Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Female Wistar rats weighing 217 g were subjected to two types of surgical stress: uncomplicated (hysterectomy) and complicated (spleen and uterus ligated, crushed, and left in situ). Liver function as assessed by amino-N conversion was measured as the capacity for urea-N synthesis preoperatively (control animals) and on Days 1, 3, and 6 postoperatively. Uncomplicated surgery transiently increased the capacity for urea-N synthesis by 30% the first postoperative day (P less than 0.001). Complicated surgery decreased the capacity for urea-N synthesis to 55% throughout the investigation period (P less than 0.001). This was not due to a general change in liver mass since galactose elimination capacity remained constant. The increase in the capacity for urea-N synthesis after uncomplicated surgery is probably due to glucagon since plasma glucagon increased whereas plasma insulin and blood glucose remained unchanged after amino acid loading. The persistent decrease in the capacity for urea-N synthesis in complicated surgery is not due to changes in these regulators: glucagon increased, insulin decreased, and the rats were hypoglycemic. All changes are expected to increase the capacity for urea-N synthesis. The mechanism for the emergence of these two distinct metabolic patterns is not known. The phenomenon is probably important for interpretation of metabolic data on clinical stress.
 ...
PMID:Contradictory effects of uncomplicated versus complicated abdominal surgery on the hepatic capacity for urea synthesis in rats. 220 48

To assess the metabolic characteristics of cirrhotic hepatocytes, a primary culture of hepatocytes was established using rat liver induced cirrhosis by CCl4 administration. Using this system, cell responsiveness to different metabolic and excretory stimuli was investigated and compared with a primary culture of normal healthy rat hepatocytes. Cirrhotic hepatocytes showed reduced protein synthesis in response to insulin and reduced urea synthesis in response to glucagon. However, DNA synthesis stimulated by insulin and EGF was significantly enhanced in cirrhotic hepatocytes. No significant difference was observed in the fluorescein diacetate excretion rate. Cirrhotic hepatocytes showed impairment of antipyrine metabolism and conjugation and excretion of unconjugated bilirubin. These results suggest indirectly that cirrhotic hepatocytes may be less functionally mature than normal healthy hepatocytes.
 ...
PMID:[Studies on metabolic characteristics of cirrhotic rat hepatocytes using primary culture]. 221 64

Rates of fat mobilization (glycerol turnover), and fuel utilization and energy expenditure (indirect calorimetry) were measured in normal subjects and injured or septic patients maintained on high or low iv intakes of glucose as their sole nutrient source during 3-day periods. Regimens were given consecutively to each subject in random order. Concentrations of glucose, glycerol, fatty acids, 3-hydroxybutyrate, urea, insulin, and glucagon were determined in plasma, and of epinephrine and norepinephrine in urine. In normal subjects, there was no increase in energy expenditure with increasing glucose, although estimated costs of glucose storage as glycogen or fat could account for an increase of 4%. Thus, storage costs of glucose do not necessarily constitute an obligatory increase in energy expenditure. Rates of glycerol turnover and fat oxidation, and plasma glycerol concentrations were lower with the high than the low rate of glucose infusion, and lower than values reported by others during fasting or glucose infusion. Rates of fat oxidation were higher and glucose oxidation lower in patients than in controls, even though insulin concentrations were more than twice as high in patients. This confirms previous studies comparing injured and septic patients to depleted patients or historical controls. Triglyceride cycle activity was higher in the injured and septic patients than in normal subjects, and could account for from 6% to 15% of the increase in energy expenditure, in agreement with reports for burn patients.
 ...
PMID:Effects of glucose on fuel utilization and glycerol turnover in normal and injured man. 229 2

