Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The survival of adult rat hepatocytes in monolayer culture was studied in the presence of different hormones (neurotensin, oxytocin, thyrotropin releasing hormone, luteinizing hormone releasing hormone, cholecalciferol, bradykinin, substance P, aldosterone, melanocyte stimulating hormone, 3,3',5-triiodo-1-thyronine, corticosterone, human growth hormone, glucagon, insulin, progesterone, testosterone, estradiol, and dexamethasone phosphate) or growth factors (fetal bovine serum). For this purpose trypan blue exclusion, lactate dehydrogenase, and DNA and protein content were measured at 24 and 72 h of culture. 10(-7) M Dexamethasone, a mixture of eight hormones, 10% fetal bovine serum, and a combination of the latter two supplements caused a more than 64% higher DNA content at 72 h when compared to control cultures. A striking agreement of these results with changes of lactate dehydrogenase leakage was observed, whereas trypan blue exclusion gave erratic results. Considerable changes of cell arrangement apparently specific for each supplement were observed by low magnification microscopy. It is concluded that glucocorticoids and fetal bovine serum have an outstanding effect on cell viability and that DNA or protein content or both are reliable indicators of cell viability in amitotic cultures.
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PMID:Influence of hormones and growth factors on viability, DNA, and protein content of adult hepatocytes in primary culture. 405 11

The effects of 23 agonists on the rates of cellular 32P efflux and lactate dehydrogenase (LDH) release were tested in a perfused rat heart preparation which had been prelabelled in vitro with [32P]Pi. Some 13 compounds produced detectable changes at high doses within 10 min, and in most cases a polyphasic response was observed. Six classes of compound gave rise to substantial effects, as follows. Catecholamines and glucagon produced a transient initial stimulation of Pi efflux, followed by a long-term inhibition of Pi transport and an increased rate of LDH release. These effects were clearly different from the response seen after treatment with dibutyryl cyclic AMP, which had a slower, stimulatory, effect on Pi output in doses which gave rise to a pronounced inotropic effect, and produced a marked increase in both coronary flow and LDH release. Carbachol also gave rise to a large transient stimulation of Pi efflux, which was followed by smaller sustained increase in Pi output without any obvious effect on LDH release. Dibutyryl cyclic GMP had no effect on Pi efflux or LDH release. Insulin decreased the rate of Pi efflux, although the loss rate partially recovered towards the control value after prolonged exposure to the hormone. Insulin had no obvious inotropic effects and produced no change in the rate of LDH release. Corticosteroids increased the rate of Pi efflux, although the loss rate partially declined towards the control value with prolonged exposure to the hormones. Corticosteroids produced a very slight inotropic response, and large doses sometimes increased the rate of LDH release from the tissue. Aldosterone slightly stimulated Pi output. A small, transient and somewhat variable stimulation of Pi efflux was observed with vasopressin and angiotensin, whereas tri-iodothyronine was slightly inhibitory, but adenosine, histamine, spermidine, des-Asp1-angiotensin, prolactin, parathyroid substances, calcitonin and somatostatin had no significant effects under our experimental conditions. Ouabain stimulated Pi efflux in doses that had no detectable inotropic effect. It is suggested that Pi efflux involves the electroneutral transport of NaH2PO4 across the cardiac plasmalemma and that many of the hormonal effects might be explained by changes in the intracellular [Na+] and pH in addition to changes in the intracellular [Pi].
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PMID:Some hormonal effects on myocardial phosphate efflux. 609 15

To investigate the role played by glucagon in the regulation of plasma potassium, we have examined the behaviour of this ion during four 2 h infusions of saline, glucagon (200 ng/min), cyclic somatostatin (priming dose of 50 microgram followed by 5.8 microgram/min) and somatostatin plus glucagon in 6 normal volunteers. Glucagon alone produced no change in potassium, despite an increase in insulin. Somatostatin, in addition to depressing insulin, produced a slight but significant (P < 0.01) increase in potassium (delta max: 0.2-0.8 mmol/1: mean +/- SEM, 0.4 +/- 0.1). Infusion of somatostatin together with glucagon suppressed the glucagon-induced increase in insulin and greatly augmented the increase in blood glucose. Potassium rose significantly more (P < 0.02) than after somatostatin alone (delta max: 0.5-1.3 mmol/l; mean 0.9 +/- 0.1), indicating that hyperkalaemia results from hyperglucagonaemia in the absence of insulin. Evidence is presented that this last phenomenon is not mediated by hyperglycaemia or by a reduction in aldosterone secretion. It is suggested that low blood insulin and increased glucagon could be one of the mechanisms that underlie or magnify the hyperkalaemia observed in cases of serious stress or decompensated diabetes.
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PMID:Influence of glucagon on plasma levels of potassium in man. 610 87

