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 untreated type II (non-insulin-dependent) diabetic subjects were given 15, 25, 35, and 50 g glucose orally. Plasma glucose, insulin, C-peptide, glucagon, urea nitrogen, alpha-amino acid nitrogen, and lactate concentrations were measured, and net 5-h postprandial areas were calculated. The net glucose-area response to the ingested glucose dose (with the 0-time value as a constant baseline) was best described by a second-order polynomial equation, whereas insulin-area response was best described by a third-order equation. In a separate study, 5 untreated type II diabetic subjects were given only water, and the same metabolites and hormones were measured. Data from this study indicated that the baseline was not constant during the 5 h of study but decreased progressively. The net glucose-area and insulin-area responses to ingested glucose dose (with the decreasing baseline) were then best described by third-order equations. Glucagon, alpha-amino acid nitrogen, and lactate concentrations were exquisitely sensitive to a rise in glucose and insulin concentrations. These were all decreased with the lowest concentration of glucose used. At this dose of glucose, the increase in insulin was only 15 microU/ml.
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PMID:Effects of dose of ingested glucose on plasma metabolite and hormone responses in type II diabetic subjects. 267 94

The biologic activities of three synthetic analogues of CCK-4 (Trp-Met-Asp-Phe-NH2) in which (i) the C-terminal residue Phe was N-methylated (peptide I); (ii) the C-terminal Phe residue was N-methylated and Ser is substituted for Met in position 2 (peptide II); (iii) Pro was substituted for Trp in position 1 and the C-terminal amino nitrogen was methylated (peptide III), have been described. Peptides I and II have been found to inhibit the release of both insulin and glucagon, while peptide III was found to be a potent releasing agent for insulin and an inhibitor for glucagon.
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PMID:Effect of some novel synthetic analogues of CCK-4 on insulin and glucagon secretion. 269 15

Diet-induced thermogenesis after ingestion of a mixed meal was investigated in eight patients with documented liver cirrhosis and in eight age- and sex-matched healthy controls. Respiratory gas exchange was measured continuously for one hour in the basal state and for three hours after ingestion of a mixed liquid meal, consisting of 17% kJ protein, 28% kJ lipids and 55% kJ carbohydrates and dispensed to correspond to 60% of the individually computed energy expenditure. Arterial substrate and hormone concentrations were determined before and at timed intervals for three hours after the meal. Urine was collected for determination of nitrogen excretion. The patients' oxygen uptake, energy expenditure and respiratory quotient were similar to those of the controls in the basal state. After the meal, pulmonary oxygen uptake and energy expenditure rose markedly in both groups during the first hour and were subsequently stable. The average increase in oxygen uptake above basal during the whole study period was 21.2 +/- 1.8% and 22.3 +/- 1.2% (NS) in patients and controls, respectively. The corresponding increase in energy expenditure was 24.8 +/- 2.0% in the patients and 24.9 +/- 1.4% in the controls (NS). The respiratory quotient was elevated throughout the postprandial period in both groups but the quotient was significantly higher in the patients (P less than 0.05-0.001), suggesting a greater proportion of carbohydrate oxidation. The basal arterial concentrations of insulin and glucagon were significantly higher in the patients. After the meal the insulin level increased 10- to 20-fold in both groups. Glucose concentration rose significantly in both groups to a maximum of 8.82 +/- 1.00 and 8.03 +/- 0.95 mmol/l in patients and controls, respectively, at 60 min after the meal. This was accompanied by a fall in the levels of glycerol and ketone bodies in both groups, indicating decreased lipolysis. It is concluded that both the basal energy expenditure and the thermogenic response to a mixed meal are similar in patients with liver cirrhosis and in healthy controls. The patients' carbohydrate oxidation rose to a greater extent after the meal, probably as a consequence of excessive increases in insulin concentration, demonstrating that insulin resistance in these patients may be compensated for by postprandial hyperinsulinaemia.
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PMID:Diet-induced thermogenesis in patients with liver cirrhosis. 272 Nov 26

Efficient treatment of deep denutrition should promote the restoration of normal intestinal villous structure and the return to a positive nitrogen balance. To determine whether the plasma measurement of lipoproteins could serve as sensitive indexes of villous architecture and/or nitrogen balance, these parameters were compared in rats starved for three days and refed three types of diets containing either whey proteins (WP), whey protein hydrolysate (WPH), or amino acids, known to differ in their capacity to promote restoration of normal villous architecture. Starvation lowered the concentration of triglycerides and phospholipids but not cholesterol. Apolipoprotein AI and AIV concentrations were also significantly lowered (30% and 40%, respectively), but ApoE was significantly increased by 40%. Upon refeeding with all three diets, plasma lipids progressively returned to control values except for triglycerides, which were significantly elevated by the protein and peptide diets. Apoprotein AI continued to decrease for 24 hours on the peptide and amino acid diets. Control levels were restored in all groups after 48 hours. ApoAIV increased progressively in parallel with the restoration of the intestinal mucosa; after 48 hours of refeeding, plasma concentrations of apo AIV were significantly correlated with jejunal villous height and protein content (P less than .01). ApoE was depressed below control levels in the WP and WPH groups at 24 and 48 hours and restored only after 96 hours. Because ApoE was affected, both in the fed state and during refeeding by the form of dietary nitrogen, it may prove to reflect nitrogen balance and/or insulin: glucagon balance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum lipids and apolipoproteins in the rat refed after starving: influence of the molecular form of nitrogen (protein, peptides, or free amino acids). 276 11