The effect of glucagon on the relation between urea synthesis and blood amino acid concentration was studied in seven healthy volunteers. Alanine was given as prime-continuous infusions and, after 1 hr for equilibration, the urea nitrogen synthesis rate was measured in two periods of about 2 hrs as urinary excretion corrected for accumulation and intestinal hydrolysis. During one of the periods, glucagon was infused to obtain a constant concentration of 200-1200 ng/l. The spontaneous urea synthesis during the alanine infusion was 86-141 mmol/hr and linearly related to the alanine concentrations of 1.33-2.99 mmol/l. The hepatic clearance of alanine-nitrogen to urea-nitrogen, assessed by the ratio between the increase in the urea synthesis rate and alanine concentration, was 23 +/- 4 l/hr (mean +/- S.D.). Glucagon increased the rate of urea synthesis by 35 +/- 11 mmol/hr (p less than 0.02) and decreased the alanine concentration by 0.22 +/- 0.06 mmol/l (p less than 0.01). Glucagon increased the hepatic nitrogen clearance to an average of 42 +/- 13 l/hr (p less than 0.01). The difference between infusion of amino-nitrogen and appearance of urea-nitrogen was +15 +/- 10 mmol/hr during alanine infusion alone and -11 +/- 25 mmol/hr during exogenous glucagon. The loss of nitrogen could be accounted for by depletion of non-alanine amino acids from the blood. Glucagon increases the efficacy of urea synthesis, which may be of importance for catabolism by changing the hepatic contribution to nitrogen homeostasis.
 ...
PMID:Glucagon increases hepatic efficacy for urea synthesis. 230 30

Glutamine is an important amino acid because of its key role in the transfer of both carbon and nitrogen between tissues in the body. Specific tissues are usually associated with either net synthesis or net utilization of glutamine, but the liver plays a central role in glutamine homeostasis, in that it can shift to function in either capacity. This capability, along with the localization of urea biosynthesis in the periportal hepatocytes, focuses attention on the transport mechanisms in hepatocytes for uptake and release of glutamine. Active transport of glutamine by hepatocytes is mediated by a Na(+)-dependent activity termed system N, which exhibits a rather narrow substrate specificity mediating uptake of histidine and asparagine as well as of glutamine. This secondary active transport system allows for the net accumulation of glutamine against a concentration gradient and maintenance of intracellular concentrations of glutamine between 4 and 8 mM in the face of a plasma concentration of 0.6 mM. Utilization of the Na+ electrochemical gradient as a driving force ensures that the system N carrier catalyzes a unidirectional transport event favoring the cytoplasm. It is obvious from the glutamine gradient across the plasma membrane that efflux of this amino acid is typically slower than accumulation; measurement of saturable, Na(+)-independent glutamine transport by system L substantiates this proposal. However, it is clear that under certain metabolic conditions the liver represents a source of glutamine for other tissues in the body and net efflux must occur. The system N transport activity in hepatocytes is regulated by hormones such as insulin, glucagon, and glucocorticoids, as demonstrated both in vivo and in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Characteristics and regulation of hepatic glutamine transport. 240 55

To understand better impairment of glucose utilization in diabetics during a hyperosmolal state, in vitro models were established to evaluate the effects of hyperosmolality on basal glucose uptake as well as glucagon dependent glucose release by isolated hepatocytes. In these studies simulating a hyperglycaemic (40 mmol glucose) and hyperosmolal (up to 500 mosm kg-1, NaCl as added solute) state basal hepatic glucose uptake was reversibly suppressed by 19% when osmolality was increased by as little as 10 mosm kg-1. No such effects on glucose uptake by isolated hepatocytes could be attained when the incubation's fluid osmolality was augmented by the addition of urea or mannitol. Estimations of the transport rates of 3-O-methylglucose and uptake of 2-deoxyglucose at 400 vs. 300 mosm kg-1 revealed that impaired intracellular enzymatic activity but not the transport rate of glucose into the cell were responsible for the hyperosmolal defect as uptake was more reduced (P less than 0.025) by increased osmolality for 2-deoxyglucose (16%) than for 3-O-methylglucose (13%). Glucagon dependent glucose release from isolated hepatocytes was diminished by 17.8% when the osmolality was raised to 400 mosm kg-1 by NaCl as added solute. These data obtained in vitro support the clinical contention that a hyperosmolal state, which corresponds to a loss of fluid in excess of solutes, is able to impair basal hepatic glucose uptake as well as glycogenolytic glucagon action on the liver.
 ...
PMID:Effect of hyperosmolality on basal and hormone-stimulated hepatic glucose metabolism in vitro. 249 70

