonidine in a dose of 50 micrograms and 0.5 mg respectively. The effects of yohimbine (1, 20, 50 micrograms) and verapamil (0.5 mg) on basal IR-ANF were also studied. Plasma IR-ANF was measured by radioimmunoassay with prior extraction on heat-activated Vycor glass. Clonidine injection in a dose of 50 micrograms caused a marked increase of plasma IR-ANF from 34.0 +/- 7.0 pg/ml (mean +/- S.E.M.) to 457.1 +/- 66.3 pg/ml. Clonidine-stimulated ANF secretion was partially inhibited by yohimbine from 457.1 +/- 66.3 pg/ml (mean +/- S.E.M.) to 99.9 +/- 23.1 pg/ml. Moreover, yohimbine in highest doses (50 micrograms) decreased the basal plasma IR-ANF from 34.0 +/- 7.0 pg/ml (means +/- S.E.M.) to 6.8 +/- 3.6 pg/ml. Verapamil did not alter basal and clonidine stimulated IR-ANF. These results indicate the important role played by alpha 2-adrenergic receptors in mediating ANF release.
Animals↗
Plasma immunoreactive atrial natriuretic factor (IR-ANF) increases markedly after alpha 2-adrenergic stimulation with clonidine in normally-hydrated rats.
Clonidine, an alpha 2-adrenergic agonist, induced a marked, dose-related increase of plasma IR-ANF in normally-hydrated rats. Maximal ANF release was observed at 10 min after injection of 50 micrograms clonidine, rising from 40.5 +/- 4.6 pg/ml (X +/- SEM) to 1064.4 +/- 22.4 pg/ml. This effect on plasma IR-ANF was partially blocked by pretreatment with 0.8 mg naloxone, whereas synthetic Arg8-vasopressin (AVP) did not inhibit clonidine's action. These findings indicate that increased ANF release may be involved in the mechanism of clonidine-induced diuresis. The clonidine's effect on ANF release may be mediated via activation of opioid receptors besides stimulation of alpha 2-adrenergic receptors.
Animals↗
The role of opiate, dopaminergic, and adrenergic systems in the hypothalamo-pituitary dysfunction in obesity.
UNLABELLED: In order to evaluate the role of opiate, dopaminergic and adrenergic systems in the mechanism of hypothalamo-pituitary disturbances in obesity, 9 obese women and 14 healthy women were investigated. Serum GH, LH, beta-endorphin and cortisol concentrations were measured after administration of clonidine, an alpha 2-adrenergic receptor agonist, and naloxone, an opiate antagonist. Additionally, PRL levels were measured after administration of the dopamine receptor blocker metoclopramide. An impaired GH response to clonidine and naloxone was found in obese women. However, a marked increase in beta-endorphin was observed in obese patients after clonidine administration. Naloxone did not cause any significant change in beta-endorphin release. Neither clonidine nor naloxone induced any change in LH release. Serum PRL concentrations in response to metoclopramide were significantly higher in obese patients than in healthy women. IN CONCLUSION: Disturbed activity in opiate, adrenergic, and dopaminergic systems may be of pathogenetic importance in a hypothalamo-pituitary dysfunction in obesity. The occurrence of hypothalamic amenorrhoea as well as the presence of abnormalities of the central nervous system regulation of GH, PRL, ACTH, cortisol, insulin and vasopressin output might point to a generalized hypothalamo-pituitary dysfunction in obesity.
Adolescent↗
The effect of clonidine on pituitary hormone secretion in physiological and pathological states.
The purpose of this study was to evaluate the effect of clonidine--an alpha 2-adrenergic agonist--and naloxone--an opiate antagonist--on pituitary hormone release. The study involved 43 women: 20 menopausal women, 9 untreated women with ACTH-dependent Cushing's disease, and 14 healthy women. Serum GH, ACTH, LH, FSH, TSH, cortisol, and plasma beta-endorphin concentrations were measured with RIA methods. A significant increase in GH and a significant decrease in ACTH and in cortisol was observed after clonidine injection in healthy women. Clonidine caused a significant decrease in LH concentration in the luteal phase of the menstrual cycle. However, naloxone induced the opposite effect on pituitary hormone release. In Cushing's disease, ACTH significantly decreased in response to clonidine. In postmenopausal women with hypertension a decrease in blood pressure, a marked decrease in the number of hot flashes, as well as a diminution in amplitude and frequency of LH pulsatility was found. Conclusions are as follows: (1) Clonidine may be useful in the treatment of hypertensive menopausal women; and (2) a diminution in ACTH, beta-endorphin, and cortisol release in response to clonidine was observed in Cushing's disease.
Adrenocorticotropic Hormone↗
Detection of endogenous LH-like and FSH-like activities in human prostate.
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Aged↗
The role of opiate peptides in the mechanisms leading to the disturbances of pulsatile secretion of LH in hyperprolactinaemic women.
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Adult↗
The effect of naloxone on the secretion of pituitary hormones in patients with acromegaly, microprolactinomas, Cushing's disease and Nelson's syndrome.
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Cushing Syndrome↗
The effect of naloxone on ATCH and beta-endorphin in patients with Cushing's disease.
Endogenous opiates may be important in the control of ACTH secretion in men. The effect of opiate receptor blockade by naloxone on ACTH, beta-endorphin-like substance and cortisol release was studied in healthy women and in 9 patients with Cushing's disease. In the healthy subjects, ACTH, beta-endorphin and cortisol levels were increased in response to naloxone. However, in 3 our of the 9 patients with Cushing's disease, a paradoxical decrease in serum ACTH, cortisol and beta-endorphin concentrations was observed after naloxone administration. In the patients with a paradoxical response to naloxone, transsphenoidal microadenomectomy was ineffective.
17-Hydroxycorticosteroids↗