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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated sheep hepatocytes were used to obtain estimates of kinetic parameters, identify substrate preference and interactions and study regulation of gluconeogenesis. Respective Vmax estimates for propionate, pyruvate and alanine conversion to glucose were 59.5, 12.8 and 21.5 mol glucose formed X (h X g dry weight)-1. Respective KS estimates for propionate and pyruvate were 1 mM and 18 to 40 microM. Rates of lactate utilization varied among cell preparations, possibly because of loss of lactate dehydrogenase during isolation. Dihydroxyacetone and glycerol were utilized for glucose synthesis at similar rates of 8.6 and 8.7 mumol glucose formed X (h X g dry weight)-1, respectively. Respective rates of glucose synthesis from 5 mM fructose and 10 mM galactose were 63.2 and 31.4 mumol X (h X g dry weight)-1. Maximum rates of pyruvate carboxylase and phosphoenolpyruvate carboxykinase were estimated to be 101.6 and 160.4 mumol substrate converted X (h X g dry weight)-1, respectively. Neither butyrate nor acetate accelerated gluconeogenesis from propionate while acetate increased glucose synthesis from pyruvate, presumably through activation of pyruvate carboxylase. Glucagon stimulated gluconeogenesis from propionate. Dibutyrylcyclic AMP mimicked the effect of glucagon, implying that the glucagon effect is translated via the adenyl cyclase system as in rats. The kinetic parameters established in these experiments should be useful in future experiments and in computer modeling analyses of ruminant liver and whole animal metabolism where Michaelis-Menten type equations are widely used.
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PMID:Gluconeogenesis in isolated lamb hepatocytes. 381 90

The effect of feeding high amounts of polyols on rat metabolism was studied. Adult male rats were fed the basal diet or the same diet to which had been added either galactitol, mannitol or xylitol for 8 wk (final polyol level 200 g/kg diet). Although all three polyols retarded the growth rate of the animals, the polyols were well tolerated. The four experimental groups did not differ significantly (P greater than 0.01) in the following analyses: blood lactic acid and serum transaminases, amylase, lactate dehydrogenase, triglycerides, insulin, glucagon and corticosterone. Compared to rats fed the basal diet, galactitol rats had higher blood hemoglobin levels (P less than 0.01); those fed galactitol or mannitol had lower blood glucose (P less than 0.001 and P less than 0.01, respectively), and those fed mannitol had higher blood pyruvic acid (P less than 0.01). Rats fed any of the polyols had lower serum total cholesterol and liver ascorbic acid (P less than 0.001) than control rats. Rats fed mannitol had higher liver glycogen levels (P less than 0.001) than control rats. Irrespective of the structural differences between the pentitol and the hexitols, a number of common metabolic effects were found. The proposed mechanisms of these effects include 1) the slow absorption and the rapid intraluminal metabolism of the polyols and 2) the similar handling of these polyols in the liver by a dehydrogenase.
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PMID:Metabolic effects in rats of high oral doses of galactitol, mannitol and xylitol. 392 94

The survival of adult rat hepatocytes in monolayer culture was studied in the presence of different hormones (neurotensin, oxytocin, thyrotropin releasing hormone, luteinizing hormone releasing hormone, cholecalciferol, bradykinin, substance P, aldosterone, melanocyte stimulating hormone, 3,3',5-triiodo-1-thyronine, corticosterone, human growth hormone, glucagon, insulin, progesterone, testosterone, estradiol, and dexamethasone phosphate) or growth factors (fetal bovine serum). For this purpose trypan blue exclusion, lactate dehydrogenase, and DNA and protein content were measured at 24 and 72 h of culture. 10(-7) M Dexamethasone, a mixture of eight hormones, 10% fetal bovine serum, and a combination of the latter two supplements caused a more than 64% higher DNA content at 72 h when compared to control cultures. A striking agreement of these results with changes of lactate dehydrogenase leakage was observed, whereas trypan blue exclusion gave erratic results. Considerable changes of cell arrangement apparently specific for each supplement were observed by low magnification microscopy. It is concluded that glucocorticoids and fetal bovine serum have an outstanding effect on cell viability and that DNA or protein content or both are reliable indicators of cell viability in amitotic cultures.
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PMID:Influence of hormones and growth factors on viability, DNA, and protein content of adult hepatocytes in primary culture. 405 11

