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)

Rats weighing 220 g were injected sc with zinc protamin glucagon 20 micrograms once daily (recurrent hyperglucagonemia) and zinc protamin glucagon 60 micrograms three times daily (chronic hyperglucagonemia); the controls received the vehicle three times daily. In the first group blood glucagon rose to above 200 ng/liter for 5 h every day; in the second group it constantly stayed above 600 ng/liter. After both 2 (n = 5) and 14 (n = 5) days treatment the control total blood alpha-amino-nitrogen (AAN) concentration was 4.3 +/- 0.1 mmol/liter, and the urea nitrogen synthesis rate was 4.9 +/- 0.4 mumol/(min.100 g BW) (mean +/- SEM) in controls. In recurrent hyperglucagonemic rats, treated for both 2 (n = 5) and 14 (n = 5) days, total AAN was 3.6 +/- 0.2 mmol/liter (P less than 0.05 vs. control) and urea nitrogen synthesis rate 4.5 +/- 0.8 mumol/(min.100 g BW). In chronic hyperglucagonemic, treated for both 2 (n = 5) and 14 (n = 5) days, total AAN was 2.2 +/- 0.1 mmol/liter (P less than 0.05 vs. control) and UNSR 7.9 +/- 0.8 mumol/(min.100g BW) (P less than 0.05 vs. control). The urea excretion was identical in controls and during recurrent hyperglucagonemia, but it was increased by 50% during chronic hyperglucagonemia. Food intake was the same in all groups. N Balances decreased from 10 mmol/24 h to 5 mmol/24 h (P less than 0.05) by chronic hyperglucagonemia. The total organ N content did not change by recurrent hyperglucagonemia, but in chronic hyperglucagonemia it decreased to 65-85% (P less than 0.01) in carcass, intestines, liver, and kidneys. In conclusion chronic but not recurrent hyperglucagonemia increases the rate of urea synthesis and decreases the blood amino acid concentration. This is suggested to be a reason for the loss of N from organs by chronic hyperglucagonemia.
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PMID:Loss of nitrogen from organs in rats induced by exogenous glucagon. 304 48

We previously have shown that ingested beef protein is just as potent as glucose in stimulating a rise in insulin concentration in type II diabetic patients. A synergistic effect was seen when given with glucose. Therefore, we considered it important to determine if other common dietary proteins also strongly stimulate an increase in insulin concentration when given with glucose. Seventeen type II (non-insulin-dependent) untreated diabetic subjects were given single breakfast meals consisting of 50 g glucose, or 50 g glucose plus 25 g protein in the form of lean beef, turkey, gelatin, egg white, cottage cheese, fish, or soy. The peripheral plasma concentrations of glucose, insulin, glucagon, alpha amino nitrogen, urea nitrogen, free fatty acids, and triglycerides were measured. Following ingestion of the meals containing protein, the plasma insulin concentration was increased further and remained elevated longer compared with the meal containing glucose alone. The relative area under the insulin response curve was greatest following ingestion of the meal containing cottage cheese (360%) and was least with egg white (190%) compared with that following glucose alone (100%). The glucose response was diminished following ingestion of the meals containing protein with the exception of the egg white meals. The peripheral glucagon concentration was decreased following ingestion of glucose alone and increased following all the meals containing protein. The alpha amino nitrogen concentration varied considerably. It was decreased after glucose alone, was unchanged after egg white ingestion, and was greatest after ingestion of gelatin. The free fatty acid concentration decrease was 4- to 8-fold greater after the ingestion of protein with glucose compared with ingestion of glucose alone.
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PMID:The insulin and glucose responses to meals of glucose plus various proteins in type II diabetic subjects. 305 32

