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 endocrine response to stress is complex. Elevations in the serum concentrations of the "classic" stress hormones, epinephrine and cortisol, occur following many kinds of physiologic challenge and are accompanied by elevations in corticotropin, GH, and glucagon levels. These changes are probably responsible for the hyperglycemia and hypercatabolism common to most critical illness. If volume depletion is present, vasopressin, renin, and aldosterone secretion are also likely to be stimulated. These hormones, if present in excess, may produce fluid retention and hyponatremia. In some critically ill patients, there is a dissociation of renin and aldosterone production called hyperreninemic hypoaldosteronism, but the clinical importance of this syndrome is poorly understood. Thyroid hormone metabolism is commonly affected by critical illness, which results in characteristic abnormalities of thyroid function testing known as the euthyroid sick syndrome. The reproductive axis is exquisitely sensitive to physiologic stress; hypogonadotropic hypogonadism is a common finding in critical illness. The ongoing challenge to the clinician is to determine whether seemingly abnormal hormone measurements in critically ill patients reflect an appropriate homeostatic response to severe illness or, instead, whether they denote an independent metabolic disorder that might actually cause or contribute to the patient's unstable condition. In view of the exceedingly complex (and poorly understood) interactions involved in the human response to a severe illness, a thoughtful approach to the whole patient is essential and far preferable to indiscriminate hormone testing. Such testing, at best, may be uninterpretable in light of the clinical circumstances or, at worst, may lead to therapeutic misadventures.
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PMID:The endocrine response to critical illness. 780 93

This article describes some of the alterations that occur in the neuroendocrine system during sepsis. With a goal of better management of the patient with sepsis, an overview of the endocrine system, its hormones, and its close relationship to the nervous system is presented. The importance of hormone target cell receptor coupling, specific mechanisms of action that result in physiological changes, and regulation of hormone secretion are detailed. The roles and effects of catecholamines, glucagon, cortisol, and growth hormone are explored. Sick euthyroid syndrome, alterations in ADH, the renin-angiotensin-aldosterone axis, and PTH secretion are also examined.
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PMID:Hormonal response in sepsis. 794 87

To determine whether renal reserve capacity was preserved in patients with chronic glomerulonephritis with well-preserved kidney function, and how sodium was handled in proximal and distal tubules, 13 healthy control subjects and 13 patients with biopsy-verified chronic glomerulonephritis were studied before and during a continuous 120-min amino-acid infusion. Glomerular filtration rate (GFR), renal plasma flow (RPF), and tubular function evaluated by the lithium clearance method, were determined during six clearance periods of 30 min each. Plasma concentrations of angiotensin II, atrial natriuretic peptide (ANP), aldosterone, arginine vasopressin (AVP), glucagon, amino acid and serum osmolality were determined before, 60, and 120 min after infusion. GFR and RPF increased about 10% in both groups; filtration fraction (FF) was unchanged. Proximal tubular reabsorption of sodium and water decreased, and distal tubular reabsorption of sodium and water increased, and thus the net excretion of sodium and water was unchanged. Angiotensin II and aldosterone were reduced in control subjects, but not in the patients. ANP and glucagon increased equally in both groups. Most amino acids increased two- or threefold. It is concluded that renal reserve capacity and glomerulotubular balance are intact in patients with chronic glomerulonephritis with well-preserved renal function, but there is an abnormal lack of suppression of the renin-angiotensin-aldosterone system in response to an amino acid infusion in these patients.
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PMID:Renal haemodynamic changes, renal tubular function, sodium and water homeostatic hormones in patients with chronic glomerulonephritis and in healthy humans after intravenous infusion of amino acids. 809 Mar 30

Recently, hydrocortisone (HC) has been shown significantly to enhance interleukin-4 (IL-4)-induced in vitro IgE synthesis. For investigation of possible effects of synthetic corticosteroids but also of effects of other important human hormones, peripheral blood mononuclear cells (PBMC) were incubated with IL-4 and various concentrations of the hormones. IgE secreted in the supernatant was determined after a 14-d culture period. Like HC, all synthetic corticosteroids potentiated IgE secretion. A minor effect was noted for the mineralocorticoid aldosterone. No modulating effect on IL-4-induced IgE formation was observed for adrenocorticotropic hormone (ACTH), somatotropin (STH), thyroid-stimulating hormone (TSH), triiodothyronine, thyroxine, epinephrine, noradrenaline, insulin, and glucagon.
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PMID:Synthetic glucocorticoids potentiate IgE synthesis. Influence of steroid and nonsteroid hormones on human in vitro IgE secretion. 809 35

