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)

Ten undernourished patients receiving total parenteral nutrition and undergoing major intestinal surgery were restarted on intravenous feeds identical to their pre-operative regimens within 24 h of their operation. Five, chosen at random, received post-operatively 1-2 units insulin/kg body weight/24 h with their feed, while the other five received the feed only. Pre-operatively, and 2 h after commencing their post-operative feeds, rates of whole-body protein synthesis and breakdown were measured over a 9-h period following intravenous injection of a single tracer dose of 15N-glycine by the ammonia and urea end-product methods. During these 9-h study periods measurements were also made of blood glucose, plasma insulin and glucagon, urinary ammonia, nitrogen, creatinine and 3-methylhistidine. Blood glucose and plasma insulin and glucagon concentrations rose post-operatively whether or not insulin was given, but the increment in insulin concentration was significantly greater when insulin was given. Apparent nitrogen balance was positive pre-operatively and became less so post-operatively whether insulin was given or not. Similarly, post-operative increments in urinary excretion of ammonia, creatinine and 3-methylhistidine were not altered by addition of insulin. Protein turnover, as estimated by the ammonia end-product method, tended to rise post-operatively, but there was no significant difference between the increases observed with or without insulin. The urea end-product method suggested that there was no change in whole-body protein turnover after surgery, whether or not insulin was given. This study does not support the clinical use of insulin as a means of modifying protein metabolic losses after major surgery.
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PMID:The effect of surgical trauma and insulin on whole-body protein turnover in parenterally-fed undernourished patients. 642 Mar 74

Glucagon has been shown to lower blood lipids and to decrease food intake and body weight in short-term studies in man and animals. There is evidence of decreased secretion of glucagon in human obesity. The Zucker obese rat suffers from a genetic type of obesity and has an absolute reduction in circulating glucagon concentration. The effect of long-term administration of glucagon on the body weight in obese Zucker rats was studied. Glucagon caused a marked (-20%) reduction of body weight in obese Zucker rats with no change in feed intake. Urine glucose, urea nitrogen, creatinine, and ketone content, as well as serum triglyceride, cholesterol, alkaline phosphatase, creatinine, and insulin levels remained unchanged. Weights of perirenal fat, kidneys, and heart also remained unchanged. However, glucagon injection in obese Zucker rats caused significant decrease in serum glucose, and increases in SGOT, liver weight, and liver lipid and glycogen content. Further investigations are needed concerning the safety of chronic glucagon administration for weight control.
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PMID:Suppression of weight gain by glucagon in obese Zucker rats. 672 36

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 purpose of this study was to ascertain whether selected components of the uremic milieu adversely affected glomerular filtration rate (GFR), the glomerular protein filtration barrier, or the integrity of the proximal renal tubular brush border membrane. To achieve these goals, GFR and the excretion rates of albumin and of brush border derived-renal tubular epithelial antigens (RTE) were measured in normal rats and in rats with experimental nephropathies before and after the intravenous infusion of concentrated urine. This experimental protocol uniformly produced severe biochemical manifestations of uremia (for example 10-50-fold increases in BUN and creatinine, hyperphosphatemia, hyperkalemia, metabolic acidosis). However, despite these perturbations, GFR, albuminuria, and RTE excretion remained constant. To assess the influence of uremic hormonal derangements on renal function, GFR, albuminuria, and RTE excretion were measured in normal rats before and after inducing acute serum elevations of seven hormones whose concentrations are known to be increased in uremia (parathyroid hormone, growth hormone, insulin, glucagon, gastrin, prolactin, gastric inhibitory peptide). Again, GFR, albuminuria, and RTE excretion were not adversely affected. These results suggest that glomerular capillary function and proximal tubular brush border membranes are acutely resistant to many of the solute and hormonal derangements which are characteristic of uremia.
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PMID:A search for nephrotoxic factors within the uremic milieu. 715 30