Chicks of king penguin (Aptenodytes patagonica), while only 3-4 months old, tolerate 4-6 months of fasting when they are abandoned by their parents during the subantarctic winter. The body mass of nine chicks, which were followed during this natural winter fast, was 13.1 kg at capture and 3.4 kg after 150 days of fasting, a 74% decrease. The longer phase II (129 days) was marked by lipid mobilization and protein sparing, as indicated by a continuous increase in plasma levels of free fatty acids, glycerol, and beta-hydroxybutyrate, whereas plasma alanine, uric acid, and urea remained stable at low values. In phase III, by contrast, plasma concentrations of lipid-derived metabolites decreased, while plasma alanine, uric acid, and urea increased markedly, indicating an increase in protein utilization. Plasma insulin concentration did not significantly change during either phase II or phase III. Plasma glucagon remained constant during phase II and at the beginning of phase III but increased 2.6 times afterward. Plasma corticosterone increased only slightly during the first 4 months of the fast but reached very high values at the end of phase II and the beginning of phase III (4.7 times basal values); moreover, it further increased 3.1 times before phase III was stopped. Altogether, these data accord with the idea that the outstanding resistance of king penguin chicks to starvation is due to the ability to extensively prolong the situation of protein sparing, which seems to require the maintenance of low plasma concentrations of corticosterone and insulin for up to 4 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma hormone levels in relation to lipid and protein metabolism during prolonged fasting in king penguin chicks. 306 Mar 95

The effects of subclinical NH3 toxicity on circulating and regulatory hormone concentrations were investigated in seven Hereford steers. Ammonium chloride (NH4Cl) was infused via a right jugular vein catheter at a rate of 12 mumol NH4Cl.kg BW-1.min-1 for 240 min. This was preceded (PRE) and followed (POST) by saline infusions of 120 and 180 min, respectively. Blood samples were taken at 20-min intervals via a left jugular vein catheter. Metabolite and hormone concentrations during NH4Cl and POST periods were compared to PRE values using the Student's t-test procedure. Plasma NH3 was elevated rapidly (P less than .001) and peaked at 503 micrograms/dl 220 min into NH4Cl infusion. Plasma urea-N and glucose increased (P less than .001) 39 and 12%, respectively, during NH4Cl infusion and remained elevated 180 min POST. Whole blood L-lactate concentrations peaked (P less than .05) at 18% above PRE between 160 and 240 min into the NH4Cl infusion and gradually returned to PRE values, whereas pyruvate levels were not altered (P greater than .10). Plasma nonesterified fatty acids peaked (P less than .001) at 94% above PRE levels 40 min into NH4Cl infusion, thereafter declining to PRE concentrations. Whole blood acetoacetate and beta-hydroxybutyrate concentrations were not altered (P greater than .10) by NH4Cl administration. Plasma insulin concentration decreased (P less than .05) 26 to 46% during NH4Cl infusion and increased (P less than .05) 89 to 122% during POST. Plasma glucagon levels were not altered by NH4Cl infusion, so molar insulin:glucagon ratio changes resembled those of insulin. Plasma epinephrine, norepinephrine and dopamine did not vary (P greater than .10) with treatment. These results support the hypothesis that the hyperglycemia observed during hyperammonemia may result from an under-utilization of glucose by insulin-sensitive tissues.
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PMID:Subclinical ammonia toxicity in steers: effects on blood metabolite and regulatory hormone concentrations. 306 22

In order to study the effect of hyperglucagonaemia on nitrogen metabolism in diabetes, zinc protamine glucagon 60 micrograms was injected subcutaneously 3 times daily for 4 weeks into streptozotocin diabetic rats (n = 5), adequately treated with long acting insulin. This raised the plasma concentration of glucagon to 725 +/- 125 (mean +/- SEM), which is not different from that found in portal blood of uncontrolled diabetic rats: 400 +/- 75 ng/l. The controls were 5 diabetic rats treated with insulin alone and 5 non-diabetic rats. Compared with control rats the nitrogen balance was reduced (p less than 0.05) and the nitrogen contents of carcass, heart, intestines, and kidneys were reduced by 15-30% (p less than 0.05) in the glucagon treated rats. The hepatic capacity of urea synthesis and the alanine elimination rate were determined in the 3 above-mentioned groups, and confirmed in 3 identical groups followed for only 2 weeks; and in addition in a group of glucagon treated diabetic rats, where the long acting glucagon was substituted by neutral insulin the last two days before investigation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exogenous hyperglucagonaemia in insulin controlled diabetic rats increases urea excretion and nitrogen loss from organs. 306 29