The plasma potassium concentration is determined both by external potassium balance and by the distribution of potassium between extracellular and intracellular fluid compartments, i.e., "internal potassium balance." Whenever external potassium balance is altered, the resultant change in the plasma potassium concentration is strongly influenced by concomitant alterations in internal potassium balance. Several factors alter internal potassium balance independently of changes in external balance. Acid-base disturbances produce shifts of potassium into or out of cells, but attempts to quantify these effects are not likely to be clinically useful. Hypertonicity produces a shift of potassium out of cells. Several hormones (insulin, aldosterone, catecholamines, glucagon, and growth hormone) may have roles in internal potassium balance. Digitalis and succinylcholine, by producing efflux of potassium from cells, may cause hyperkalemia. Potassium is released from skeletal muscle during exercise, causing an increase in the plasma potassium concentration. The periodic paralyses are associated with well-defined transient alterations in internal potassium balance.
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PMID:Internal potassium balance and the control of the plasma potassium concentration. 626 28

The 41-residue ovine corticotropin releasing factor (CRF) was administered iv and intracerebroventricularly (icv) to merino sheep. A significant rise in plasma ACTH, beta-lipotropin (beta LPH) and cortisol was demonstrated after the administration of 200 micrograms, iv. A highly significant correlation between the increments in plasma ACTH and beta LPH was observed. The plasma ACTH rise was evident within 5 min and was abolished by the prior administration of 0.4-4.0 mg dexamethasone. No significant rise in plasma GH, LH, PRL, insulin, glucagon, pancreatic polypeptide, met-enkephalin, angiotensin II, aldosterone, or vasopressin could be demonstrated. Although smaller doses of CRF (50 ng to 5 micrograms) were effective when given icv, the ACTH response was more delayed. It is concluded that CRF stimulates a rapid increase in the secretion of ACTH and beta LPH in sheep. Suppression of this response by dexamethasone indicates that glucocorticoids are capable of acting on the pituitary to inhibit the ACTH response to CRF. The delayed response when CRF is given icv may be due to diffusion. The action of CRF appears to be relatively specific, in that the plasma concentrations of the other pancreatic, pituitary, and adrenal hormones measured were not affected.
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PMID:The hormonal actions of corticotropin-releasing factor in sheep: effect of intravenous and intracerebroventricular injection. 630 69

Two 8-yr-old children, a boy and girl, are described with Cushing's syndrome secondary to ectopic ACTH-secreting pancreatic islet cell carcinomas. The girl, seen 28 yr ago, had strong presumptive evidence of ectopic ACTH production and hypercalcemia. The boy, studied recently, had strikingly elevated concentrations of plasma ACTH (1,500 pg/ml) and beta-lipotropin (beta LPH; 2,500 pg/ml) and showed no suppression of urinary 17-hydroxycorticoids or cortisol with low and high dose dexamethasone. He had increased plasma calcitonin (257 pg/ml), glucagon (442 pg/ml), lactate dehydrogenase (497 IU/liter), and alpha-fetoprotein (5,144 pg/ml). He also had hypokalemic alkalosis with elevated plasma deoxycorticosterone (70 ng/ml) and PRA (6.9 ng/ml.h) but normal plasma aldosterone (8.2 ng/dl) and 18-hydroxycorticosterone (7.6 ng/dl). Preoperative localization of the tumor was accomplished by computed tomographic scan of the abdomen with concurrent barium enema. Cell-free translation of the tumor mRNA produced authentic proopiomelanocortin of 35,000 mol wt, indicating that the ACTH and beta LPH were produced by the tumor from a common precursor. After removal of a large amount of metastatic tissue from the boy, clinical progression of the remaining tumor was monitored by measuring plasma ACTH and beta LPH. Episodic secretion of ACTH and beta LPH was demonstrated by taking frequent plasma samples while suppressing pituitary ACTH with oral dexamethasone. Chemotherapy and radiation proved ineffective in controlling the growth of his tumor.
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PMID:Endocrine, histological, and biochemical studies of adrenocorticotropin-producing islet cell carcinoma of the pancreas in childhood with characterization of proopiomelanocortin. 630 81

