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)

To study the hormonal and metabolic effects of prostacyclin (PGI2), 6 healthy women were infused iv with PGI2 (1, 2, 4, and 8 ng/kg/min. each for 20 min) dissolved in glycine buffer, or with glycine buffer only. Serial blood samples collected before, during and after the infusion were assayed for FSH, LH, prolactin, growth hormone, thyrotrophin, oestradiol, progesterone, testosterone, cortisol, thyroxine, triiodothyronine, renin, aldosterone, glucose, insulin, glucagon, cholesterol, high density lipoprotein-cholesterol, triglycerides, alkaline phosphatase, alanine and aspartate aminotransferases, bilirubin, sodium, potassium, chloride, calcium, inorganic phosphorous, creatinine and uric acid. PGI2 infusions were accompanied by increased levels of prolactin, growth hormone and cortisol, probably due to the stressful side-effects during PGI2 infusion. In addition, plasma renin activity, glucagon and blood glucose increased, whereas the other variables measured did not change. These PGI2-effects should be kept in mind, when PGI2 is used in clinical practice.
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PMID:Hormonal and metabolic effects of intravenous infusion of prostacyclin in healthy women. 675 11

Chromium is involved in normal glucose metabolism. To test whether chromium is also associated with the exercise-induced increases in glucose utilization, urinary chromium excretion, serum glucose, insulin, and glucagon of nine male runners (23-46 yr) were evaluated. Blood samples were taken prior to, immediately following, and 2 h after a strenuous 6-mile run. Urine samples were also taken at these times, and total daily urine collections were made the day of the run and the following day. Mean serum glucose for all runners immediately after running was 185 +/- 19 mg/dl compared with 90 +/- 1 mg/dl (mean +/- SE) prior to running. Mean serum glucagon immediately after running was significantly elevated compared with that observed prior to or 2 h after running; serum insulin levels were not altered significantly. Mean urinary chromium concentration was increased nearly five-fold 2 h after running; similar results were obtained when chromium concentration was expressed per mg of creatinine. Total daily urinary Cr excretion was approximately two times higher the day of running compared with the following nonrun day. Daily urinary excretion of sodium, potassium, and calcium were measured to determine if exercise had a general nonspecific effect on renal function; daily urinary excretion of these was not changed by exercise. These data demonstrate that accompanying the exercise-induced changes associated with increased glucose utilization, there is a significant increase in chromium excretion.
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PMID:Effect of exercise (running) on serum glucose, insulin, glucagon, and chromium excretion. 675 38

The hemodynamic, hormonal and electrolyte effects of prenalterol, a synthetic selective beta 1 agonist, were studied in six patients with New York Heart Association functional class II and III heart failure. Prenalterol was infused incrementally at 60, 120 and 240 nmol/min, each rate for 24 hours, producing steady-state plasma prenalterol levels of 52 +/- 3, 121 +/- 6 and 194 +/- 9 nmol/1, respectively (mean +/- SEM). Hemodynamic and hormonal measurements were performed before, during and after prenalterol administration under conditions of constant body posture and a regulated intake of dietary sodium and potassium. Prenalterol induced a statistically significant increase in cardiac index (from 2.6 +/- 0.2 to 3.1 +/- 0.3 1/min/m2), with parallel increases in stroke index (from 28 +/- 2 to 34 +/- 2 ml/beat/m2). Forearm blood flow measurements increased (from 2.9 +/- 0.5 to 4.1 +/- 0.6 ml/min/100 g), while calculated systemic vascular resistance fell, as did pulmonary capillary wedge pressure (from 13.7 +/- 1.6 to 10.5 +/- 1.7 mm Hg). The drug did not alter heart rate, arterial pressure, right heart pressures or the frequency of ventricular premature beats. Prenalterol increased plasma renin activity (from 2.9 +/- 0.8 to 6.6 +/- 1.8 nmol/1/hour), angiotensin II (from 59 +/- 12 to 89 +/- 22 pmol/1), urinary aldosterone excretion (from 41 +/- 10 to 78 +/- 34 nmol/day) and plasma insulin (from 10.6 +/- 2.2 to 19.8 +/- 3.9 mU/1). Circulating catecholamines, cortisol, glucose, glucagon or pancreatic polypeptide did not change. Dose-response studies in five patients showed dose-dependent increments in hemodynamic variables, while hormonal changes plateaued at the second dose level. We conclude that prenalterol infusion augments myocardial contractility, reduces systemic vascular resistance, and stimulates insulin release and the renin-angiotensin-aldosterone system.
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PMID:Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure. 682 3