The effects of 23 agonists on the rates of cellular 32P efflux and lactate dehydrogenase (LDH) release were tested in a perfused rat heart preparation which had been prelabelled in vitro with [32P]Pi. Some 13 compounds produced detectable changes at high doses within 10 min, and in most cases a polyphasic response was observed. Six classes of compound gave rise to substantial effects, as follows. Catecholamines and glucagon produced a transient initial stimulation of Pi efflux, followed by a long-term inhibition of Pi transport and an increased rate of LDH release. These effects were clearly different from the response seen after treatment with dibutyryl cyclic AMP, which had a slower, stimulatory, effect on Pi output in doses which gave rise to a pronounced inotropic effect, and produced a marked increase in both coronary flow and LDH release. Carbachol also gave rise to a large transient stimulation of Pi efflux, which was followed by smaller sustained increase in Pi output without any obvious effect on LDH release. Dibutyryl cyclic GMP had no effect on Pi efflux or LDH release. Insulin decreased the rate of Pi efflux, although the loss rate partially recovered towards the control value after prolonged exposure to the hormone. Insulin had no obvious inotropic effects and produced no change in the rate of LDH release. Corticosteroids increased the rate of Pi efflux, although the loss rate partially declined towards the control value with prolonged exposure to the hormones. Corticosteroids produced a very slight inotropic response, and large doses sometimes increased the rate of LDH release from the tissue. Aldosterone slightly stimulated Pi output. A small, transient and somewhat variable stimulation of Pi efflux was observed with vasopressin and angiotensin, whereas tri-iodothyronine was slightly inhibitory, but adenosine, histamine, spermidine, des-Asp1-angiotensin, prolactin, parathyroid substances, calcitonin and somatostatin had no significant effects under our experimental conditions. Ouabain stimulated Pi efflux in doses that had no detectable inotropic effect. It is suggested that Pi efflux involves the electroneutral transport of NaH2PO4 across the cardiac plasmalemma and that many of the hormonal effects might be explained by changes in the intracellular [Na+] and pH in addition to changes in the intracellular [Pi].
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PMID:Some hormonal effects on myocardial phosphate efflux. 609 15

1. Effect of glucagon on amylase secretion and lactic dehydrogenase (LDH) release from functionally intact dissociated pancreatic acinar cells and acini was studied. 2. In dissociated rat pancreatic acinar cells, the rate of amylase secretion was increased by 70% with bethanechol (maximally effective concentration, 10(-4) M) and 125% with A23187 (10(-5) M), but the response to cholecystokinin-pancreozymin (CCK-PZ) was inconsistent. In dissociated cells from mouse pancreas, the increases amounted to 78% with bethanechol (10(-4) M), 134% with A23187 (10(-5) M) and 82% with CCK-PZ (maximally effective concentration, 0 . 01 u. ml.-1). Glucagon in concentrations ranging from 10(-7) to 10(-4) M increased amylase secretion by 3, 26, 67 and 80%, whereas secretin (10(-8)--10(-5) M) increased amylase secretion by 8, 39, 88 and 138%. LDH release was increased with A23187 in concentrations greater than 10(-6) M. 3. CCK-PZ, bethanechol and A23187 used in maximal concentrations potentiated the effect of a submaximal dose of glucagon whereas secretin did not have an additive or a potentiating effect. 4. Pancreatic acini were approximately 3 times more responsive to secretagogues than cells. The dose--response curves to bethanechol, glucagon and CCK-PZ for increase in amylase secretion were similar. LDH release was not increased by these agents. Cytochalasin B (5 microgram ml.-1) which is known to disrupt the integrity of luminal membrane inhibited the amylase secretion stimulated by glucagon, bethanechol and CCK-PZ. 5. Glucagon inhibited incorporation of a mixture of fifteen 14C-labelled amino acids (algal profile, Schwarz Mann) into perchloric acid precipitable proteins in dissociated mouse pancreatic acini within 30 min. 6. In 'pulse-chase' experiments, glucagon decreased the specific activity of zymogen granules isolated by differential centrifugation, from pancreatic lobules (120 min) and increased the specific activity of radiolabelled proteins in the medium (60 and 120 min). 7. It is concluded that glucagon increased digestive enzyme secretion from pancreatic acinar cells by a direct action (in contrast to its reported indirect effect in vivo) and decreased digestive enzyme synthesis. The data on transport and secretion do not support the suggested role of glucagon as an inhibitor in the intact animal.
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PMID:Effect of glucagon on digestive enzyme synthesis, transport and secretion in mouse pancreatic acinar cells. 616 27