Splanchnic and systemic hemodynamics and plasma levels of aldosterone, glucagon and plasma renin were investigated in 12 patients with advanced cirrhosis before and 2 wk (14.6 +/- 2.8 days) and 2 mo (60.8 +/- 10.5 days) after orthotopic liver transplantation. Liver transplant was followed by significant (p < 0.01) changes in systemic hemodynamics at 2 wk, with a marked reduction in cardiac index (4.9 +/- 0.8 vs. 3.7 +/- 0.7 L/min.m2) and increases in mean arterial pressure (79 +/- 8 vs. 101 +/- 11 mm Hg) and peripheral vascular resistance (721 +/- 149 vs. 1,274 +/- 253 dyn.sec.cm-5). Two months after liver transplant, we saw further significant increases in peripheral vascular resistance (1,700 +/- 341 dyn.sec.cm-5; p < 0.05) without changes in cardiac index. Hepatic venous pressure gradient, very high before transplantation, was normal 2 wk after liver transplant (18.7 +/- 3.0 vs. 2.1 +/- 0.8 mm Hg; p < 0.01). Hepatic blood flow rose markedly from 1.03 +/- 0.46 to 2.25 +/- 0.79 L/min (p < 0.01) and was still elevated at 2 mo (1.84 +/- 0.74 L/min). Azygos blood flow had not changed after 2 wk with respect to pretransplant values (0.65 +/- 0.26 vs. 0.69 +/- 0.39 L/min) but had decreased significantly at 2 mo (0.39 +/- 0.16 L/min; p < 0.05). The elevated aldosterone, plasma renin and glucagon levels found in our cirrhotic patients before transplantation decreased to near-normal values 2 wk after the procedure. These results suggest that most of the hemodynamic and humoral abnormalities characteristic of advanced cirrhosis are reversed after liver transplant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and humoral changes after liver transplantation in patients with cirrhosis. 844 25

The effects of a 2-h intravenous infusion of glucagon 5 ng kg-1 min-1 or placebo on glomerular filtration rate (GFR), renal plasma flow (RPF), tubular sodium handling as judged by the lithium clearance method, and plasma concentrations of angiotensin II (AngII), aldosterone (Aldo), and atrial natriuretic factor (ANF) were investigated in two groups of healthy human volunteers, glucagon group (n = 10), and placebo group (n = 10). Glucagon infusion resulted in a maximal increase in plasma concentrations of glucagon of 400%. GFR increased 5.9% (range 1.3-12.4, p < 0.001) through the whole infusion period, whereas RPF only increased transiently during the first hour of infusion 6.5% (range 2.6-15.3, p < 0.05). Whereas filtered load of sodium increased significantly in response to glucagon infusion (p < 0.001), urinary sodium excretion was unchanged. Neither of these variables were affected by placebo. As judged from assessments of tubular sodium handling derived from the renal clearance of lithium, the increased filtered load of sodium resulted in an increase in the output of sodium from the proximal tubules of a similar magnitude, and an increase in absolute reabsorption of sodium in the distal tubules totally counterbalancing this increased input to the distal tubules. These alterations in tubular sodium handling did not involve Ang II, Aldo, or ANF. We conclude that an increase in plasma concentration of glucagon within the physiological range is capable of inducing a small and sustained increase in GFR, whereas RPF increases only transiently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of intravenous glucagon infusion on renal haemodynamics and renal tubular handling of sodium in healthy humans. 845 99

Seven days of dosing with either 30 mg or 60 mg of lansoprazole were compared with placebo in a double-blind, randomized, three-way cross-over study in 12 male healthy volunteers. Twenty-four-hour intragastric pH was measured after 7 days of dosing with each regimen, as well as 3 and 7 days after the end of dosing. During dosing with placebo, intragastric pH was above 4 for a median of 51 minutes. pH values were significantly raised to above 4 for 8.45 and 8.33 hours on Day 7 of dosing with lansoprazole 30 and 60 mg, respectively, but returned to normal by the third day after stopping dosing. No clinically relevant influence on endocrine function (serum concentrations of insulin, aldosterone, testosterone, parathormone, glucagon, T3, T4, TSH, LH, FSH, STH, prolactin, circadian cortisol profile, ACTH test) was observed. No serious adverse clinical or laboratory events were noted.
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PMID:The effects of lansoprazole, 30 or 60 mg daily, on intragastric pH and on endocrine function in healthy volunteers. 848 72