Metabolic effects of a trickle challenge with the equivalent of 10,000 infective Ostertagia ostertagi larvae per day were investigated in 12 calves allocated to infected, pair-fed control or ad libitum-fed control groups. Changes in hormone levels reflecting abomasal, pituitary and pancreatic function were monitored using radioimmunoassay techniques previously validated for use in cattle. A range of metabolic profile parameters and blood metabolites was also measured. Feed intake of the infected calves began to decline as blood gastrin and pepsinogen levels reached a peak. The depression in appetite recorded in this group was responsible for significant increases in plasma urea and non-esterified fatty acid levels and associated with an increase in growth hormone/insulin ratio. No significant difference in glucagon levels was recorded between groups. A decline in blood albumin values was also shown in the infected group and associated with a drop in nitrogen digestibility. A significant depression in circulating calcium levels was related to either the hypoalbuminaemia or impaired mineral absorption in the intestine. A decrease in plasma cholesterol values in the infected group was associated with changes in digestive function.
 ...
PMID:Ostertagia ostertagi infection in the calf: effects of a trickle challenge on the hormonal control of digestive and metabolic function. 259 87

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.
 ...
PMID:Effects of dose of ingested glucose on plasma metabolite and hormone responses in type II diabetic subjects. 267 94

Two experiments involving 3- to 5-d-old dairy calves were carried out. In Experiment 1, lime-treated corn flour (Nixtamal) supplied 50 to 100% of carbohydrates in a milk substitute based on sodium caseinate, lard, and cerelose. In Experiment 2, partially hydrolyzed fish protein concentrate replaced 50% of 67% of proteins in milk substitutes based on skim milk powder, lard, and 35% Nixtamal. Increasing the proportion of carbohydrates supplied by Nixtamal was associated with a linear decrease of postprandial serum glucose and insulin. Postprandial fluctuations in blood glucose were less in calves fed Nixtamal than in controls. Nixtamal probably was trapped within the casein clot in the abomasum, leading to delayed rate of passage of Nixtamal carbohydrates into the intestine. Replacing skim milk protein with hydrolyzed fish protein in diets containing Nixtamal had no effect on blood glucose or insulin but elevated free essential amino acids, which promoted glucagon secretion. More uniform concentrations of blood essential amino acids and glucose were related to lower blood urea at 54 d in calves fed diets based on hydrolyzed fish protein and Nixtamal, than that of control calves. It is suggested that more uniform postprandial blood glucose concentrations might reduce amino acid degradation for energy purposes and stimulate protein synthesis. Young dairy calves may adapt to milk substitutes based on Nixtamal and hydrolyzed fish protein despite changes in the concentration patterns of several blood components.
 ...
PMID:Blood responses of calves fed milk substitutes containing hydrolyzed fish protein and lime-treated corn flour. 267 72

Acid-urea extract of rat brain was examined by glucagon-like peptide-1 (GLP-1) specific radioimmunoassay. A single peak was observed which co-eluted with GLP-1(7-36)amide on gel filtration and anion exchange chromatography. In contrast, GLP-1(1-37) was not detected under our experimental conditions. The fact that GLP-1 (7-36)amide, but not GLP-1(1-37), was present in rat brain suggests that preproglucagon was processed in the brain in the same manner as in the intestine and not as in the pancreas.
 ...
PMID:Identification of glucagon-like peptide-1(7-36) amide in rat brain. 272 60


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>