1. The effect of membrane stabilizers and cytochalasin-B on amylase secretion, basal and induced by ionophore A23187, CCK-PZ, bethanechol and glucagon, was studied in dissociated mouse pancreatic acinar cells. 2. Cytochalasin-B did not affect basal or secretagogue-stimulated amylase secretion. 3. Membrane stabilizers [thymol (10(-7)-10(-4) M), chlorpromazine (10(-7)-10(-4) M) and propranolol (10(-7)-10(-5) M) did not alter basal release of amylase. At higher concentrations of thymol (10(-3) M), chlorpromazine (10(-3) M) and propranolol (10(-4) M), dissociated acinar cells were lysed as indicated by an increase in release of lactic dehydrogenase (LDH). 4. Ionophore A23187, CCK-PZ (maximal effective concentrations, 0.01 u. ml.-1), bethanechol (maximal effective concentrations, 10(-4) M) and glucagon increased amylase secretion in a dose-dependent fashion. Concentrations of CCK-PZ and bethanechol beyond optimal levels decreased amylase secretion. Concentrations of ionophore A23187 and glucagon when tested beyond 10(-6) M and 10(-4) M respectively increased the release of LDH. In concentrations that were non-toxic, membrane stabilizers blocked the stimulating effect of cholecystokinin-pancreozymin and bethanechol on amylase secretion but did not alter the response to A23187 and glucagon. 5. Unlike bethanechol, glucagon neither increased the uptake of 45Ca nor did it alter the release of 45Ca from cells previously loaded with 45CaCl2. 6. These data provide evidence that stimulus-secretion coupling in dissociated pancreatic acinar cells is basically similar to cells in situ. The effect of glucagon is consistent with the model in which hormone-dependent mobilization of Ca2+ from intra- or extracellular sources is bypassed leading to digestive enzyme secretion.
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PMID:Amylase release from dissociated mouse pancreatic acinar cells stimulated by glucagon: effect of membrane stabilizers. 616 45

1. The effect of octapeptide of cholecystokinin-pancreozymin (CCK(8)), bethanechol, cholera toxin, glucagon and vasoactive intestinal polypeptide (VIP) on amylase secretion and lactic dehydrogenase (LDH) release from isolated rat pancreatic acini was studied.2. In isolated rat pancreatic acini, in the absence of theophylline in the medium, amylase secretion was increased by 65-78% with 10(-7) and 10(-6) M-cholera toxin. In the presence of theophylline, amylase secretion was increased by 43-56% with 10(-7) and 10(-6) M-cholera toxin following a 90 min incubation. No effect was observed in the presence of theophylline at 30 and 60 min. The effect of cholera toxin was potentiated by CCK(8) at 60 and 90 min.3. In the absence of theophylline in the medium, amylase secretion was increased by 81-118% with 10(-5) and 10(-4) M-glucagon and 86% with 10(-6) M-VIP at 60 min. In the presence of theophylline in the medium, amylase secretion was increased by 53-246% with 10(-9) to 10(-6) M-glucagon and 111-158% with 10(-7) and 10(-6) M-VIP respectively. The effect of glucagon and VIP was potentiated by CCK(8).4. Potentiation of the rate of amylase release due to glucagon (10(-5) M) and VIP (10(-6) M) occurred during the first 15 min of incubation.5. Release of LDH was not increased by any of these agents.6. It is concluded that cyclic AMP rise (due to cholera toxin, glucagon and VIP effect) increased amylase secretion from rat pancreatic acinar cells. This effect is less marked than in the guinea-pig pancreas and is potentiated by agents mobilizing cellular Ca(2+) (CCK(8) and bethanechol).7. These data indicate species-specific variation in the action of cyclic AMP in the pancreas.
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PMID:Role of cyclic adenosine monophosphate in amylase release from dissociated rat pancreatic acini. 618 68

