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 multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

A high glomerular filtration rate (GFR) is often found early in insulin-dependent diabetes mellitus (IDDM). It has been suggested that high circulating glucose, glucagon, and GH levels could play a role in this increase in GFR. On the other hand, patients with IDDM in poor metabolic control also have high circulating ketone body levels. This study was undertaken to determine whether exogenous D,L-3-hydroxybutyric acid at two infusion rates (40 and 30 mumol kg-1 min-1) for 180 min altered renal plasma flow (RPF), GFR, and the excretion rate of total protein, beta 2-microglobulin, and albumin in 11 normal (N) subjects and 11 IDDM patients in whom euglycemia was achieved and maintained using the insulin-glucose clamp technique. RPF and GFR were measured by a priming-continuous infusion of [125I]hippurate and [51Cr]EDTA, respectively. The 40 mumol kg-1 min-1 D,L-3-hydroxybutyric acid infusion increased RPF and GFR in both N and IDDM subjects. Mean RPF increased from 588 +/- 78 (+/- SD) to 706 +/- 129 mL min-1 1.73 m-2 in N and from 671 +/- 101 to 781 +/- 99 in IDDM. GFR increased from 121 +/- 11 to 151 +/- 15 ml min-1 1.73 m-2 in N and from 136 +/- 11 to 191 +/- 16 in IDDM. The filtration fraction also was significantly higher in IDDM than in N during the D,L-3-hydroxybutyric acid infusion. The 30 mumol kg-1 min-1 D,L-3-hydroxybutyric acid infusion increased RPF and GFR to a somewhat lesser extent in both groups. D,L-3-hydroxybutyric acid infusions increased the tubular reabsorption rate of ketone bodies and sodium. The increase in tubular sodium reabsorption rate was correlated significantly to that in the tubular ketone body reabsorption rate. A significant decrease in urinary pH was found during the D,L-3-hydroxybutyric acid infusion. D,L-3-Hydroxybutyrate sodium salt (30 mumol kg-1 min-1) also was infused in 5 of the 11 diabetic patients. A similar increase in GFR and RPF occurred. Both total protein and beta 2-microglobulin, but not albumin, excretion rates increased during D,L-3-hydroxybutyric acid (40 mumol kg-1 min-1) infusion in N and IDDM subjects. D,L-3-Hydroxybutyric acid infusion did not change plasma glucagon, GH, or renin activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glomerular filtration rate is increased in man by the infusion of both D,L-3-hydroxybutyric acid and sodium D,L-3-hydroxybutyrate. 329 5

Physical injury of any sort--accidental injury, burns or elective surgery--provokes an immediate neuroendocrine response. Neural input arising from the cerebral cortex, damaged tissues and receptors detecting fluid loss leads to increased secretion of ACTH, growth hormone, prolactin and vasopressin from the pituitary, and to a general activation of the sympathetic nervous system, with rises in adrenaline and noradrenaline concentrations. Secondary changes include stimulation of cortisol and aldosterone and inhibition of insulin and somatomedin secretion. The glucagon concentration and plasma renin activity may also be increased, either immediately or after a delay. The duration of these responses generally depends upon the severity of the injury and differs considerably between hormones, for reasons that are not understood. The only endocrine changes consistently seen at later times after trauma are an increase in insulin secretion, which supersedes the initial suppression, and decreases in the concentrations of T3 and gonadal steroids. Some of the changes in steroid, thyroid and pancreatic hormones differ temporally or even qualitatively from those of their usual stimuli and are unexplained. The initial neuroendocrine response to injury can be construed as playing a defensive role, but the function of the later changes is not understood; it seems likely that they are adaptive in nature, but the scope for therapeutic intervention remains unclear.
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PMID:The neuroendocrinology of physical injury. 332 96

In order to evaluate the pathogenesis of the systemic hyperdynamic circulation in portal hypertension, serum concentration of eight kinds of hormones including glucagon (Glu), aldosterone (Ald), renin (Ren), and epinephrine (Adr), and the hemodynamic parameters were measured in a series of 30 patients, of whom 23 were patients with liver cirrhosis, 3 were with Banti's disease, 2 with chronic active hepatitis, and 2 with pre-cirrhotic change. The average cardiac index was 4.6l/min, m2, with normal PCWP of 6.7 mmHg. CI. and SVR. showed significant inverse correlation of r = -0.767 (p less than 0.01), however, PCWP and CI did not have any significant correlation. Average serum concentrations of Glu, Ald, and Ren were 160 pg/ml, 139 pg/ml, and 5.4 ng/ml, respectively, all of which were increased up to 2.5 times above the normal values. Adr, norepinephrine, cortisol, estrone and estradiol were within normal limits. Of the eight hormones being measured, only Glu had significant correlation with both liver function tests and the cardiac index (r = 0.479, p less than 0.05). Neither Ald nor Adr had significant correlation with hemodynamic parameters.
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PMID:[Systemic hyperdynamic circulation and serum hormone concentrations in portal hypertension]. 352 13