The effect of carbohydrate overfeeding on protein metabolism was studied in 11 healthy men. Total urinary nitrogen output during 10 days of carbohydrate overfeeding (1,600 extra kcal/day) decreased 27% relative to nitrogen excretion during 10 days of weight maintenance, indicating protein accretion during over-feeding. However, postabsorptive nitrogen excretion did not change, which means that the positive nitrogen balance associated with overfeeding results from enhanced postprandial nitrogen retention. Overfeeding reduced postabsorptive glucose concentrations 4 +/- 1% and increased glucose production rate 14 +/- 2% and glucose clearance 17 +/- 4%. Overfeeding increased plasma concentrations of insulin, glucagon, and 3,5,3'-triiodothyronine approximately 20%. Alanine and branched-chain amino acid concentrations were increased after overfeeding, but serine, threonine, and asparagine concentrations were reduced. Postabsorptive leucine flux, which is an index of proteolysis, was measured using L-[1-13C]leucine as a tracer. Overfeeding increased leucine flux 13 +/- 2% compared with values after 10 days on a weight-maintenance diet. If it is assumed that overfeeding did not alter the fraction of 13CO2 not recovered in breath, there was no change in the portion of leucine flux that was oxidized. Thus the difference between flux and oxidation, which is a theoretical index of protein synthesis, increased 12 +/- 3% after overfeeding. These data suggest that excess caloric intake, without an increase in protein intake, stimulates post-absorptive proteolysis and protein synthesis.
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PMID:Stimulation of protein turnover by carbohydrate overfeeding in men. 278 3

Four-day fasting in the conscious dog is associated with enhanced ammoniagenesis in both the gut and kidneys and a switch in the hepatic glutamine balance from net uptake to that of net production. In the present study we examined the role that the rise in portal venous ammonium ions plays in regulating nitrogen metabolism in vivo. Three groups of 18- to 24-h fasted conscious dogs with catheters surgically implanted in the femoral artery and in the hepatic, portal, and renal veins for 17-21 days were studied. On the day of the study, one group (n = 6) received intraportal ammonium acetate at 3.0 mumol.kg-1.min-1 intended to result in portal venous ammonium ion levels slightly above those seen in the 4-day fasted dog. Another group (n = 5) received an equimolar infusion of sodium acetate, and a third group (n = 6) received saline (0.9%) and acted as controls. Organ balances across the liver, extrahepatic splanchnic tissues (gut), and kidneys were estimated by the arteriovenous differences multiplied by blood flows. All of the load of ammonium acetate infused intraportally was taken up by the liver. As a result there was an immediate switch in hepatic glutamine balance from that of net uptake to net production similar to that seen in the 4-day fasted dog. Simultaneously, net hepatic production of urea nitrogen doubled. These occurred with no change in acid-base balance or no change in circulating arterial or portal venous levels of insulin and glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of ammonium ions in regulating hepatic glutamine synthesis during fasting. 280 34

The results of the few studies on the effect of the thyroid status on nitrogen metabolism have been inconclusive and/or contradictory. In an attempt to elucidate this important relationship, we have studied the effect of experimental hypo- and hyperthyroidism on urea biosynthesis and related processes. We have found that the capacity of the liver to synthesize urea was increased in hypothyroid rats, as were the activities of the urea cycle enzymes; there were also changes in the activities of some related enzymes and in the levels of intermediates and amino acids. Isolated hepatocytes from these rats showed an increased capacity for urea synthesis. In hyperthyroid rats the picture was more complicated, since there was no change in the urea-synthesizing capacity of the liver, although there were changes in some enzymes and metabolites. Our results suggest that there may be more endogenous proteolysis in hypothyroidism which would increase ammonia production, the ammonia being used primarily for urea biosynthesis and, to a lesser extent, for glutamate and aspartate synthesis. These overall effects might be the result of an increase in glucagon and/or cAMP, which, as is well known, increase the urea-synthesizing capacity of liver. In hyperthyroidism, on the other hand, the changes in nitrogen metabolism could be the result of an increase in protein synthesis, a decrease in catabolic activity, or both.
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PMID:Effect of thyroid hormones on urea biosynthesis and related processes in rat liver. 284 5

