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)

In hepatocytes from starved streptozocin-induced diabetic rats, vanadate increases the glycolytic flux because it raises the levels of fructose-2,6-bisphosphate (Fru-2,6-P2), the main regulatory metabolite of this pathway. This effect of vanadate on Fru-2,6-P2 levels is time and dose dependent, and it remains in cells incubated in a calcium-depleted medium. Vanadate is also able to counteract the decrease on Fru-2,6-P2 levels produced by glucagon, colforsin, or exogenous cAMP. However, vanadate does not modify 6-phosphofructo-2-kinase and pyruvate kinase activities, but it does counteract the inactivation of these enzymes induced by glucagon. Likewise, Fru-2,6-P2ase activity is also not affected by vanadate. In addition, vanadate is able to increase the production of both lactate and CO2 in hepatocytes from streptozocin-induced diabetic rats incubated in the presence of glucose in the medium. Vanadate behaves as a glycolytic effector in these cells, and this effect may be related to its ability to normalize blood glucose levels in diabetic animals.
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PMID:Activation by vanadate of glycolysis in hepatocytes from diabetic rats. 193 97

The VFA, also known as short-chain fatty acids, are produced in the gastrointestinal tract by microbial fermentation of carbohydrates and endogenous substrates, such as mucus. This can be of great advantage to the animal, since no digestive enzymes exist for breaking down cellulose or other complex carbohydrates. The VFA are produced in the largest amounts in herbivorous animal species and especially in the forestomach of ruminants. The VFA, however, also are produced in the lower digestive tract of humans and all animal species, and intestinal fermentation resembles that occurring in the rumen. The principal VFA in either the rumen or large intestine are acetate, propionate, and butyrate and are produced in a ratio varying from approximately 75:15:10 to 40:40:20. Absorption of VFA at their site of production is rapid, and large quantities are metabolized by the ruminal or large intestinal epithelium before reaching the portal blood. Most of the butyrate is converted to ketone bodies or CO2 by the epithelial cells, and nearly all of the remainder is removed by the liver. Propionate is similarly removed by the liver but is largely converted to glucose. Although species differences exist, acetate is used principally by peripheral tissues, especially fat and muscle. Considerable energy is obtained from VFA in herbivorous species, and far more research has been conducted on ruminants than on other species. Significant VFA, however, are now known to be produced in omnivorous species, such as pigs and humans. Current estimates are that VFA contribute approximately 70% to the caloric requirements of ruminants, such as sheep and cattle, approximately 10% for humans, and approximately 20-30% for several other omnivorous or herbivorous animals. The amount of fiber in the diet undoubtedly affects the amount of VFA produced, and thus the contribution of VFA to the energy needs of the body could become considerably greater as the dietary fiber increases. Pigs and some species of monkey most closely resemble humans, and current research should be directed toward examining the fermentation processes and VFA metabolism in those species. In addition to the energetic or nutritional contributions of VFA to the body, the VFA may indirectly influence cholesterol synthesis and even help regulate insulin or glucagon secretion. In addition, VFA production and absorption have a very significant effect on epithelial cell growth, blood flow, and the normal secretory and absorptive functions of the large intestine, cecum, and rumen. The absorption of VFA and sodium, for example, seem to be interdependent, and release of bicarbonate usually occurs during VFA absorption.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Energy contributions of volatile fatty acids from the gastrointestinal tract in various species. 218 1

Recent studies have suggested the beneficial effects of essential fatty acids in postoperative patients receiving total parenteral nutrition. While there is abundant information on the role of glucose and amino acids on insulin release, the effect of essential fatty acids on endocrine pancreatic secretions is not clear. Since linoleic and linolenic acids are constituents of TPN solutions as well as dietary fat, our aim was to examine their effect on the endocrine pancreatic function, using isolated islets. In each experiment, six islets microdissected from three mice were preperifused at the rate of 1 ml/min with Krebs-Ringer bicarbonate (KRB) buffer pH 7.4 containing 2% bovine albumin and 5.5 mM glucose (basal) with continuous supply of 95%/5%, O2/CO2 for 1 hr, after which basal samples were collected on ice every minute. The perifusion was continued for 20 min after the addition of a mixture of 10 mM linoleic acid and 5 mM linolenic acid to the KRB. During each perifusion phase, effluent samples were also collected for insulin and glucagon assay. The mean integrated area under the curve/20 min showed an increase in both insulin and glucagon secretions with the addition of fatty acids. Hence insulin increased from a basal 3154.8 +/- 953.7 to 8393.0 +/- 2073.1 pg (P less than 0.025, n = 6) and glucagon increased from 193.7 +/- 46.9 to 1566.1 +/- 411.2 pg (P less than 0.0025, n = 5). The fatty-acid-induced insulin but not glucagon secretion was blocked by the addition of 2 mM palmoxirate an inhibitor of fatty acid oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of endocrine pancreatic secretions by essential fatty acids. 218 12