The effect of oral prednisolone treatment on renal haemodynamics, tubular function and various hormones during amino acid infusion was studied in 14 normal men. A balanced amino acid solution was infused for 120 min, before and after 4 days of prednisolone treatment (40 mg day-1). During amino acid infusion before prednisolone glomerular filtration rate, renal plasma flow, urinary sodium excretion, fractional excretion of sodium, lithium clearance, fractional excretion of lithium, serum insulin (s-insulin), plasma glucagon (p-glucagon) and s-growth hormone increased, whereas p-atrial natriuretic peptide, p-aldosterone, p-vasopressin and s-insulin-like growth factor 1 were unchanged, and potassium excretion and fractional excretion of potassium fell. After prednisolone treatment the most important differences during amino acid infusion were a significantly lower fractional excretion of sodium after 120 min (before prednisolone 26%; after prednisolone-7%; p < 0.05), a more pronounced increase in s-insulin after 120 min (before 118%; after 200%; p < 0.05) and a lower s-potassium. In conclusion, amino acid infusion increased fractional sodium excretion in healthy men, and this increase was reduced by prednisolone due to increased reabsorption in the distal tubules. It is suggested that the more pronounced the increases in plasma insulin and the decrease in serum potassium are mediators of the increased distal tubular sodium reabsorption during amino acid infusion during prednisolone treatment.
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PMID:Effect of prednisolone on amino acid-induced changes in renal haemodynamics and tubular function. 886 68

The purpose of the study was to evaluate renal functional reserve [RFR is the difference between glomerular filtration rate (GFR) at rest and maximal GFR after stimulation] in a controlled study in normal pigs. Our basic hypothesis was that a decreased RFR may be used as an early indicator of renal deterioration, i.e. a test to disclose significant obstruction as opposed to simple dilatation in hydronephrosis. During various forms of stimulation (amino acids, captopril and dopamine), we measured changes in GFR, renal plasma flow (RPF), tubular reabsorption of sodium and water, net uptake from plasma to the kidney of three salt and water homeostatic hormones (angiotensin II, aldosterone and atrial natriuretic peptide) and of glucagon, which is thought to play a key role as mediator of the GFR increase during amino acid infusion. We found the largest GFR increase during combined infusion of amino acids and dopamine (+13%), but compared with a non-stimulated control group, the GFR increase was statistically non-significant. RPF increased by 57% during stimulation with amino acids plus dopamine (P < 0.001), while tubular reabsorption of sodium and water, and renal uptake of angiotensin II, aldosterone and atrial natriuretic peptide showed no significant differences between control and stimulation groups. The renal uptake of glucagon increased significantly during amino acid stimulation with no concomitant GFR increase. We conclude that in this experimental, non-obstructed model, RFR is a very insensitive measure, which cannot be used to discriminate between obstruction and simple dilatation in hydronephrosis. Further, our study does not support the hypothesis that glucagon is involved in GFR changes after amino acids.
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PMID:Renal functional reserve in pigs: renal haemodynamics, renal tubular function and salt and water homeostatic hormones during amino acid and dopamine stimulation. 901 58

101 male Wistar rats (body mass 180-200 g) received a single dose of ethanol in two concentrations--96% and 30%. High ethanol concentrations produced a direct damage to gastric and duodenal mucosa. 30% ethanol inhibited secretion of glucagon, insulin and aldosterone. This inhibition rapidly changes for the hormones rise in the blood. Hydrocortisone was high over the experiment. Previous intake of mineral water prevents damage to the gastroduodenal mucosa induced by 96% ethanol and modifies the hormonal response provoked by 30% ethanol as evident from reduced expression of the two phases.
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PMID:[The effect of the preliminary intake of mineral waters in acute alcoholic intoxication (an experimental study)]. 944 9


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