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)

In idiopathic or generalized epilepsy, serum glucose and cholesterol concentrations tend to be low, especially just before the seizure. Glucose tolerance curves are abnormal and variable. The electrolyte balance is disturbed, and epileptics tend to go readily into alkalosis. Serum [Na+] is usually unaffected, but [K+] is normal to low between attacks and increases during and after the seizure. Serum [Cl-] is usually high just before the seizure. Epileptics are generally mildly hypocalcemic, especially in the period before the seizure. Serum urea and nonprotein nitrogen values are low between paroxysms but increase after the seizure. Serum protein concentration is usually normal. Stress, which releases epinephrine and corticotropin, results in high serum citrate concentration, which probably contributes to decreased serum [Ca2+] just before a seizure. In the healthy individual, any increase in serum citrate is accompanied by increasing [Ca2+]. In the rabbit, convulsions can be induced with corticotropin, a result of increased serum citrate concentration coupled with a decrease in [Ca2+]. The net result is severe hypo-ionic-calcemia. A similar phenomenon has been reported in a few humans. Administration of insulin causes serum citrate concentrations to decrease. Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic.
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PMID:Clinical biochemistry of epilepsy. I. Nature of the disease and a review of the chemical findings in epilepsy. 22 Nov 36

The most common ectopic production of a pituitary hormone is the one of ACTH leading to Cushing's syndrome. Ectopic ACTH-hypersecretion is the cause of Cushing's syndrome in 10-15% of all cases. The ACTH-secreting tumours are often oat-cell carcinomas of the lung, less frequently pancreatic cancers, hypernephromas, or C-cell carcinomas of the thyroid. Some of these tumours may be benign or semi-benign as the rare carcinoid tumours and cause great problems in the differential diagnosis of ACTH-dependent hypercortisolism. Out of 173 of our patients with Cushing's syndrome observed in the last 12 years 21 were caused by ectopic ACTH-production. Of these 21 patients 13 have a small cell carcinoma of the lung. The ectopic ACTH-syndrome often has typical clinical features caused by the levels of ACTH and cortisol leading to hypocalcemic alkalosis with muscle weakness and wasting, carbohydrate intolerance, and hypertension with oedema. The survival time in many of these patients is not long enough to allow them to develop typical signs of Cushing's syndrome though they are often highly pigmented. These patients are easily diagnosed. However, patients with small tumours which do not cause very elevated ACTH-levels and who have the more typical clinical signs of full-blown Cushing's syndrome are difficult to recognize. For the differential diagnosis of ACTH-dependent Cushing's syndrome the corticotropin-releasing hormone (CRH) stimulation test and dexamethasone suppression test with high doses are helpful. In special cases the venous sampling procedure for ACTH-measurements is necessary, also CT or NMR is helpful. Ectopic CRH-production is a rare cause of ACTH-dependent Cushing's syndrome. Patients with ectopic CRH-production and consecutive ACTH-hypersecretion from the pituitary have not been studied extensively. There are especially no well documented results of the use of the CRH-stimulation test in vivo in this group of patients with Cushing's syndrome. On the other hand, in the documented cases, not only CRH-, but also ACTH-production was found in the tumours. So far, this rare cause of ACTH-dependent Cushing's syndrome has to be excluded or confirmed by the measurement of endogenous CRH-levels. But until now we have not been able to detect one single case of ectopic CRH-production using a sensitive homologous CRH-radioimmunoassay over a period of more than 8 years in which we have seen nearly 120 newly diagnosed patients with ACTH-dependent Cushing's syndrome. Only in the plasma and tumour tissue of two patients of other groups have we found high CRH-levels.
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PMID:Ectopic production of ACTH and corticotropin-releasing hormone (CRH). 132 73

A 36-year-old patient developed marked pigmentation, marked myopathy and severe hypokalaemic alkalosis which at first pointed towards an ectopic ACTH syndrome. The dexamethasone test at a high dose indicated cortisol suppression. A mediastinal tumour was seen radiologically, but the sella was of normal size. Computed tomography provided indirect signs of a sellar space-occupying lesion which suggested an ectopic production of corticotropin-releasing factor (CRF) as cause of the Cushing's syndrome. CRF concentration in antecubital venous blood was markedly elevated to 280 ng/l. The mediastinal tumour was excised and proved to be a carcinoid histologically. Postoperatively the CRF concentration fell to 70 ng/l. An extract of the carcinoid contained 15.5 ng/g wet-weight of CRF and 254 ng/g wet-weight of beta-endorphin. The patient died 5 weeks postoperatively of sepsis with bilateral pneumonia. At autopsy the hypophysis was of normal size but showed nodular ACTH-cell hyperplasia. This was thus a case of Cushing's syndrome resulting from ectopic CRF production in a mediastinal carcinoid tumour.
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PMID:[Cushing's syndrome in CRF-producing mediastinal carcinoid]. 230 1

