Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary responsibility for the induction of various acute phase reactions has been ascribed to interleukin 1 (IL-1), tumor necrosis factor (TNF), or IL-6, suggesting that these cytokines may have many overlapping activities. Thus, it is difficult to identify the cytokine primarily responsible for a particular biologic effect, since IL-1 and TNF stimulate one another, and both IL-1 and TNF stimulate IL-6. In this work, the contribution of IL-6 in radioprotection, induction of adrenocorticotropic hormone (ACTH), and induction of hypoglycemia was assessed by blocking IL-6 activity. Administration of anti-IL-6 antibody to otherwise untreated mice greatly enhanced the incidence of radiation-induced mortality, indicating that like IL-1 and TNF, IL-6 also contributes to innate resistance to radiation. Anti-IL-6 antibody given to IL-1-treated or TNF-treated mice reduced survival from lethal irradiation, demonstrating that IL-6 is also an important mediator of both IL-1- and TNF-induced hemopoietic recovery. A similar IL-1/IL-6 interaction was observed in the case of ACTH induction. Anti-IL-6 antibody blocked the IL-1-induced increase in plasma ACTH, whereas recombinant IL-6 by itself did not induce such an increase. Anti-IL-6 antibody also mitigated TNF-induced hypoglycemia, but did not reverse IL-1-induced hypoglycemia. It is, therefore, likely that TNF and IL-1 differ in their mode of induction of hypoglycemia. Our results suggest that an interaction of IL-6 with IL-1 and TNF is a prerequisite for protection from radiation lethality, and its interaction with IL-1 for induction of ACTH.
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PMID:Role of interleukin 6 (IL-6) in protection from lethal irradiation and in endocrine responses to IL-1 and tumor necrosis factor. 131 Oct 16

Endogenous opioid peptides have a role in the regulation of the hypothalamic-pituitary-adrenal axis. Recently, beta-endorphin (EP) has been thought to inhibit CRF release in vivo and in vitro. In the present study we examined the effects of central administration of EP on ACTH secretion and gene expression of both CRF in the hypothalamus and POMC in the anterior pituitary gland (AP) during basal and insulin-induced hypoglycemia in pentobarbital-anesthetized rats. Administration of EP in the lateral ventricle decreased basal CRF levels in the median eminence and inhibited basal and hypoglycemia-induced ACTH secretion in a dose-dependent manner. Hypoglycemia-induced POMC mRNA levels in the AP and CRF mRNA levels in the hypothalamus were also dose-dependently inhibited by the administration of EP. The inhibitory effect of EP was reversed by naloxone. These results suggest that 1) central administration of EP acts through the opioid receptor to inhibit hypoglycemia-induced CRF gene expression in the hypothalamus and CRF release, which results in a decrease in ACTH secretion and POMC mRNA levels in the AP; and 2) the active site of EP is the CRF neuron in the paraventricular nucleus.
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PMID:Beta-endorphin inhibits hypoglycemia-induced gene expression of corticotropin-releasing factor in the rat hypothalamus. 131 Dec 37

We evaluated whether the brain kallikrein-kinin system plays a role in the regulation of adrenocorticotropin (ACTH) release in rats. Intracerebroventricular (icv) injection of bradykinin (0.24 nmol) increased plasma immunoreactive ACTH (irACTH) levels (from 93 +/- 4 to 200 +/- 12 pg/ml, P less than 0.01). This effect was prevented by icv kinin antagonist at 15.4 nmol/h (from 98 +/- 5 to 108 +/- 6 pg/ml; not significant). The antagonist did not alter the increase in plasma irACTH levels induced by icv corticotropin-releasing factor (CRF), arginine vasopressin, or prostaglandin E2. Melittin (7 nmol/h icv) increased plasma irACTH from 95 +/- 4 to 268 +/- 7 pg/ml (P less than 0.01). This effect was prevented by icv kinin antagonist (15.4 nmol/h), kallikrein antibodies (13 pmol/h), or indomethacin (0.28 mmol/h). ACTH response to melittin was not altered by antagonists of CRF or vasopressin. Intra-arterial injection of insulin (0.3 IU/kg body wt) reduced plasma glucose levels to a similar extent in rats given icv kinin antagonist or vehicle; the ACTH response to insulin-induced hypoglycemia was slightly less in rats given kinin antagonist than in those given vehicle (55 +/- 5 vs. 86 +/- 4 pg/ml, P less than 0.05). The brain kallikrein-kinin system may play a role in the regulation of ACTH secretion in stimulated conditions.
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PMID:Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release. 131 88

