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)

Immunoreactive glucagon (IRG) or glucagon immunoreactivity is known to be increased in the plasma of insulin-deprived pancreatectomized dogs, most of it originating in the stomach. We attempted to clarify the extent to which gastric IRG is involved in glycogenolysis in the liver of insulin-deprived, pancreatectomized dogs. Mongrel dogs underwent total pancreatectomy. IRG levels in portal vein blood increased to 760 +/- 186 pg/ml on the 4th postoperative day while the insulin levels were negligible. On the 4th postoperative day some of the dogs underwent total gastrectomy. IRG levels in the portal vein blood of pancreatectomized dogs decreased from 760 +/- 186 pg/ml to 135 +/- 44 pg/ml one hour after gastrectomy. Glucose containing insulin was then infused into both pancreatectomized and pancreatectomized-gastrectomized grups of dogs. Glycogen synthesis in the liver during glucose and insulin infusion was much the same in both groups. However, glycogen degradation after glucose and insulin infusion was completely suppressed in pancreatectomized dogs without a stomach while pancreatectomized dogs alone showed marked glycogenolysis in the liver. No difference in portal IRI and blood sugar level was found in both groups while a marked difference in portal IRG were observed. These findings indicate that the IRG released from the stomach plays a significant role i glycogen metabolism in pancreatectomized dogs.
 ...
PMID:The role of gastric glucagon immunoreactivity in pancreatectomized dogs. 701 9

In the islets of the rat pancreas, steroid diabetes induced by triamcinolon-acetonid leads to degranulation of the B cells and glycogen infiltration. The glycogen cannot be satisfactorily detected using methods like the chromic acid technique according to Bauer, staining with Best's carmine, or the usually applied periodic acid-Schiff (PAS) reaction. Glycogen detection is improved, however, when lead tetraacetate is used in place of periodic acid as oxidizing agent. When combining the carbohydrate detection method with the peroxidase--antiperoxidase (PAP) method used for immunocytochemical detection of the various pancreatic islet hormones, paraffin sections reveal that glycogen is primarily localized in granulated B cells; the degranulated B cells also contain glycogen, though in smaller amounts. In contrast, the islet cells containing somatostatin, glucagon and pancreatic polypeptide are nearly free of glycogen.
 ...
PMID:Glycogen in pancreatic islets of steroid diabetic rats. Carbohydrate histochemical detection and localization using an immunocytochemical technique. 703 7

A toxic extent has been isolated and partially purified from burnt human and mouse skin and also from sera of severely burnt patients, which causes disturbances of energy metabolism and decreased synthesis rates for glucose and urea in the perfused rat liver. Enzymatically isolated hepatocytes from rat livers were used to study the toxic effects on hormonal sensitivity, synthetic functions and ultrastructure of the cells. A decreased synthesis of urea and glycogen was found in cells from rats treated 5 days before with "toxin" and in cells, which were directly incubated with the toxic factor. Glucagon increased urea synthesis in normal cells by 33%, and a decrease of 25% was caused by insulin. Cells of rats treated with the nontoxic precursor of the toxic factor from normal skin were similar, while those treated with "toxin" produced less urea and did not react to glucagon or insulin. Glycogen synthesis was reduced in cells directly incubated with the "toxin", however, the hormonal effects were still observed. Surface alterations of "toxin" treated cells and cells of "toxin" treated rats were found by scanning electronmicroscopy. These findings provide evidence of a direct cytotoxic effect of the toxic factor from burnt skin. It is proposed that the "toxin" acts on the cellular membrane with destruction of surface and receptorproteins.
 ...
PMID:Effects of peptide hormones on urea- and glycogen-synthesis of isolated hepatocytes and the influence of a toxic factor from burnt mouse and human skin. 704 Jan 93

The effects of long-term exposure (7 wk) to hyperinsulinaemia on insulin sensitivity were studied in female rats. The rats were made hyperinsulinaemic by implantation of osmotic minipumps that were changed once a week. Elevated adrenergic activity and secretion of glucocorticoids were controlled by another minipump with propranolol and adrenalectomy with corticosterone substitution, respectively. This resulted in hyperinsulinaemia and moderate hypoglycaemia, the latter probably counteracted by overeating and increased glucagon secretion, as indicated by increased body weight and lower liver glycogen contents, respectively. Euglycaemic, hyperinsulinaemic clamp measurements showed a significantly higher glucose disposal rate (P < 0.05) in the hyperinsulinaemic rats 18.8 +/- 1.1 mg kg-1 min-1 compared with the control groups 14.6 +/- 0.4 and 15.4 +/- 0.9 mg kg-1 min-1. Insulin stimulation of 2-deoxyglucose as well as glycogen synthesis was measured in the extensor digitorum longus muscle, the red and white part of the gastrocnemius, the soleus muscle, the liver and in parametrial, retroperitoneal, and inguinal adipose tissue. No differences were found between the groups in the insulin response of the 2-deoxyglucose uptake. Glycogen synthesis was significantly elevated in all muscles in the insulin treated compared with the control rats but no differences were found in the liver. Capillary density was significantly elevated per unit muscle surface area in the soleus and extensor digitorum longus muscles of the insulin-exposed rats.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effects of long-term hyperinsulinaemia on insulin sensitivity in rats. 762 70