The effects of chronic uraemia on glucose production and nitrogen release (urea plus ammonia formation) from alanine, glutamine or serine in isolated rat hepatocytes were studied. Uraemia increased the rate of formation of urea plus ammonia from all three amino acids by 38-93% when they were present at a final concentration of 10 mmol/l. At lower concentrations (2 mmol/l) the rate of nitrogen release was not significantly increased. Hepatocytes from normal rats whose food intake had been restricted to the level of that of uraemic rats did not show the increased rates of nitrogen release. The increased rates of nitrogen release with hepatocytes from uraemic rats were not accompanied by increased rates of glucose synthesis. Instead, accumulation of metabolic intermediates occurred: lactate and pyruvate (alanine or serine as substrates) and glutamate (glutamine as substrate). Livers of uraemic rats had increased activities of glutaminase (30%) and serine dehydratase (100%). Hepatocytes from normal rats treated with phlorhizin to increase the plasma glucagon/insulin ratio behaved in a similar manner to hepatocytes from uraemic rats. They had increased serine dehydratase activity, and increased rates of utilization of serine or glutamine. The possible implications of these findings for human uraemia are discussed.
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PMID:Effects of chronic uraemia on the formation of glucose and urea plus ammonia from L-alanine, L-glutamine and L-serine in isolated rat hepatocytes. 308 21

The effects of increasing glucose intake on nitrogen balance, energy expenditure and fuel utilization were measured in malnourished adult patients receiving parenteral nutrition with constant nitrogen intake and high or low glucose intakes for 8 day periods. Energy balance, nitrogen balance, weight and temperature were determined daily. Blood samples taken at admission and at the end of days 7 and 8 of each diet were analysed for glucose, fatty acids, urea, insulin, glucagon and thyroid hormones. The effect of increasing glucose intake was to increase nitrogen balance by 0.28 +/- 0.08 (SEM) mg/kJ. A scheme is proposed, based on present and previous findings, of the separate effects of nitrogen and energy intake on nitrogen balance, permitting calculation of rates of repletion of fat and lean body mass from estimates of nitrogen intake and energy balance. Malnourished patients are shown to attain markedly positive nitrogen balances at zero or negative energy balances. Large errors in estimation of energy requirements have little effect on nitrogen balance. Changes in nitrogen balance were entirely due to changes in urea excretion. Creatinine excretion increased 12% with high glucose intake, attributed mainly to increased muscle mass (7%) and body temperature (4%). A 12% increase in resting energy expenditure was only partly due to costs of glycogen storage and lipogenesis; the remainder, about one-half, is probably due to glucose and insulin mediated increases in sympathetic activity. There were marked increases in 3,5,3'-triiodothyronine (T3) concentrations with time, but no difference between the high and low glucose diets. The T3/thyroxine ratio, an index of free T3 concentration, increased much more rapidly on the high than on the low glucose diet. Changes in T3 could not account for the effect of glucose, under these conditions, to increase resting energy expenditure.
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PMID:Effects of increasing glucose intake on nitrogen balance and energy expenditure in malnourished adult patients receiving parenteral nutrition. 310 72

