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)

The effect of glucagon on the components of the hepatic microsomal electron transport chain (NADPH oxidase, NADPH cytochrome c reductase (EC 1.6.2.4), cytochrome P-450, and NADPH cytochrome P-450 reductase), and on two representative oxidative pathways (aminopyrine N-demethylation, a type I substrate oxidation; and aniline p-hydroxylation, a type II substrate oxidation) was determined. Microsomes from rats pretreated with glucagon (300 mug/kg per day for 3 days) showed a significant decrease in NADPH oxidation and in aminopyrine N-demethylation with a prolonged hexobarbital sleeping time, and a significant increase in aniline p-hydroxylation. Microsomes from rats pretreated with a lower dose of glucagon (30 mug/kg per day for 3 days) showed a significant decrease in the microsomal N-demethylation of aminopyrine. Glucagon had no effect when added in vitro to microsomes, suggesting that the in vivo effects of glucagon are mediated indirectly in the intact animal.
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PMID:Alterations of hepatic microsomal drug metabolism by glucagon. 81 38

Abnormal glucose tolerance is often found in patients with anorexia nervosa (AN). We attempted to evaluate pancreatic B-cell functioning after intravenous glucagon administration. Fourteen patients with the restricting type of AN (percentage of ideal body weight 71.5 +/- 1.6%, mean +/- SE) and 6 patients with the bulimic type of AN (77.0 +/- 3.0%) were studied. After an overnight fast, glucagon (0.02 mg/kg) was injected i.v. into all subjects and 6 normal controls. Blood samples were obtained at 0, 5, 30, 60, 90 and 120 min to measure blood glucose (BS), serum insulin (IRI) and C-peptide (CPR). The same tests were repeated in 8 patients with restricting AN after therapy and restoration of body weight (85.9 +/- 1.0% of ideal body weight). BS responses did not differ among the groups. Peak serum levels (5 min) of both IRI and CPR in restricting AN patients were significantly lower than those in bulimic AN patients and in normal controls. BS, IRI and CPR concentrations did not change significantly following restoration of body weight. Pancreatic B-cell dysfunction after glucagon administration was observed in restricting AN patients and the abnormality persisted after short-term weight restoration.
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PMID:Pancreatic B-cell functioning after intravenous glucagon administration in anorexia nervosa. 154 50

The serum ketone response to glucagon was measured in 10 patients with IDDM and 37 with NIDDM. In both groups, serum 3-hydroxybutyrate increased significantly after intravenous injection of 1 mg glucagon. The difference between the serum level of 3-hydroxybutyrate at 30 min and basal level [delta 3-OHBA(30')] was 133 +/- 25 mumol/l in the patients with IDDM, 13 +/- 8 mumol/l in those with NIDDM treated by diet alone or with oral hypoglycemic agents and 23 +/- 13 mumol/l in those with NIDDM treated with insulin. The delta 3-OHBA(30') was significantly greater in IDDM patients than in both groups of NIDDM patients (P less than 0.001). The delta 3-OHBA(30') was greater than 87 mumol/l in eighty percent of IDDM patients, but smaller than 87 mumol/l in both groups of NIDDM patients. The delta 3-OHBA(30') was correlated with the difference between the plasma level of C-peptide at 6 min and basal level [delta CPR(6')] (r = -0.540, P less than 0.001). The delta 3-OHBA(30') was not correlated with fasting plasma levels of glucose, fructosamine or hemoglobin A1c. These observations show that measurement of the serum ketone response to glucagon is a useful marker of insulin dependency. In order to determine insulin dependency, the simultaneous measurement of concentrations of ketones and C-peptide is indicated during the glucagon stimulation test.
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PMID:Serum ketone response to glucagon as a marker of insulin dependency in diabetics. 175 81

The increase in insulin requirement at the onset of adolescence is compensated by an increase of insulin secretion. This metabolic pattern persists during adolescence but is no longer present in adults. It is supposed to depend on a decrease of insulin sensitivity of uncertain origin. We compared the metabolic pattern of late adolescent girls (13-16 year old) with young women (21-30 year old) with similar body mass indexes, testing subjects with iv glucose tolerance test (IVGTT) (glucose 0.33 g/kg) and arginine test (ATT) (arginine 30 g in 30 min). In late adolescent vs adult women we observed: i) IVTT: similar k of glucose tolerance and higher insulin and C-peptide responses; ii) ATT: unmodified plasma glucose, insulin and glucagon values, higher GH plasma levels; iii) in adolescent girls GH and CPR incremental areas significantly correlated (r = 0.755, p less than 0.05). These data show that: i) the adolescent pattern of glucose metabolism persists after completion of sexual development and, ii) there is a positive correlation between GH response to arginine and beta-cell response to glucose. So GH should play a role in the impairment of glucose metabolism during adolescence.
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PMID:Glucose tolerance and insulin release in adolescent female. 176 11