The 41-residue ovine corticotropin-releasing factor (CRF) was administered iv to five normal men. A significant rise in plasma corticotropin (ACTH), cortisol, and aldosterone was demonstrated after a dose of 200 micrograms. There was no demonstrable change in supine blood pressure, pulse rate, plasma vasopressin, renin, catecholamines, insulin, glucagon, or glucose. It is concluded that 200 micrograms ovine CRF stimulates ACTH and cortisol secretion independently of any change in peripheral plasma levels of vasopressin and catecholamines. The cortisol and ACTH responses to ovine CRF were less marked but more prolonged than those after insulin-induced hypoglycemia. The relatively small increment in plasma ACTH, which was well within the physiological range, was associated with a significant increase in plasma aldosterone. Posterior pituitary function was not affected by this dose of ovine CRF.
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PMID:The effect of ovine corticotropin-releasing factor on catecholamine, vasopressin, and aldosterone secretion in normal man. 631 53

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

Injury or stress generates a vigorous metabolic response designed to establish the metabolic priorities required for the repair of injured tissues. In this condition, hormones commonly found to be elevated in the plasma include glucagon, catecholamines, glucocorticoids, growth hormone, aldosterone, and antidiuretic hormone. This hormonal profile results in rapid lysis of body protein, an increased rate of fat oxidation, and water and salt conservation. Rates of gluconeogenesis and ureagenesis are accelerated and may result in significant losses in lean body mass, a process that, if allowed to progress, will adversely affect patient survival. Exogenous nutrients provided to the critically ill patient may be poorly tolerated and may result in complications. Dextrose and intravenous fat emulsions provide the major sources of parenteral, nonprotein energy. These energy sources may not be metabolized efficiently in these patients, even though energy expenditure in this condition is increased significantly. Measurement of urinary nitrogen losses yields evidence useful in assessing the patient's degree of stress. In this manner, the patient's energy and protein requirements may be estimated. Formulations of amino acids, including the branched-chain amino acids, in higher concentrations have been reported to have anticatabolic effects and may improve the maintenance of lean body mass in stressed individuals. The stressed patient is prone to metabolic complications and, therefore, requires more careful monitoring of fluid, electrolyte, and acid-base balance, as well as renal, pulmonary, and liver function. Nutritional status is difficult to assess, since negative nitrogen balance may persist and the visceral proteins such as transferrin become altered in stress and, therefore, may not respond to nutritional intervention alone. The goal of nutritional therapy is the preservation of lean body mass by the safe and efficacious provision of metabolic substrate, thus improving patient survival.
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PMID:Nutritional support of the critically ill patient. 640 74

The immediate effect of sudden blood loss is the activation of a variety of homeostatic responses. These include increased sympathetic activity and increased release or production of renin, angiotensin, anti-diuretic hormone, aldosterone, adrenocorticotrophic hormone, beta-endorphins, glucocorticoids, glucagon, erythropoeitin, 2-3 diphosphoglycerate, prostaglandins and complement. This may be followed by the release of many substances, some initially appropriate locally, and some the products of damaged cells, which may go on to cause both local and systemic damage. These include lysosomal enzymes, kinins, histamines, serotonin, lactic acid, free oxygen radicals, neutrophil proteases, fibrinogen degradation products, endotoxins, myocardial depressant polypeptides, and passive transferable lethal factor. The early and late effects on the cardiovascular and respiratory systems, and on the blood, brain, kidneys, gut, liver, pancreas, and on overall metabolism and cellular function, are considered in turn. Although an enormous research effort has increased our understanding of the pathophysiology of haemorrhagic shock, no special measures have yet been shown to influence morbidity or mortality in man. Management still hinges on the early recognition and treatment of bleeding, on general supportive measures, and on safeguarding each link in the oxygen delivery chain.
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PMID:Pathophysiology of haemorrhagic shock. 651 66


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