Chicks of the king penguin (Aptenodytes patagonica) can tolerate a fast of 4-6 months during the subantarctic winter. The aim of this work was to study their initial response to food deprivation. Nine chicks were starved for 18 days. Two phases of starvation were defined according to changes in the specific daily loss in body mass: it decreased by 92% in phase I (6.6 +/- 0.3 days) and remained steady and low in phase II. Phase I was marked by a large decline in protein utilization, indicated by decreases in plasma levels of alanine (58%), uric acid (89%) and urea (76%) together with a decrease in circulating corticosterone (60%) and thyroxine (75%). In phase I, plasma insulin concentration decreased (61%) in some birds, but did not change in others; plasma pancreatic glucagon was stable whereas gut-glucagon decreased by 75%. Free fatty acids and beta-hydroxybutyrate concentrations gradually rose during the fast to 5 to 6 times pre-fast levels. Glycemia remained unchanged. Phase II was characterized by no change in plasma concentrations of protein-derived metabolites and by no or little change in circulating hormone levels. From comparison with previous data, we conclude that there are similar early adjustments to food deprivation in king penguin chick, rat and man: (1) a decrease in resting metabolic rate, (2) a decrease in protein utilization, and (3) mobilization of fat stores. The key adaptations to long-term fasting in these species are therefore effectiveness in protein sparing and ability to prolong this situation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early changes in plasma hormones and metabolites during fasting in king penguin chicks. 322 Sep 86

(i) Hepatocytes isolated from adult rats were cultured for 2 to 3 weeks on collagen in a modified, serum-free Waymouth medium containing fatty acids and varying concentrations of glucocorticoid, insulin and glucagon. (ii) In the presence of all three hormones, it was possible to maintain the content of DNA, the activity of glucokinase, pyruvate kinase, hexokinase and lactate dehydrogenase at initial levels for 2 to 3 weeks. The activity of glucokinase and pyruvate kinase was affected by the concentration of insulin. (iii) The activity of alcohol dehydrogenase was stable for 3 days and declined to about 25% of the initial level after 2 weeks of culture, irrespective of the presence of hormones. (iv) Maintenance of albumin secretion was dependent on the presence of glucocorticoid, and glucocorticoid and insulin showed an additive or, at some time points, a synergistic effect on its secretion. (v) The content of cytochrome P-450 could be kept at 65% of the initial level, provided that a relatively high concentration of dexamethasone was present (10(-6) M). (vi) In the absence of hormones, urea synthesis was 70% of initial levels throughout the experimental period. With insulin and glucocorticoid present, a high concentration of glucagon (10(-8) M) was required to maintain the synthesis of urea at this level. (vii) It is concluded that hepatocyte cultures as described in the present study may be a useful, well-defined system for long-term metabolic, pharmacologic and toxicologic studies.
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PMID:Long-term culture of hepatocytes: effect of hormones on enzyme activities and metabolic capacity. 327 89

Rats with experimental diabetes due to streptozotocin (75 mg/kg body weight) and free access to food were divided into two groups. One group (n = 9) was optimally treated with insulin (glucosuria less than 4.0 mmol/24 h), using heat treated very long-acting ultralente insulin. The other group (n = 10) was poorly treated with insulin (glucosuria 20-30 mmol/24 h). The nitrogen balance and energy balance of optimally treated diabetic rats was positive and not different from the control group (n = 6). In the poorly treated diabetic rats the nitrogen balance was reduced whereas the energy balance was not different from that of control rats. After 4 weeks the fasting glucagon was: 50 +/- 21 ng/l (mean +/- SEM) in control rats, 62 +/- 18 ng/l in optimally treated diabetic rats and 249 +/- 58 ng/l in poorly treated diabetic rats (p less than 0.01). The capacity of urea nitrogen synthesis determined during alanine loading was: 9.6 +/- 1.0 mumol/(min 100 g body weight) in control rats, 10.6 +/- 1.7 mumol/(min 100 g body weight) in optimally treated diabetic rats and 17.3 +/- 1.3 mumol/(min 100 g body weight) in poorly treated diabetic rats (p less than 0.01). Nitrogen contents of carcass, heart, intestines, liver, and kidneys as determined by Kjeldahl analyses were identical in control rats and optimally treated diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Strict insulin therapy normalises organ nitrogen contents and the capacity of urea nitrogen synthesis in experimental diabetes in rats. 328 51


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