The present study evaluated a protocol for drawing large volumes of blood over an acute time frame in conscious cannulated rats with blood from cannulated donor rats simultaneously infused to maintain isovolemia. During time control (n = 6), three successive 1.5-ml blood samples were drawn at 10-min intervals with equal volumes of donor blood infused simultaneously. One milliliter of blood was drawn quickly and saved for analysis followed by an additional 3 ml of blood withdrawal to total a 15-ml/kg hemorrhage. Two subsequent 1.5-ml samples were replaced with autologous (hemorrhage) blood. During hypoxia inspired O2 was decreased to 10% after the first sample-transfusion. The sampling-transfusion protocol (time control) had no effect on blood pressure (MAP), hematocrit (Hct), blood gases, renin, or adrenocorticotropic hormone (ACTH). Hemorrhage resulted in a significant decrease in MAP, Hct, base excess, and arterial PCO2 and an increase in arterial PO2, renin activity, and ACTH. Ten percent O2 resulted in significant hypoxemia, respiratory alkalosis, and a small degree of hypotension at the 20-min sample with no change in renin and a moderate increase in ACTH. The consistency of the results with previous studies confirms the utility and efficiency of large sample-transfusion protocols for the study of blood gas and endocrine dynamics in conscious rats.
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PMID:Evaluation of a blood sample-transfusion protocol in rats: blood gases, renin, and ACTH. 284 65

A case of atypical pituitary dependent Cushing's disease is reported. The patient presented with clinical symptoms similar to those of the ectopic ACTH syndrome; notably a marked hypokalaemic alkalosis, widely fluctuating plasma cortisol levels, greatly elevated plasma ACTH levels, and failure to suppress both plasma cortisol and ACTH levels following high dose oral dexamethasone. However, a large aggressive pituitary tumour was detected by skull X-ray and computed tomography. Removal of the pituitary tumour led to full remission of the patient's Cushing's syndrome. Pro-opiomelanocortin (POMC) related peptides in the plasma and tumour tissue extract of this patient have been characterized by gel-filtration and Concanavalin-A Sepharose affinity chromatography, indicating processing of POMC in a manner more usually associated with ectopic tumours.
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PMID:A case of pituitary dependent Cushing's disease with clinical and biochemical features of the ectopic ACTH syndrome. 298 2

A patient with ectopic adrenocorticotrophic hormone (ACTH) production from a neuroendocrine tumour of the nasal roof is presented. By indirect immunoperoxidase techniques the tumour cells were shown to be distinctly positive for ACTH and beta-endorphin but negative for other peptides derived from pro-opiomelanocortin. Neither corticotropin releasing hormone (CRF) found in some tumours associated with ectopic Cushing's syndrome, nor gastrin immunoreactivity, which coexists with ACTH in normal rat pituitary and in rat and human gastrointestinal cells, were demonstrable in the tumour. A review of other, previously recognized locations of CRF/ACTH producing tumours is given to increase the awareness of the ectopic Cushing's syndrome, which may lack the classical features and is characterized by fulminant clinical course, extreme fatigue, weakness, pale facial swelling, oedema and hypokalaemic alkalosis.
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PMID:Cushing's syndrome due to an ACTH-producing neuroendocrine tumour in the nasal roof. 298 19