We have employed the primed constant infusion technique to investigate the metabolic effects of the organophosphate antidote, atropine, on glucose homeostasis in rats. This method utilizes the radioisotopes 6-3H-glucose to measure production and uptake and U-14C-glucose to measure oxidation. Our data indicate that glucose production significantly (p less than 0.05) increased (24.0 +/- 2.0 vs. 30.9 +/- 2.6 mumoles.kg-1.min-1) following atropine administration. The elevated rate of glucose turnover was associated with concomitant increases in glucose oxidation (8.3 +/- 0.6 vs. 12.0 +/- 0.8, mumoles.kg-1.min-1), the percent of glucose uptake oxidized (37.2 +/- 2.0 vs. 44.6 +/- 2.6), and the percent carbon dioxide produced from glucose (8.4 +/- 0.7 vs. 12.0 +/- 1.8). Presumably, these glucokinetic changes were mediated by elevated plasma catecholamines (Epi: 166 +/- 19 vs. 271 +/- 50 pg/ml; Norepi: 262 +/- 24 vs. 525 +/- 63 pg/ml, p less than 0.05) since other glucoregulatory hormones (insulin, glucagon, and corticosterone) were not significantly affected by atropine administration. In addition, there was no change in VO2 associated with atropine administration. These data indicate that atropine enhances glucose production and utilization; such effects could be ergogenic during exercise in thermoneutral conditions.
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PMID:Atropine: effects on glucose metabolism. 219 May 48

Paired micropuncture experiments were carried out in somatostatin-infused volume-expanded rats to examine the effects of a glucagon infusion (0.05 ng.min-1.g body wt-1) on urinary acidification and tubular handling of bicarbonate. Whole kidney and single-nephron glomerular filtration rate were not affected by glucagon. In thyroparathyroidectomized (TPTX) rats, glucagon inhibited the reabsorption of total CO2 in Henle's loop. In intact animals, however, the latter effect was not observed. In the distal tubule accessible to micropuncture, net total CO2 absorption was observed during volume expansion plus somatostatin infusion, which reversed to net total CO2 secretion during glucagon infusion in Wistar rats; thus the late distal delivery of total CO2 increased almost 80%. Marked inhibition of urinary acidification occurred in all animals as evidenced by a rise in urine pH and bicarbonate excretion. Conversely, a somatostatin infusion, which decreased the plasma glucagon concentration, stimulated net total CO2 absorption along the distal tubule and augmented final urine acidification in Wistar rats. Finally, urine-minus-blood PCO2 during alkaline diuresis was significantly reduced by glucagon infusion in bicarbonate-loaded TPTX rats. We conclude that 1) glucagon inhibits bicarbonate absorption in superficial Henle's loop in TPTX but not in intact rats, and 2) glucagon stimulates bicarbonate secretion and/or inhibits proton secretion in the distal tubule and collecting ducts, which leads to reduced urinary acidification.
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PMID:Effects of glucagon on H(+)-HCO3- transport in Henle's loop, distal tubule, and collecting ducts in the rat. 257 52

The major phenobarbital-inducible cytochrome P-450 purified from rat liver, a member of family II of the cytochrome P-450 gene superfamily, is rapidly phosphorylated by cAMP-dependent protein kinase. The phosphorylation reaches greater than 0.5 mol phosphate/mol P-450 after 5 min and is accompanied by a decrease in enzyme activity. The serine residue in position 128 was shown to be the sole phosphorylation site and a conformational change of the protein was indicated by a shift of the carbon monoxide difference spectrum of the reduced cytochrome from 450 to 420 nm. Comparison of amino acid sequences of various cytochrome P-450 families revealed a highly conserved arginine residue in the immediate vicinity of the phosphorylated serine residue which constitutes the kinase recognition sequence. It also revealed that only the members of the cytochrome P-450 family II carry this kinase recognition sequence. To find out whether this phosphorylation also occurs in vivo, the exchangeable phosphate pool of intact hepatocytes derived from phenobarbital-pretreated rats was labeled with 32Pi followed by an incubation of the cells with the membrane-permeating dibutyryl-cAMP or with the adenylate cyclase stimulator glucagon to activate endogenous kinase. As a result, a microsomal polypeptide with the same electrophoretic mobility as cytochrome P-450 became strongly labeled. Peptide mapping and immunoprecipitation with monospecific antibodies identified this protein as the major phenobarbital-inducible cytochrome P-450. It becomes phosphorylated at the same serine residues as in the cell-free phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phosphorylation of hepatic phenobarbital-inducible cytochrome P-450. 258 91