Two 8-yr-old children, a boy and girl, are described with Cushing's syndrome secondary to ectopic ACTH-secreting pancreatic islet cell carcinomas. The girl, seen 28 yr ago, had strong presumptive evidence of ectopic ACTH production and hypercalcemia. The boy, studied recently, had strikingly elevated concentrations of plasma ACTH (1,500 pg/ml) and beta-lipotropin (beta LPH; 2,500 pg/ml) and showed no suppression of urinary 17-hydroxycorticoids or cortisol with low and high dose dexamethasone. He had increased plasma calcitonin (257 pg/ml), glucagon (442 pg/ml), lactate dehydrogenase (497 IU/liter), and alpha-fetoprotein (5,144 pg/ml). He also had hypokalemic alkalosis with elevated plasma deoxycorticosterone (70 ng/ml) and PRA (6.9 ng/ml.h) but normal plasma aldosterone (8.2 ng/dl) and 18-hydroxycorticosterone (7.6 ng/dl). Preoperative localization of the tumor was accomplished by computed tomographic scan of the abdomen with concurrent barium enema. Cell-free translation of the tumor mRNA produced authentic proopiomelanocortin of 35,000 mol wt, indicating that the ACTH and beta LPH were produced by the tumor from a common precursor. After removal of a large amount of metastatic tissue from the boy, clinical progression of the remaining tumor was monitored by measuring plasma ACTH and beta LPH. Episodic secretion of ACTH and beta LPH was demonstrated by taking frequent plasma samples while suppressing pituitary ACTH with oral dexamethasone. Chemotherapy and radiation proved ineffective in controlling the growth of his tumor.
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PMID:Endocrine, histological, and biochemical studies of adrenocorticotropin-producing islet cell carcinoma of the pancreas in childhood with characterization of proopiomelanocortin. 630 81

The effect of small amounts of oral glucose on hepatic function during starvation was studied. A group of 20, nondiabetic, obese, male patients were entered into the protocol. Ten were placed on absolute caloric starvation and the other ten were placed on a starvation diet modified by the daily addition of 8 or 16 g of oral glucose. Five patients in the starved group crossed over to the modified starvation protocol and 3 of the modified starvation group were switched to the starvation group at the end of the initial dietary period. Total serum bilirubin, serum glutamic pyruvic transaminase (SGOT) and lactic dehydrogenase (LDH) were significantly lower in the modified starvation group compared to the totally starved group. When the groups crossed over the values were similarly altered; the bilirubin and SGOT reduced with the addition of small amounts of glucose and were elevated with starvation. Fasting immunoreactive insulin (IRI), glucagon, and glucose were similar in both groups; but the 90-min postprandial IRI was doubled while only a 15 mg/dl change in blood sugar was seen. The results show that small amounts of oral glucose reduces the total serum bilirubin, SGOT, and LDH elevation of starvation. It is suggested that the postprandial increase in peripheral IRI seen in modified starvation may expose the liver to pulses of portal vein insulin that may exert a protective effect thru the known hepatotrophic effects of insulin.
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PMID:Protective effect of small amounts of glucose on abnormal liver function tests during starvation. 699 90

Glucagonoma Syndrome is a rare syndrome comprising hyperglucagonemia, diabetes mellitus, necrolytic migratory erythema and hypoaminoacidemia in the setting of a glucagon producing, alpha cell tumour of the pancreas. We report a case of Glucagonoma Syndrome palliatively treated successfully with octreotide. In addition to classical clinical and biochemical findings, this patient also had a Glomus Jugulare tumour, and Empty Sella Syndrome and demonstrated an unusual pattern of plasma lactate dehydrogenase isoenzymes, features not previously reported in this syndrome.
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PMID:Glucagonoma syndrome with increased lactate dehydrogenase isoenzymes: octreotide treatment. 752 1


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