The proportion of total hepatic energy utilized for bile formation and transport of taurocholate (TC) and conjugated sulfobromophthalein (cBSP) has not been defined previously. To study this question we have measured changes in oxygen consumption by the isolated perfused rat liver and freshly isolated hepatocytes occurring in response to TC and cBSP administration, cation substitution, and glucagon infusion. The basal rates of bile formation and oxygen consumption varied considerably among different livers, and there was little or no relationship between these two variables. Administration of either TC or cBSP to the perfused liver elicited a marked choleresis but failed to alter steady-state oxygen consumption even at maximal rates of TC or cBSP transport. Similarly, incubation of hepatocytes with TC or cBSP did not alter oxygen consumption. In contrast, inhibition of Na-K-ATPase by removal of sodium and/or potassium from the medium reduced oxygen consumption by perfused rat liver and isolated hepatocytes by 27-37%, and glucagon administration increased oxygen consumption in both systems by 31-40%. These findings indicate that the oxygen requirement for bile formation and even maximal rates of TC and cBSP transport is small compared with that for the metabolic changes induced by glucagon or for hepatic Na-K-ATPase activity. This is in contrast to other epithelial tissues, such as kidney and rectal gland, in which oxygen utilization for transepithelial solute and water transport constitutes a large fraction of both total and Na-K-ATPase-dependent oxygen consumption.
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PMID:Oxygen consumption by rat liver: effects of taurocholate and sulfobromophthalein transport, glucagon, and cation substitution. 684 48

The frequency of persistent or intermittent hyperkalemia in patients with diabetes is unknown. In 405 predominantly insulin-treated patients, major hyperkalemia was not common (< 5.0 mEq/L in 2.5%). In ten insulin-treated patients sampled hourly from 8 AM through 8 PM, major intermittent hyperkalemia was not detected (< 4.8 mEq/L in all samples). However, mean plasma potassium values paralleled mean glucose values; these variables were significantly correlated in seven of ten patients. In contrast, there were no relationships between plasma potassium and plasma free insulin, glucagon, epinephrine, or norepinephrine values. We conclude that (1) hyperkalemia--fasting or intermittent--does not occur commonly in patients with diabetes, and (2) hyperglycemia, but not insulin or epinephrine lack or glucagon excess, appears to be a direct determinant of plasma potassium but is not a sufficiently potent determinant to commonly produce clinically important hyperkalemia in insulin-treated diabetic patients.
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PMID:Hyperkalemia and hyperglycemic increments in plasma potassium in diabetes mellitus. 700 40

The acute effects of glucagon (mol. wt. 3500) and its interactions with insulin were studied in the forearm during eight studies in seven normal, post-absorptive males. The protocol consisted of a 2 h baseline, 1 h glucagon perfusion (mean glucagon increment, 691 +/- 50 pg/ml), 1 h perfusion of both insulin and glucagon (mean insulin increment of 105 insulin and glucagon (mean insulin increment of 105 /- 13 mU/l) and a 30 min recovery period. Simultaneous arterial (A), deep venous (DV), and superficial venous (SV) blood samples were obtained at 30 min intervals. Perfusion of glucagon resulted in a decrease in (A-DV) non-esterified fatty acids of -0.128 +/- 0.057 mmol/l (n = 7, p less than 0.05) and (A-SV) non-esterified fatty acids of -0.081 +/- 0.36 mol/l (n = 7, p less than 0.05), as well as a change in deep compartment uptake of glycerol after 60 min of -0.044 +/- 0.019 mumol/min/100 ml of forearm tissue (n=6, p less than 0.05), indicating increased lipolysis. There was also a decrease in net glucose uptake as reflected by a change in (A-Dids of -0.081 +/- 0.36 mol/l (n = 7, p less than 0.05), as well as a change in deep compartment uptake of glycerol after 60 min of -0.044 +/- 0.019 mumol/min/100 ml of forearm tissue (n=6, p less than 0.05), indicating increased lipolysis. There was also a decrease in net glucose uptake as reflected by a change in (A-Dids of -0.081 +/- 0.36 mol/l (n = 7, p less than 0.05), as well as a change in deep compartment uptake of glycerol after 60 min of -0.044 +/- 0.019 mumol/min/100 ml of forearm tissue (n=6, p less than 0.05), indicating increased lipolysis. There was also a decrease in net glucose uptake as reflected by a change in (A-DV) of -0.24 +/- 0.09 mmol/l (n = 7, p less than 0.025) and (A-SV) of 0.10 +/- 0.05 mmol/l (n = 7, p less than 0.05). There was also a net decrease in deep arteriovenous differences of potassium in six of seven subjects. Insulin levels, similar to those found after a meal, rapidly reversed the effects of glucagon on non-esterified fatty acid, glucose and potassium. These effects persisted throughout the recovery period.
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PMID:The acute metabolic effects of glucagon and its interactions with insulin in forearm tissue. 702 Dec 78