Protein catabolism following injury is associated with elevated levels of the stress hormones cortisol, glucagon, and the catecholamines. To study the effect of hormonal blockade on catabolic responses to surgery, 16 dogs underwent general anesthesia, a standard abdominal operation, and implantation of aortic and caval catheters. Five received phentolamine and propranolol continuously, at doses which block catecholamine effects. To prevent the rise in both catecholamines and cortisol, 6 received a high epidural anesthetic (T4-S3), started preoperatively and continued for 24 hr. Five dogs served as controls. Hindquarter amino acid flux was measured at 6 and 24 hr post-op. Pre- and post-op skeletal muscle biopsies were analyzed for amino acids. Urinary nitrogen was measured over 24 hr. Urinary nitrogen excretion was unaffected by treatment, but urinary creatinine fell from 0.039 +/- 0.002 g/24 hr X kg for controls to 0.03 +/- 0.002 for the epidural group and 0.031 +/- 0.001 for alpha and beta blockade (P less than 0.05). Hindquarter amino acid nitrogen efflux was decreased from -19.05 +/- 4.06 mumole/min X kg in controls to -8.98 +/- 0.86 in the epidural and -6.89 +/- 1.21 in the alpha- and beta-blockade groups (P less than 0.05). The urinary nitrogen loss, glutamine efflux, and fall in muscle glutamine produced by the operation were not prevented by either form of hormonal blockade, but hindquarter nitrogen efflux was diminished. Hormonal blockade inhibits net skeletal muscle protein catabolism without altering whole-body nitrogen loss. Hormones and other factors must be responsible for the increased ureagenesis that occurs following injury.
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PMID:Hormonal blockade modifies post-traumatic protein catabolism. 286 76

The postprandial release of immunoreactive insulin, glucagon, gastrin, somatostatin, pancreatic polypeptide (PP), and gastric inhibitory polypeptide (GIP) was studied in parallel with the absorption of sugars and amino acids in conscious pigs. Six pigs fitted with permanent catheters in the portal vein and arterial blood system as well as within an electromagnetic flow probe around the portal vein received successively at 3-day intervals, three meals of 800 g each containing 0, 14, or 28% protein (semisynthetic diets based on fish protein). Blood samples were collected and portal blood flow was recorded during a postprandial period of 8 h. For the same level of feed intake, an increase in the dietary protein concentration led to a higher alpha-amino nitrogen absorption and to a lower appearance of reducing sugars in the portal vein; in addition, the carbohydrate absorption efficiency (amounts absorbed as a percentage of amounts ingested) was reduced, showing the competition between the absorption of amino acids and glucose. The largest absorption occurred during the first 4 h after the meal, but neither the digestion of proteins nor that of carbohydrates were finished 8 h after the meal since portoarterial differences could still be observed. All test meals induced a rise of portal and peripheral concentrations of insulin, gastrin, somatostatin, and PP, and of the systemic level of GIP. Glucagon increased after the 28% protein meal only. The rise of plasma insulin paralleled that of blood glucose, and bore a significant positive relationship to the systemic GIP level in the early postprandial period. In terms of absolute amounts, portoarterial concentration gradients increased postprandially. Insulin release was significantly the highest after intake of the 14% protein diet. The gastrin response was significantly correlated to the amount of protein. Similarly the release of glucagon and somatostatin tended to increase with increasing dietary amount, but differences failed to reach significance (P less than 0.05), except for glucagon 2 h after the meal. There were very close relationships between the hourly amounts of alpha-amino nitrogen absorbed and gastrin and glucagon production, as between insulin and PP secretions. From the present results, the induction of physiological increments of plasma peptide concentration in 60-kg pigs would require infusion rates of about 50-250 micrograms/h for insulin, 1-4 micrograms/h for gastrin 17, 5-10 micrograms/h for glucagon and somatostatin, and 5-50 micrograms/h for PP.
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PMID:Metabolic and hormonal effects of test meals with various protein contents in pigs. 286 30

We investigated the roles of insulin and glucagon as mediators of changes in glucose and alanine kinetics during the hypermetabolic response to injury in 10 burn patients by infusing somatostatin with and without insulin replacement. Glucose and alanine kinetics were measured by primed-constant infusions of 6,6-d2-glucose and [3-13C]alanine. The basal rate of glucose production and alanine flux were significantly elevated in all patients. Lowering both hormones simultaneously caused an insignificant reduction in glucose production, but plasma glucose rose significantly (P less than 0.01), because of reduced clearance. Alanine flux and total plasma amino nitrogen increased significantly (P less than 0.05) above basal. Selectively lowering glucagon concentration decreased glucose production (P less than 0.05), and exogenous glucose was infused to maintain euglycemia. Alanine flux and total plasma amino nitrogen remained unchanged. In severely burned patients hyperglucagonemia stimulates increased glucose production, basal insulin suppression glucose production, stimulates basal glucose clearance, and is important for regulation of plasma amino acid concentrations, and the selective lowering of glucagon while maintaining basal insulin constant normalized glucose kinetics.
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PMID:Role of insulin and glucagon in the response of glucose and alanine kinetics in burn-injured patients. 287 83


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