The stress response in humans commonly includes elevations in plasma concentrations of glucocorticoids, catecholamines, glucagon, growth hormone, aldosterone, and renin, resulting in alterations in the metabolism of glucose and other energy substrates, and in increased sodium and water retention. In severe illness, triiodothyronine and sometimes thyroxine are decreased without evidence of clinical hypothyroidism. Antidiuretic hormone may be elevated in bacterial meningitis and other central nervous system disorders, as well as in acute asthma, chronic ventilator therapy, pneumothorax, atelectasis, and postoperatively. Increased ADH concentration can lead to significant hypoosmolality and hyponatremia with adverse effects on the patient. In the setting of severe intracerebral insults, ADH may be inappropriately low, resulting in diabetes insipidus. Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Either situation leads to hyperglycemia. Disturbances in calcium, phosphorus, and magnesium homeostasis may occur relatively frequently in the critically ill patient in response to therapeutic interventions, or illness-induced altered metabolism. It is not always clear when an altered metabolic or hormonal state is an appropriate response to a stress, or represents decompensation of the body's mechanisms for coping with that stress. It is important, however to recognize the common responses of the organism to severe illness, and to monitor for treatable abnormalities which occur.
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PMID:Endocrine manifestations of critical illness in the child. 354 20

In a randomised, double-blind, cross over trial, 25 patients with mild to moderate primary hypertension were given nifedipine 20-40 mg twice daily and labetalol 200-400 mg twice daily after a 4 week period on placebo, followed by the two drugs in combination. The BP during placebo therapy was 164/108 mmHg supine and 159/110 mmHg standing. After monotherapy with nifedipine for 6 weeks the supine BP was reduced by 18/13 mmHg and the standing BP by 20/12 mmHg; with labetalol the corresponding figures were 26/15 mmHg and 28/21 mmHg, respectively. The combined therapy induced a larger fall in BP, by 36/22 mmHg supine and by 39/24 mmHg standing; in 21 of 23 patients the BP became normal. The heart rate (HR) decreased during labetalol treatment alone and on the combined therapy. With nifedipine alone, the HR was unchanged in the supine position and increased on standing. Nifedipine increased plasma renin activity (PRA) and urinary aldosterone excretion (uA), whereas labetalol reduced both. During combination therapy, PRA and uA remained unchanged. There was a slight fall in HDL-cholesterol during treatment with labetalol alone and in combination with nifedipine. The fasting blood glucose increased slightly during treatment with each of the drugs, but neither caused a change in the concentrations of glycosylated haemoglobin A1, serum insulin, C-peptide, or plasma glucagon. Adverse effects as a rule were well tolerated and were related to the pharmacological effects of the drugs. Only 2 patients left the trial, both during labetalol treatment.
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PMID:Antihypertensive and metabolic effects of nifedipine and labetalol alone and in combination in primary hypertension. 390 21

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

A study was made of change in hormone secretion in 243 patients with alimentary-constitutional and hypothalamic obesity. Activation of the somatostatin mechanism, a decrease in somatotropic and thyrotropic function of the hypophysis, an increment of corticotropin, beta-lipotropin and vasopressin levels in the blood, disturbance of circadian fluctuations of hormone secretion, an increase in insulin and C-peptide secretion, a decrease in glucagon secretion and triiodothyronine and cortisol levels in the blood, activation of the renin-aldosterone system and cortisol secretion rate were equally expressed both in alimentary-constitutional and primary hypothalamic obesity. The central mechanisms of the regulation of endocrine functions were incorporated in a pathological process even in alimentary-constitutional obesity. Disorders of the hypothalamic regulation lay in the basis of both types of obesity.
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PMID:[Comparative evaluation of the hormonal changes in alimentaro-constitutional and hypothalamic obesity]. 395 72

The submandibular glands of mice and rats are not fully developed at birth. In early postnatal life, differentiation of acini takes place before that of granular convoluted tubule (GCT) cells. The latter develop from striated duct cells, and first appear in both species around 15 days of age. In mice their full development gets under way by 20 days of age and is rapid in males and slow in females, resulting in a clear sexual dimorphism in adults. In rats, GCT development is more protracted, and accelerates around 40 days of age, with no sexual dimorphism seen at any time. The course of postnatal development of several GCT cell products is correlated with the cytodifferentiation of these cells. Reliable data are available for the development of amylase, proteases (including kallikrein), renin, epidermal growth factor, and nerve growth factor. Preliminary information exists for a glucagon-like substance. Cytodifferentiation of GCT cells is under hormonal control. Androgens alone can not precociously induce GCT cells, but thyroid hormones can do so, acting either alone or synergistically with androgens.
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PMID:Postnatal developmental changes in submandibular glands of rats and mice. 616 Jan 81

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6


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