To determine whether the postprandial pattern of carbohydrate metabolism differs after ingestion of an identical amount of glucose as either a drink or as a part of a mixed meal, normal subjects were studied on two occasions. On both occasions, hepatic and extrahepatic glucose metabolism were assessed using the dual isotope and forearm catheterization techniques as well as indirect calorimetry. Plasma glucose, insulin, and C-peptide concentrations and rate of systemic entry of ingested glucose all were lower (P less than 0.05) during the first 15 min after the mixed meal than after the glucose drink. The integrated C-peptide response was greater (P less than 0.05) after the mixed meal, whereas the integrated suppression of glucagon was greater (P less than 0.05) after the glucose drink. Despite these differences in circulating hormone concentrations, after the first 15 min, the rates of systemic entry of ingested glucose, endogenous glucose release, incorporation of carbon dioxide into glucose, and glucose and lipid oxidation as well as nonoxidative glucose storage were virtually the same after the mixed meal and the glucose drink. We conclude that the pattern of postprandial carbohydrate metabolism after ingestion of a glucose meal is remarkably similar to that after ingestion of a more traditional mixed meal. These data suggest that insights regarding the pattern of postprandial carbohydrate metabolism derived from previous studies employing only a glucose drink are likely to pertain to those observed when healthy individuals ingest a meal that contains protein and fat.
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PMID:Comparison of the pattern of postprandial carbohydrate metabolism after ingestion of a glucose drink or a mixed meal. 264 12

In order to clarify the regulatory mechanism of BAT function, the effects of noradrenaline (NA) (6mM), insulin (I) (40nM), glucagon (G) (400nM) and nerve growth factor (NGF) (2-10nM), alone or in combination, were investigated directly in BAT from neonatal rats (ca. 3 days old), cultured in 10% fetal bovine serum-medium 199 in 95% air-5% CO2 gas phase at 33 degrees C for 1 to 2 weeks. I stimulated lipid accumulation and enlarged outgrown cell size, but mitochondria in the cells of tissue block were smaller and their cristae less distinct. I + G enlarged nucleus and cytoplasm, and suppressed the lipid accumulation induced by I, but mitochondria in the cells of tissue block were larger and their cristae became more prominent than those of I-added cells. G induced the similar changes to those by I + G. I + NA also induced the similar effects to those by I + G, but their mitochondria size did not differ from that of I-added cells. NGF caused the similar effects of those by G, inducing the development of mitochondria, rough endoplasmic reticulum and Golgi complex. These results suggest that multiple factors such as NA, I, G and NGF regulate differentiation and functional development of BAT.
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PMID:[Studies on regulation of the function of thermogenic tissue, brown adipose tissue (BAT) by means of tissue culture method]. 265 88

Using isolated rat hepatocytes, we studied the effect of epidermal growth factor (urogastrone) (EGF-URO) on the incorporation of [3-14C]pyruvate into glucose and glycogen, on the incorporation of [U-14C]glucose into glycogen, and on the oxidation of [U-14C]glucose to 14CO2. The effects of EGF-URO were compared with those of glucagon and insulin. EGF-URO, with an EC50 of 0.2 nM, enhanced by 34% (maximal stimulation) the conversion of [3-14C]pyruvate into glucose; no effect was observed on the oxidation of glucose to CO2 and on the incorporation of either pyruvate or glucose into glycogen. The effect of EGF-URO on pyruvate conversion to glucose was observed only when hepatocytes were preincubated with EGF-URO for 40 min prior to the addition of substrate. Glucagon (10 nM) increased the incorporation of [3-14C]pyruvate into glucose (44% above control); however, unlike EGF-URO, glucagon stimulated gluconeogenesis better without than with a preincubation period. Neither insulin nor EGF-URO (both 10 nM) affected the incorporation of [U-14C]glucose into glycogen during a 20-min incubation period. However, at longer time periods of incubation with the substrate (60 instead 20 min), insulin (but not EGF-URO) increased the incorporation of [14C]glucose into glycogen; EGF-URO counteracted this stimulatory effect of insulin. In contrast with previous data, our work indicates that EGF-URO can, under certain conditions, counteract the effects of insulin and, like glucagon, promote gluconeogenesis in isolated rat hepatocytes.
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PMID:Effects of epidermal growth factor (urogastrone) on gluconeogenesis, glucose oxidation, and glycogen synthesis in isolated rat hepatocytes. 268 20

Glucagon was injected directly into the medial amygdala (AMYG) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the AMYG of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, cholesterol ester, free fatty acids and phospholipids but decreased those of 14C transfer into triglyceride. However, the glucagon injection into the AMYG of rabbits with lesions of stria terminals or into the parietal cortex of intact rabbits had no effects on the hepatic acetate metabolism. These observations support the hypothesis that the AMYG is a part of the glucagon-sensitive brain regulator system in the hepatic acetate metabolism.
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PMID:Influence of microinjection of glucagon into the amygdala on hepatic acetate metabolism in rabbits. 273 41


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