We studied the effect of chronic hypoxia on the renin, adrenocorticotropin (ACTH), aldosterone, and corticosterone responses to acute hemorrhage in conscious male rats with chronic femoral arterial catheters. Rats were exposed to 21, 12.5, or 10% O2 (n = 7 per group). At 42 h of exposure, animals underwent a rapid 6 ml/kg hemorrhage. O2 at 12.5 and 10% led to significant hypoxemia (arterial PO2 = 52 +/- 1 and 43 +/- 1 Torr, respectively) and respiratory alkalosis. Significant increases in plasma sodium to 145 +/- 2 meq/l and decreases in plasma potassium to 3.53 +/- 0.12 meq/l were also observed during hypoxia. Hypoxia per se had no significant effect on blood pressure, plasma renin activity, ACTH, and corticosterone. O2 at 12.5% led to a significant reduction in aldosterone levels (0.9 +/- 0.8 ng/dl) compared with normoxia (4.2 +/- 0.9 ng/dl). The mean arterial pressure, plasma renin activity, and aldosterone responses to hemorrhage were unaltered by hypoxia. ACTH and corticosterone responses to hemorrhage were potentiated by exposure to 10% O2. We conclude that chronic exposure to severe hypoxia augments the pituitary-adrenal but not the renin-aldosterone response to hemorrhage.
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PMID:Renin, ACTH, and adrenocortical function during hypoxia and hemorrhage in conscious rats. 300 36

Studies of whole body balances of non-metabolizable base (NB) and several electrolytes and of the acid-base status of blood and urine during development of corticotropin-induced alkalosis in the weanling rat were carried out in order to identify the primary source of base and factors instrumental in maintenance of the alkalotic state. The data were compared to baseline and running control values and to the results of whole carcass analysers. Primary accumulation of NB was accounted for by ongoing gastrointestinal NB absorption in the weight-losing animal, distributed to extracellular and non-extracellular compartments of the body. An increase in the rate of renal excretion of non-metabolizable acid (NA), from negative values to zero, corresponded to an increased load of endogenous sulphuric acid and a reduced rate of gastrointestinal NB absorption. Accordingly, the renal response did not per se contribute to the induction of extracellular alkalosis. Maintenance of alkalosis occurred in spite of ample chloride in the renal tubular lumen and a moderate increase in relative extracellular volume. In the absence of evidence of overloading (with base) or malfunction of the kidney, corticotropin-induced alkalosis is classifiable as a 'set-point disturbance' of acid-base metabolism in which fluctuations in the (non-renal) load of NA lead to commensurate changes in renal NA excretion at an elevated extracellular pH. Withdrawal of corticotropin injections was followed by prompt restoration of a normal extracellular acid-base status and a return to reference values for renal NA excretion despite a marked fall in the balance of NB. This observation supports a concept of the extracellular compartment as the immediate reference system of the kidney.
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PMID:Corticotropin-induced alkalosis in the weanling rat and its relation to the balance of non-metabolizable base. 631 53

Early alterations in fluid, electrolytes, and their regulating hormones were investigated in men exposed to 6,000 m simulated altitude (2 h-ascent, 2 h-sojourn, 2 h-return). Hematocrit and serum protein rose with elevated serum osmolality and reduced urine flow upon arrival at 6,000 m, suggesting decreased plasma volume probably due to hypotonic fluid shift to intracellular spaces. Serum K declined reflecting respiratory alkalosis. The exposure raised plasma antidiuretic hormone (ADH), plasma renin activity (PRA), serum cortisol and aldosterone. Increases both in ADH and aldosterone showed close correlations with that in cortisol, suggesting that ADH may be elevated by hypoxic stress in addition to elevated serum osmolality and decreased plasma volume, and that increased secretion of adrenocorticotropin may be the main cause of increased aldosterone, though PRA involvement cannot be excluded. These rises in ADH and aldosterone may act to retain body water, and the latter may exaggerate alkalosis; thus, these hormonal changes may be related to acute mountain sickness.
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PMID:Hormonal disturbances of fluid-electrolyte metabolism under altitude exposure in man. 637 81

Experiments on white rats found that both chronic acidosis and chronic alkalosis cause fasting hyperglycemia and decreases glucose tolerance. In hypophysectomized animals, alkalosis causes similar effects and acidosis leads to hypoglycemia. Acute acidosis stimulates insulin and corticotropin secretions acute alkalosis reduces blood insulin and corticotropin levels and increases glucagon concentration. Chronic acidosis and alkalosis decrease insulin secretion and stimulates corticotropin secretion. Glucagon levels remain increased in chronic alkalosis. It has been concluded that primary cause of diabetogenic action of chronic acidosis is glucocorticoid hyperfunction and exhausting stimulation of B cells with glucose. Alkalosis causes a direct inhibitory action on B cells and activates A cells of Langerhans' islets.
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PMID:[The mechanisms of disorders of carbohydrate metabolism in changes to the acid-base balance]. 811 90


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