Male Sprague-Dawley rats (initial weight 400 g) were fed a 0.5% lactalbumin diet containing required amounts of all other known essential nutrients for 14 weeks. The body weights averaged 250 g after depletion when the animals were randomly assigned to four groups of four or five. Rats of one group were killed for baseline analyses on day 0 of repletion. The remaining three groups were repleted for 14 days with a complete L-amino acid diet containing 20% protein equivalent and 0, 0.75 or 1.5% Arg . HCl. Daily feed intakes averaged 11, 15 and 17 g and daily weight gains were 3.3, 7.4 and 8.3 g, respectively. Average values for corresponding groups were: nitrogen balance--116, 187 and 190 mg/day; urinary orotate--4.6, 0.8 and 0.15 mg/day; carcass lipid--27, 37 and 40 g/100 g dry matter. Liver weights per 100 g body weight for 0 arginine exceeded other groups by 40%. There were no differences in creatinine index, nor in plasma concentrations of insulin, glucagon and albumin. The maximal rate of recovery from protein-calorie malnutrition of mature rats required an exogenous source of arginine. Urinary orotic acid excretion provided a reliable measure for determining when arginine needs for maximal rate of repletion were not met.
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PMID:Arginine requirement of mature protein-malnourished rats for maximal rate of repletion. 726 76

Nocturnal hypoglycemia in insulin-treated diabetic persons is often difficult to recognize clinically. It has been suggested that a useful biochemical test to demonstrate this would be the increased excretion of cortisol in the urine during the overnight period. However, of six diabetic persons who had nocturnal hypoglycemia (less than or equal to 2.5 mmol/L), plasma cortisol profiles and overnight urinary cortisol-creatinine ratios were abnormal in only one. In four others the plasma cortisol levels and cortisol excretion indices were indistinguishable from either a normal control group or a group of five diabetic subjects who did not develop nocturnal hypoglycemia. The remaining patient had a raised urinary cortisol-creatinine ratio, but did not show increased plasma levels of cortisol, growth hormone, or glucagon during the hypoglycemic phase. These data do not support the usefulness of the urinary cortisol-creatinine index as a marker of nocturnal hypoglycemia in diabetes.
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PMID:Nocturnal cortisol release during hypoglycemia in diabetes. 734 60

Blood samples were taken before and immediately after 80 km and 40 km rides held on consecutive days and analysed for haematocrit, blood glucose and lactate, plasma sodium, potassium, calcium, albumin, free fatty acids (FFA), glycerol, bicarbonate, insulin, cortisol, glucagon, urea, creatinine, uric acid, bilirubin and alkaline phosphatase. Unusually hot weather probably contributed to haemoconcentration with a significant (P < 0.001) increase in haematocrit and plasma albumin. A fall in blood glucose, with a rise in FFA and glycerol were consistent with long distance riding and were associated with a reduction in plasma insulin and a rise in cortisol and glucagon. The results suggested that the horses were working aerobically and the small increase in blood lactate was likely to be a result of reduced tissue perfusion. Plasma urea, creatinine and bilirubin increased during the 80 km ride and were still high the next morning. Blood samples were taken from 2 horses that became exhausted and were forced to retire and the results from these animals indicate the slow rate of recovery. It is suggested that haemoconcentration with reduced tissue perfusion might contribute to exhaustion during long distance exercise and that the speed of recovery might be improved by the intravenous administration of balanced electrolyte solutions.
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PMID:Further studies on the metabolic effects of long distance riding: Golden Horseshoe Ride 1979. 743 43

Blood samples were taken before and after a cross country race over the marathon distance of 42 km. There was a rise in blood glucose and plasma free fatty acids and glycerol associated with a rise in plasma cortisol and glucagon but the fall in insulin was not significant (P > 0.05). Plasma potassium and albumin concentrations increased, calcium decreased and there was no change in sodium or bicarbonate concentrations. There was an increase in plasma urea, creatinine, uric acid, bilirubin and isocitrate dehydrogenase but no change in alkaline phosphatase. There was a rise in plasma creatine kinase. These results of a competitive race are compared with those of the 80 km non-competitive Golden Horseshoe Ride.
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PMID:A biochemical study of the Arab Horse Society's marathon race. 746 99

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy. 762 22


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