Isolation and culture techniques for hepatocytes from whole livers of the cynomolgus monkey, Macaca fascicularis, are described. Hepatocytes were isolated by two-step perfusion of livers, using collagenase with hyaluronidase; fructose and trypsin inhibitor were included to reduce cell loss. Yields from a single liver average 4 X 10(9) cells with viabilities of 90.8 +/- 5.7%. Cells, plated on collagen substrates, were assessed for changes in morphology and various marker enzyme activities over a period of 7 d in culture. Cells exhibited a morphology similar to that observed for this species in vivo; little change in attached and spread cells was observed over the length of time monitored. Enzyme activities for catalase, succinate dehydrogenase, and tyrosine aminotransferase were observed to decrease significantly (though considerable activity remained), whereas acid phosphatase and 5'-nucleotide phosphodiesterase remained unchanged. Activity of cytochrome P-450 reductase was observed to increase slightly for the first 2 d, then decrease to about 60% of initial levels. Activity of alpha-mannosidase was stable for 4 d but was observed to be increased at Day 7. Cells were observed to retain metabolic responsiveness, demonstrated by glucose production by both gluconeogenesis and glycogenolysis in response to glucagon stimulation. The monkey hepatocytes obtained by methods described here thus retain hepatocellular morphology and activity through at least 1 wk in culture without medium or culture modification.
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PMID:Isolation and culture of hepatocytes from the cynomolgus monkey (Macaca fascicularis). 197 77

Subcellular fractionation of liver homogenates from treated rats was carried out in order to study the mechanism of action of the gastrointestinal polypeptides on glucoronidation. Rats were treated for 90 min with an intravenous infusion of secretin (0.4 cU/h/100 g body weight), glucagon (100 micrograms/h/100 g body weight) and vasoactive intestinal polypeptide (VIP) (300 ng/h/100 g body weight); controls were sham-treated rats. For comparison, another group of animals was treated with a daily injection of phenobarbitone (10 mg/kg), a well-established enzyme inducer. Treatment with the different polypeptides produced minor changes in the subcellular localization of the enzyme. The bulk of activity was always recovered in the microsomal fraction, as identified by both differential centrifugation and the enrichment in specific activity of glucose-6-phosphatase, esterase and NADPH-cytochrome c reductase. Secretin produced a specific increase of bilirubin glucuronidation, more evident in all nuclear fractions. Glucagon increased both bilirubin and p-nitrophenol glucuronidation in all subcellular fractions. VIP had a selective action on p-nitrophenol conjugation of similar extent in nuclear and microsomal fractions. The type of changes observed is suggestive of physicochemical modifications occurring into the cell, perhaps at the membrane environment of different organelles, able to modify the overall conjugation of different substrates by the cell.
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PMID:Subcellular localization of UDP-glucuronyltransferase by differential centrifugation. Changes produced by pretreatment of rats with secretin, glucagon, vasoactive intestinal polypeptide and phenobarbitone. 249 35

Fifty obese (BMI = 40.1 +/- 1.5) subjects (21 men and 21 women; average age 38.6 +/- 3.8 years) were prescribed a 600 cal/day diet (carbohydrates 30 g, proteins 60 g, lipids 10 g). Thirty patients were also given benfluorex (three tablets/day) for six months (Group A), whereas the other 20 patients (Group B) were treated with the dietary measures only. Apart from grade II and III obesity, several patients suffered from dyslipidaemia (Group A: n = 10; Group B: n = 7), non-insulin-dependent diabetes mellitus (NIDDM) (Group A: n = 4; Group B: n = 3) or IGT (Group A: n = 8; Group B: n = 6). The usual blood and biochemical tests and clinical examinations were carried out on Days 0, 90 and 180, together with the OGTT and glucagon test to determine blood glucose levels, IRI and CPR. There was no statistical difference between the weight loss of Group A and that of Group B. In Group A there was a statistically significant reduction (p less than 0.001) in total cholesterol, triglycerides, total/HDL-cholesterol and beta/alpha-lipoproteins and a significant increase in HDL-cholesterol and alpha-lipoproteins (p less than 0.001), whereas in Group B only a significant reduction in triglycerides (p less than 0.001) was observed. In NIDDM patients treated with benfluorex, normalisation of basal blood glucose levels was accompanied by an improvement in the OGTT blood glucose curve which was statistically significant relative to Group B. Benfluorex was well tolerated by all patients and no adverse event was reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of benfluorex in obese patients with metabolic disorders. 259 99