The isolated working rat heart was adapted for simultaneous determination of glycogen synthesis and degradation using a dual isotope technique. After prelabeling of glycogen with [U-14C]glucose, glycogenolysis was determined continuously from the washout of 14CO2 plus [14C]lactate. Glycogen synthesis was determined during the same period from incorporation of [5-3H]glucose. In the absence of added hormones, hearts were predominantly glycogenolytic (1.5 mumol/min/g, dry weight), and there was simultaneous synthesis (11% of the rate of glycogenolysis). The percentage of glucose taken up by the heart that could traverse the glycogen pool as a consequence of glycogen turnover was minor (5%). Insulin (10 milliunits/ml) predictably stimulated glycogen synthesis (3.6-fold) and nearly abolished glycogenolysis. Addition of glucagon (1 microgram/ml) increased contractile performance and initially stimulated glycogenolysis (3.8-fold) until glycogen was largely depleted. Net tritium incorporation was unaffected by glucagon. Both hormones stimulated glycolytic flux from exogenous glucose (3H2O from [5-3H]glucose) as well as total glycolytic flux (3H2O plus glycogenolysis). The initial stimulation in total glycolytic flux with glucagon was largely from glycogen, explaining the lag in stimulation from exogenous glucose. The relationship between the specific radioactivity and amount of glycogen remaining after different degrees of glycogenolysis suggests that the preference of glycogenolysis for newly synthesized glycogen is only partial.
 ...
PMID:Glycogen turnover in the isolated working rat heart. 772 42

Long term feeding a sucrose-rich diet (SRD) to normal Wistar rats led to multiphasic changes in the activity of the pyruvate dehydrogenase complex (PDH), characterized by a significant decrease in PDHa (active form) in the short term on SRD (3 weeks) when compared to control rats fed the standard chow (STD). Although PDHa returned spontaneously to control values in the medium term (6-8 weeks) on SRD, an even more pronounced decrease was recorded when rats were kept long term on the SRD (15 weeks). Low PDHa levels recorded in the short and long term were accompanied by a two fold increase in heart acetyl-CoA concentration and the acetyl-CoA/CoASH ratio. Tissue long-chain acyl-CoA and triacylglycerol levels were also significantly higher in SRD fed rats. Spontaneous normalization of all the above metabolic parameters was observed during the medium term on SRD. Glucose-6-phosphate levels remained within control values during the short and medium term, in contrast to a two fold increase recorded in the long term on SRD. Glycogen concentrations were found moderately elevated only in the long term. Citrate concentrations were slightly increased in the short and greatly in the long term, and the fructose-2,6-bisphosphate/citrate ratio was found significantly decreased only during the long term on SRD. After 3 weeks on SRD, the protal vein Insulin/Glucagon (I/G) molar ratio was three times higher in SRD than STD rats, as opposed to an unchanged I/G ratio found in the long term.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Multiphasic metabolic changes in the heart of rats fed a sucrose-rich diet. 783 21

Functional recovery following ischemia and reperfusion in the isolated working rat heart perfused with glucose (11 mM) was examined in relation to pre- and postischemic levels of ATP, glycogen, glucose 6-phosphate, and the lactate-to-pyruvate ratio. The following variables were studied: feeding and fasting in vivo, addition of L-lactate (10 mM), dl-beta-hydroxybutyrate (10 mM), glucagon (0.01 and 1 micrograms/ml), and a 15-min anoxic perfusion before ischemia in vitro. Recovery was assessed as the percentage of preischemic power. Good correlation was found between functional recovery and the postischemic content of glycogen. Glycogen depletion by anoxia or glucagon before ischemia impaired recovery. There was no relationship among lactate produced, or the lactate-to-pyruvate ratio, and recovery. The addition of lactate or beta-hydroxybutyrate to hearts from fed rats increased the content of glycogen and glucose 6-phosphate, whereas addition of lactate, but not beta-hydroxybutyrate, improved recovery. There was a linear relationship between glycogen content and glucose 6-phosphate levels. In conclusion, the degree of return of oxidative metabolism and of net glycogen resynthesis reflects postischemic recovery of function. The results also suggest a role for anaplerosis of the citric acid cycle as an additional determinant of postischemic recovery.
 ...
PMID:Metabolic recovery of isolated working rat heart after brief global ischemia. 806 97