To study the relationship between islet hormonal secretion and intracellular content of five elements, a rat islet perifusion technique was used in 24 paired experiments. Control and experimental chambers each containing 100 islets, received 2.8 and 16.7 mM D-glucose, respectively. Effluent was collected frequently for hormone measurements. At eight different time intervals form 0--30 min islets were fixed and prepared for scanning electron microscopy. Over 900 unobscured alpha and beta cells were selected by size and shape criteria. Energy dispersive x-ray analysis was applied to each single cell to determine relative content of calcium (Ca), potassium (K), sodium (Na), chlorine (Cl), and phosphorus (P). Experimental chambers exhibited typical acute (0--9 min) and second phase (10--30 min) insulin secretion in association with suppression of glucagon release after 10 min. At 2 min an abrupt upward K spike in both alpha and beta cells was followed at 3--4 min with a 1.5- to 2-fold rise of Ca and a reciprocal decrease in K, Na, Cl, and P. From 3 to 30 min biphasic insulin secretion. Reduced alpha cell calcium after 6 min preceded suppression of glucagon secretion. After 2 min K related inversely to Ca content in both alpha and beta cells. These results could not be reproduced when D-galactose was substituted for D-glucose. We conclude that sequential changes of Ca content that are reciprocally related to K are predictive of beta cell insulin release and suppression of alpha cell glucagon secretion.
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PMID:Fluctuations of calcium, phosphorus, sodium, potassium, and chlorine in single alpha and beta cells during glucose perifusion of rat islets. 702 94

The effects of two loop diuretics, bumetanide and furosemide, on carbohydrate metabolism and electrolyte balance were assessed in 11 normal male subjects in a double-blind manner. Glucose, insulin, glucagon, and growth hormone responses to 5-hour glucose tolerance test and arginine infusion were measured during the control and drug treatment periods. Three other non-insulin-dependent diabetic subjects, receiving diuretic drug for six weeks, underwent a similar protocol. Kaliuresis and natriuresis due to diuretic administration were significant only on day 1 of treatment. There were no significant changes in total body potassium by 40K counting; net potassium loss by balance study was minimal in both the acutely treated subjects and the chronically treated patients. Effects of bumetanide and furosemide on water and electrolyte excretion did not differ. Glucose tolerance was significantly improved with bumetanide but not with furosemide. Plasma insulin, glucagon, and growth hormone levels during the oral glucose tolerance test were unaffected by either drug. Insulin levels with arginine infusion were significantly increased, and growth hormone levels decreased with bumetanide but not with furosemide. No evidence of impaired carbohydrate metabolism in the three chronically treated diabetic subjects was seen. It is concluded that the effects of bumetanide and furosemide on potassium balance and glucose utilization were minimal in this experimental setting.
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PMID:Effects of loop diuretics on carbohydrate metabolism and electrolyte excretion. 704 Apr 94

To assess the effects of dialysis or hemofiltration on carbohydrate metabolism in uremia, we performed intravenous (IV) glucose tolerance tests (IV GTTs) after an overnight fast 48 hours following the last treatment in ten patients with chronic renal failure. Samples were obtained for plasma glucose, insulin, glucagon, and growth hormone levels throughout the GTTs in addition to basal samples for levels of plasma potassium and bicarbonate. The IV GTTs were performed at the end of a four-month period of standard hemodialysis (period 1) and then at the end of a four-month period of hemofiltration (period 2). Patients had mild glucose intolerance that did not change after hemofiltration, although the exaggerated insulin responses to glucose administration did significantly decrease in period 2. The fasting hyperglucagonemia did not decrease after hemofiltration but exhibited normal suppression with IV glucose. Levels of basal plasma bicarbonate and basal plasma potassium did not change significantly in period 2. Further studies investigating the beneficial metabolic effect of hemofiltration would seem to be indicated based on the data reported herein.
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PMID:Studies of carbohydrate metabolism after hemodialysis and hemofiltration in uremic patients. 704 44

In the arginine-stimulated perfused rat pancreas, elevated concentrations of potassium ion inhibited glucagon secretion while stimulating the secretion of insulin. Decreased potassium ion produced the reverse effect. The observed inverse correlation between changes in insulin and glucagon secretion (r = -0.64; p less than 0.001) was suggestive of local interactions between islet hormones, and prompted us to determine whether potassium-induced changes in glucagon secretion were dependent upon concurrent changes in insulin release. We found that when insulin secretion was greatly suppressed, either through acute induction of diabetes with streptozotocin or by utilization of a glucose-free perfusate, no qualitative differences in glucagon responsiveness to altered potassium ion were evident, although the amplitude of these glucagon changed was enhanced. Similarly, when exogenous insulin (20,000 mU/l) was added to the perfusate in order to render potassium-induced changes in endogenous insulin secretion insignificant, glucagon responsiveness to altered potassium ion was maintained. Exogenous insulin alone had no effect on arginine-stimulated glucagon secretion. We conclude that any indirect effects of potassium ion on arginine-stimulated glucagon secretion are not mediated by insulin, but could be related to changes in somatostatin secretion.
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PMID:Potassium ion concentration alters glucagon secretion independently of insulin secretion in the isolated rat pancreas. 704 31


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