Dietary iron deficiency in rats results in increased blood glucose turnover and recycling. We measured the rates of glucose production in isolated hepatocytes from iron-sufficient (Fe+) and iron-deficient (Fe-) rats to assess the intrinsic capacity of the Fe- liver to carry out gluconeogenesis. Low-iron and control diets were given to 21-day-old female rats. After 4-5 wk, hemoglobin concentrations averaged 4.1 g/dl in the Fe- and 14.3 g/dl in the Fe+ animals. In the hepatocytes from Fe- rats, there was a 35% decrease in the rate of glucose production from 1 mM pyruvate + 10 mM lactate, a 48% decrease from 0.1 mM pyruvate + 1 mM lactate, a 39% decrease from 1 mM alanine, and a 48% decrease from 1 mM glycerol. The addition of 5 microM norepinephrine or 0.5 microM glucagon to the incubation media produced stimulatory effects on hepatocytes from both Fe- and Fe+ rats, resulting in the maintenance of an average difference of 38% in the rates of gluconeogenesis between the two groups. Studies on isolated liver mitochondria and cytosol revealed alpha-glycerophosphate-cytochrome c reductase and phospho(enol)pyruvate carboxykinase activities to be decreased by 27% in Fe- rats. We conclude that because severe dietary iron deficiency decreases gluconeogenesis in isolated rat hepatocytes, the increased gluconeogenesis demonstrated by Fe- rats in vivo is attributable to increased availability of gluconeogenic substrates and upregulation of the pathway.
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PMID:Iron deficiency decreases gluconeogenesis in isolated rat hepatocytes. 260 20

In an attempt to define the pancreatic B cell function in the elderly, we subjected 88 non-obese individuals (aged between 21 and 88) to an oral glucose tolerance test (OGTT), a simple glucagon test (SGT) and OGTT-glucagon test, in which the plasma glucose, insulin and serum C-peptide (CPR) were measured. We investigated heterogeneity in glucose intolerance in the elderly and its relationship to atherosclerosis. In the OGTT and SGT test, the insulin responses (SIRI/SPG ratios) for normal, borderline and DM1 (fasting plasma glucose less than 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) groups of the elderly (60 and above) were not significantly different from those for normal group of young and middle-aged (below 60) and were significantly higher for elderly group than for the young and middle-aged group in each glucose tolerance group. But the insulin responses for the DM2 (fasting plasma glucose greater than or equal to 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) group of the elderly were not significantly different from those for the DM1 and DM2 groups of young and middle-aged. The insulin responses of normal, borderline and DM1 groups of the elderly with atherosclerosis were significantly higher than those of the comparable groups without atherosclerosis, while the insulin responses of the borderline and DM1 groups of the elderly with atherosclerosis were similar to those of the control group of the young. In the OGTT-glucagon test, there were no differences in the insulin response or serum CPR response among the normal, borderline and DM1 groups of the elderly, and these responses were significantly higher for the elderly group than the for young and middle-aged group in each glucose tolerance group. But these responses for the DM2 group of the elderly were not significantly different from those for the DM1 and DM2 groups of the young and middle-aged. These results indicate that the pancreatic B cell function of the normal group in the elderly remains favorable while mildly impaired glucose tolerance was exhibited by the borderline and DM1 groups, who are comparable with the normal group of the young and middle-aged. But this function was clearly reduced in the DM2 group of the elderly. These findings suggest that there is a subgroup in the elderly, which has clinically evident atherosclerosis, mild glucose intolerance and high insulin response. Their pancreatic B cell function remains favorable.
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PMID:[Pancreatic B cell function and glucose intolerance in the elderly]. 265 22

To evaluate the effect of total pancreatectomy on the secretion of human growth hormone, twenty-six patients undergoing total pancreatectomy and twelve healthy subjects (controls) were investigated. Blood glucose (BG), plasma insulin (IRI), C-peptide (CPR), immunoreactive glucagon (IRG) and human growth hormone (HGH) levels were determined. In the glucose tolerance test, the mean basal blood glucose level in the patients before operation was significantly higher than the level in the controls. The basal blood glucose level in the patients after operation was still higher than the level before operation. The responses of IRI, CPR, and IRG secretion after arginine infusion in the patients before operation were less than those in the controls. After operation, arginine infusion did not alter the levels of IRI, CPR and IRG. The mean basal HGH levels were not significantly different between the controls and the patients before and after operation. However, a statistically significant correlation was shown between the basal values of plasma HGH and those of plasma IRI in the patients after operation. Thus, it suggested that the basal secretion of HGH is closely related to the exogenous plasma insulin levels in the pancreatectomized patients. After arginine infusion, the HGH levels in the patients before operation were lower than the those in the controls, but insignificant. After operation, mean HGH levels were significantly lower than those before operation. These findings suggested the absence of pancreatic endocrine function caused by total pancreatectomy resulted in decreased responses of HGH secretion after arginine infusion.
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PMID:[Influence of total pancreatectomy on the secretion of human growth hormone and the endocrine pancreas]. 305 67


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