Six control subjects underwent an insulin tolerance test before and after the administration of therapeutic doses of imipramine hydrochloride for 10 days to investigate effects of tricyclic antidepressants on hypothalamic-pituitary-adrenal axis response to hypoglycemia. The mean steady-state tricyclic blood level was 141 (SD = 66) ng/ml. Baseline levels of glucose, cortisol, and adrenocorticotropic hormone (ACTH) were not affected by the administration of imipramine. After administration of imipramine for 10 days, subjects uniformly had a significantly lower glucose nadir than before its administration (before imipramine: mean = 32 mg/dl; SD = 5; after imipramine: mean = 24 mg/dl; SD = 6). There was no difference in ACTH or cortisol response before and after the administration of imipramine. These findings suggest that imipramine hydrochloride increases sensitivity to the hypoglycemic effects of insulin, but does not alter the counterregulatory response of ACTH and cortisol.
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PMID:Imipramine effect on hypothalamic-pituitary-adrenal axis response to hypoglycemia. 131 83

The effect of corticotropin-releasing hormone (CRH), independent of adrenocorticotropin hormone (ACTH), was evaluated in nine healthy individuals. Cortisol release and corresponding ACTH production were determined after separate intravenous administration of ovine-CRH (1 micrograms/kg BW) and insulin inducing hypoglycemia (0.1 u/kg BW). Adrenocorticotropin hormone (1-24; 250 micrograms intravenous bolus) revealed an adequate adrenal reserve capacity in all subjects. At the time of peak cortisol response following CRH and insulin administration, IR-cortisol increments were 14 +/- 1 micrograms/dl and 9 +/- 1 micrograms/dl (mean +/- SE), respectively (p less than .05); whereas ACTH (IR-ACTH) increments were 40 +/- 10 ng/l and 53 +/- 14 ng/l, respectively. The cortisol increment/ACTH increment ratios were 0.53 +/- 0.09 and 0/36 +/- 0.09, respectively (p less than 0.05), suggesting an ACTH-independent effect of CRH on cortisol production. The authors speculate that CRH may have a direct effect on the human adrenal gland or it may release ACTH-like factors that stimulate the human adrenal cortex.
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PMID:Corticotropin-independent effect of ovine corticotropin-releasing hormone on cortisol release in man. 131 20

Insulin-induced hypoglycemia is a metabolic stress that stimulates secretion of adrenocorticotropic hormone (ACTH) and cortisol in a number of animal species. Dexamethasone is a potent synthetic glucocorticoid that suppresses the secretion of ACTH and cortisol. Both ACTH and cortisol exhibit complex secretory patterns demonstrating ultradian and circadian rhythms. This work investigated the pattern of ACTH and cortisol response to hypoglycemia in goats and the effect of dexamethasone on this response. Five goats were pretreated with dexamethasone (0.1 mg/kg) and 5 with saline. Blood samples were taken every 2 min for 60 min before and 60 min after administration of insulin (2.5 IU/kg, i.v.). Immunoreactive ACTH and cortisol were measured in all samples and glucose in selected samples. Data sets were analyzed for significant pulses with the Cluster Analysis program. Complete data sets were compared as well as those for each 30-min interval. Plasma glucose was lower than preinsulin levels at 10 min, declined rapidly between 10 and 30 min, and remained low 30-60 min after insulin injection in both treatment groups. Controls showed a rapid rise in ACTH and cortisol beginning 30 +/- 10 min postinsulin. The increase in mean plasma hormone levels during hypoglycemia was predominantly due to an increase in amplitude of secretory pulses for ACTH and cortisol compared with the 30 min before insulin. Dexamethasone significantly lowered mean ACTH and cortisol levels and prevented alteration in plasma ACTH and cortisol secretion during hypoglycemia but did not totally ablate pulsatile activity of either hormone. The amplitude of ACTH and cortisol pulses was significantly decreased by dexamethasone treatment. The frequency of cortisol but not ACTH pulses was also significantly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsatile ACTH and cortisol in goats: effects of insulin-induced hypoglycemia and dexamethasone. 131 9