Insulin, glucagon, somatostatin, and PP cells were found by immunotopochemical and electron-optical techniques in the islets of Langerhans of the sand rat, proving that the islets in this species also contain the four basic cell types known to be found in the islets in mammals in general. The ratio of A cells to B cells was 1:4 (19.1% A cells to 80.9% B cells). The pancreas of the sand rat contained assemblages of various numbers of neurons in the intralobal and interlobular connective tissue. They did not seem related in any regular fashion to specific blood vessels or branches of the pancreatic ducts. No bundles of nerve fibers were found by either light or electron microscopy. Nonmyelinated nerve fibers were detected by electron microscopy in the stroma of the islets. In the sand rat the neuroinsular complexes are formed by the penetration of single nerve cells into the pancreatic islets. In the NH or long-term group the islets exhibited signs of stimulation. The number of islets was higher than normal (polynesia), with the islets themselves enlarged (macronesia). Double islets in the secretory ducts of the exocrine pancreas were frequent. The increase in islet size was due to hyperplasia of the B cells. The numbers of beta-granules in the B cells varied considerably. Glycogen was demonstrated in some islets. The fusion of beta-granules was shown in electron microscopic pictures. The electron-opaque centers of these granules were brighter than the others and appeared to have partly dissolved. The organelles of the B cells (ER, Golgi apparatus, and mitochondria) were well developed, this also being a sign of cell stimulation. No changes were observed in the B and PP cells. Stimulation of the islet cells was even more pronounced in the diabetic group. Due to hyperplasia, the islets in this group were significantly larger not only than those in the control group, but also than those in the NH group. The pancreata of this group of sand rats contained numerous small islets. Although necrotic B cells were found in the large islets of the pancreas, none were discovered in the small islets. The small islets were considered to be "regenerated" islets. Granulation was slight in the remaining functioning B cells. The hypophyses of the control group contained the GH, LTH, FSH, LH, and TSH cell types typical of this organ in other species. In the sand rat the granules of these cell types are of about the same size as has been stated for other rodents.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Histophysiology of the obesity-diabetes syndrome in sand rats. 808 78

Glycogen synthesis and degradation were studied in cultured rat hepatocytes prelabeled by incubation with [14C]glucose or [14C]galactose. During prelabeling about 75% of the accumulated glycogen was synthesized from glucose and about 25% from gluconeogenic precursors. Following the labeling period, glycogen synthesis and degradation were estimated at 5 and 12.5 mM glucose and varying concentrations of insulin and glucagon. At 12.5 mM glucose and 10 nM insulin the accumulation of glycogen was comparable to in vivo values, whereas the level of radioactivity in prelabeled glycogen remained constant. Further addition of 0.1 nM glucagon resulted in constant values of both content and radioactivity of glycogen. Increasing the concentration of glucagon to 10 nM resulted in a parallel decrease of content and radioactivity in glycogen. At 5 mM glucose, 10 nM insulin, and 0.1 nM glucagon both the content and the radioactivity of glycogen were constant, whereas addition of 10 nM glucagon resulted in a parallel decrease of content and radioactivity of glycogen, which was 64% higher than that observed with 12.5 mM glucose. In the absence of insulin, prostaglandin D2 had effects similar to those of 10 nM glucagon, whereas no effects was observed in the presence of insulin. From these results and from calculated rates of glucose 6-phosphate formation, it is concluded that the rate of glycogen degradation is less than 10% of the rate of synthesis under conditions favoring glycogen accumulation. At conditions favoring glycogen degradation (10 nM insulin plus 10 nM glucagon or prostaglandin in the absence of insulin) no synthesis could be detected. Results from cells prelabeled with [14C]galactose suggested that glycogen degradation is not an absolutely ordered process, but that some random degradation takes place.
 ...
PMID:Absence of glycogen cycling in cultured rat hepatocytes. 811 7

Several lines of evidence indicate that glycolysis is especially important for normal diastolic relaxation and for the maintenance of cellular ion homeostasis in myocardium. To elucidate whether the glycolytic flux of ATP contributes to diastolic tone and to the regulation of intracellular Ca2+, myocardial content of sugar phosphates ([SP]) and intracellular Ca2+ concentration ([Ca2+]i) were measured in isolated, perfused ferret hearts using nuclear magnetic resonance. Glucose and acetate were used as substrates for glycolysis and oxidative phosphorylation, respectively. Glycogen was effectively depleted after 15-min perfusion with glucagon (2 mg/liter), as verified by the lack of rise in [SP] during exposure to iodoacetate (100 microM) in substrate-free perfusate. Despite the fact that glycolytic flux had been blocked both by iodoacetate and by absence of substrate, end-diastolic left ventricular pressure (EDP) remained unchanged (P > 0.15, n = 6). The subsequent addition of glucose to the perfusate led to SP accumulation and a marked rise in EDP, with a significant correlation between EDP and [SP] (r = 0.86 +/- 0.04, P < 0.01, n = 6). A similar correlation was observed when glucose in the perfusate was replaced by 2-deoxyglucose (r = 0.78 +/- 0.09, P < 0.01, n = 3). Fluorine nuclear magnetic resonance measurements of [Ca2+]i verified that EDP faithfully reports changes in diastolic [Ca2+]i under the present experimental conditions. Thus, intracellular Ca2+ overload is caused by the accumulation of SP rather than by the inhibition of glycolysis per se. Glycolysis may appear to be important because its by-products are deleterious, and not necessarily because glycolytically derived ATP plays a favored role in ion homeostasis.
 ...
PMID:Mechanism of the diastolic dysfunction induced by glycolytic inhibition. Does adenosine triphosphate derived from glycolysis play a favored role in cellular Ca2+ homeostasis in ferret myocardium? 813 61


<< Previous 1 2 3 4 5 6 Next >>