The clinical and laboratory findings in 76 patients with isolated corticotropin deficiency (10 of our own and 66 from literature) were analyzed with the following observations. With the exceptions of hyperpigmentation and hyperkalemia, the similarity of symptoms and signs to those of Addison's disease and their reversibility by glucocorticoids indicate that most, but not all, manifestation of isolated corticotropin deficiency is caused by glucocorticoid deficiency. Isolated corticotropin deficiency seems to be of pituitary origin in most patients, as shown by lack of corticotropin response to insulin-induced hypoglycemia, vasopressin, or corticotropin-releasing factor. Secretion of other pituitary hormones is frequently abnormal, which is mostly attributable to glucocorticoid deficiency. Although the pathogenesis of isolated corticotropin deficiency is unknown in most patients, association with other autoimmune endocrinopathies, postpartum onset in women, or serum antipituitary antibodies suggests an autoimmune pathogenesis in some patients. In two of our 10 patients, cancer developed during glucocorticoid treatment. More observations of complications and long-term prognosis following glucocorticoid therapy are needed for optimal clinical decision making.
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PMID:Isolated corticotropin deficiency in adults. Report of 10 cases and review of literature. 132 48

The purpose of these studies was, first, to determine whether hypertonic saline (HS) infusion or nitroprusside (NiPr)-induced hypotension augments the vasopressin (AVP) and adrenocorticotropic hormone (ACTH) responses to insulin (Ins)-induced hypoglycemia and, second, to determine whether neurohypophysectomy could attenuate the augmentation. Conscious, male dogs (n = 8) underwent two different types of experiments. In the first, Ins was preceded by either a 30-min infusion of normal saline (control) or HS to raise plasma osmolality and AVP. HS augmented the AVP response but diminished the ACTH response to Ins. In the second group of experiments, Ins was preceded by a controlled decrease in mean arterial pressure using NiPr, which led to an increase in AVP and ACTH. The initial ACTH and AVP response to Ins was augmented by NiPr, but this early augmentation was not sustained. Neurohypophysectomy attenuated the early augmentation of the ACTH response to Ins by NiPr, but did not alter the final ACTH level achieved. We conclude that HS augmented the AVP but inhibited the ACTH response to Ins probably because of expansion of plasma volume. Concomitant hypotension led to an augmentation of the early but not sustained AVP and ACTH response to Ins. Neurohypophysectomy eliminated this augmentation, suggesting a role for AVP from the neural lobe in the early ACTH response to combined hypotension and Ins-induced hypoglycemia.
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PMID:Effect of hypotension and hyperosmolality on vasopressin and ACTH responses to hypoglycemia in conscious dogs. 132 17

Concurrent effects of benzodiazepines on stress-induced activation of the three classical "stress" systems: pituitary-adrenal, adrenomedullary, and sympathoneural systems have not been extensively investigated in humans. In the present study, the effects of alprazolam (1.5 mg) on plasma levels of adrenocorticotropin hormone (ACTH), epinephrine, norepinephrine, dihydroxyphenylglycol (DHPG, the intraneuronal metabolite of norepinephrine), and mood states were examined in 10 healthy volunteers undergoing glucoprivic stress. Glucoprivic stress was induced by intravenous administration of the glucose analog, 2-deoxyglucose (2DG), at a dose (50 mg/kg) that impairs cellular glucose metabolism and produces a state comparable to hypoglycemia. Alprazolam and 2DG were administered in a double-blind, placebo-controlled manner. 2DG produced robust elevations in plasma ACTH and epinephrine levels, modest elevations in plasma norepinephrine levels, and decreases in plasma DHPG levels. Alprazolam significantly attenuated the 2DG-induced increases in plasma ACTH and epinephrine, but did not significantly effect plasma norepinephrine and DHPG. These data suggest that benzodiazepines attenuate metabolic stress-induced activation of the pituitary-adrenal and adrenomedullary systems but do not effect 2DG-related effects on peripheral sympathoneural function. The possible mechanisms involved are discussed.
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PMID:Effects of alprazolam on pituitary-adrenal and catecholaminergic responses to metabolic stress in humans. 133 13

Immunoreactive corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH) are present in the plasma of the brain dead patients. These hypothalamic hormones may reflect some residual brain function after brain death. To examine the hypothalamic function, insulin-induced hypoglycemia and arginine infusion were performed in brain dead patients. Plasma CRH and GHRH were present initially, but levels did not increase significantly for 120 minutes after insulin injection. GH, adrenocorticotropic hormone, and cortisol levels did not increase either. Arginine load did not induce GH. These results suggest that hypothalamic hormones in the plasma after whole brain death do not reflect hypothalamic functions. The hormones may originate from extrahypothalamic sources such as the pancreas or adrenal gland.
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PMID:Absence of response to hypothalamic stimulation test in brain death. 137 98


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