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)

1. Rat livers were dissociated into their constituent cells by perfusion through the portal vein with a medium containing collagenase, and hepatocytes separated from non-parenchymal cells. 2. It is shown that the procedure described by Wisher & Evans [(1975) Biochem. J. 146, 375-388] for preparation of plasma membranes from liver tissue when applied to isolated hepatocytes also yielded subfractions of similar morphology and marker-enzyme distribution. 3. Thus the distribution of alkaline phosphodiesterase, 5'-nucleotidase and the basal and glucagon-stimulated adenylate cyclase among two 'light' vesicular and one 'heavy' junction-containing plasma-membrane subfractions paralleled that reported for tissue-derived plasma-membrane subfractions. 4. Increased recoveries and specific activities of plasma-membrane marker enzymes were obtained when soya-bean trypsin inhibitor was included in the collagenase-containing perfusion media used to dissociate the liver. 5. Polyacrylamide-gel-electrophoretic analysis of the corresponding plasma-membrane subfractions prepared from liver tissue and isolated hepatocytes were generally similar. 6. The results indicate that the functional polarity of the hepatocyte's plasma membrane is retained after tissue dissociation. The damage occurring to plasma-membrane ectoenzymes by the collagenase-perfusion procedure is discussed.
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PMID:Preparation of plasma-membrane subfractions from isolated rat hepatocytes. 88 Feb 46

1 Subcutaneous administration of glucagon (1 and 0.5 mg/kg) 30 min before the injection of carrageenin or dextran into the rat's paw reduced oedema and the local exudation of Evans blue previously given intravenously. 2 The effect persisted after removal of the adrenal medulla but not after adrenalectomy. 3 When glucagon (1 mg/kg, s.c.) was given daily after a local reaction to Freund's adjuvant injected into the paw had developed, a decrease in the reaction was observed up to 12 days. Blood sugar levels remained within the normal range. 4 Glucagon may exert an anti-inflammatory effect through the release of adrenal corticosteroids and thus help modulate inflammatory reactions.
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PMID:Anti-inflammatory action of glucagon in rats. 118 50

We studied the natural course of disease in spontaneously diabetic rats, Long Evans Tokushima Lean (LETL) rats, to determine whether it showed similar pathogenetic heterogeneity to that of patients with insulin-dependent diabetes mellitus (IDDM) with regard to the relationships between age at onset, rapidity of disease progress, and degree of beta-cell function at the time of its manifestation. Type 1 diabetes developed in 35 rats (6.3%) between 40 and 140 days of age. Eight rats that became diabetic at age 69 days or less were more severely ketotic at the time of first detection of glycosuria and showed more rapid deterioration than seven rats that became diabetic later after birth (mean plasma 3-hydroxybutyrate levels, 4,707 +/- 1,215 pmol/L v 1,390 +/- 859 pmol/L; mean +/- SEM, P < .01). The mean plasma levels and pancreatic content of immunoreactive insulin (IRI) of the early onset rats, 47 +/- 13 pmol/L and 19 +/- 12 pmol/g tissue weight, were significantly lower (P < .01) than the corresponding values of the late-onset rats, 262 +/- 52 pmol/L and 348 +/- 87 pmol/g tissue weight, respectively. Both values were markedly lower than the mean values of 25 nondiabetic LETL rats, 976 +/- 122 pmol/L and 3,488 +/- 628 pmol/g tissue weight. Plasma immunoreactive glucagon (IRG) levels were significantly increased in the diabetic groups (early onset, 57 +/- 13 pmol/L; late-onset, 51 +/- 12 pmol/L; nondiabetic, 18 +/- 1 pmol/L; P < .01). These changes in pancreatic hormone levels of the early onset and late-onset rats were compatible with the histological features of their pancreatic islets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation between residual beta-cell function and age at onset of spontaneous diabetes in Long Evans Tokushima lean rats. 146 Nov 46

Spontaneously occurring neoplasms and non-neoplastic proliferative changes of the pancreatic cells in aging Sprague-Dawley and Long-Evans rats were examined for the presence and distribution of pancreatic hormones using immunocytochemical techniques. Islet cell tumors were indistinguishable in the two rat strains. They were composed principally of insulin-containing beta cells, but had additional and variable small proportions of cells that stained for somatostatin, glucagon, or rarely, pancreatic polypeptide. The heterogeneity in these spontaneous islet cell neoplasms was similar to that reported in humans as well as those induced in rats by streptozotocin. Hyperplasia of the islet cells also mainly affected the beta cells, but the overall pattern of immunocytochemical staining usually remained similar to that of normal islets, a point of distinction from islet cell neoplasms. In addition, rats with exocrine atrophy and fibrosis were found to have considerable disruption and focal proliferation of the islets.
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PMID:Neoplasia and hyperplasia of pancreatic endocrine tissue in the rat: an immunocytochemical study. 300 1

The inotropic responses of chronic alcoholic and control rat hearts to phenylephrine, glucagon, ouabain, and dobutamine were studied to determine if the reported beta-adrenergic subsensitivity of alcoholic rat hearts was a specific defect. Male Long-Evans rats were maintained on nutritionally-complete liquid diets for 10 to 12 months; alcoholic rats received 38% of their calories from ethanol. Dry heart weight/body weight ratios indicated an average 15% hypertrophy of the alcoholic rat hearts. The function of isolated working hearts from these animals was studied at a constant heart rate and afterload. Ventricular function curves indicated significantly lower basal function of alcoholic rat hearts, as evident from their lower peak left ventricular relaxation rate, lower isovolumic relaxation rate, and lower peak power compared to controls. The alcoholic rat hearts had significantly lower inotropic (stroke work and peak power) responses to phenylephrine, glucagon, and dobutamine compared to controls, whereas the response of the alcoholics to ouabain was not significantly different from that of controls. Oxygen supply-to-utilization ratios decreased similarly in alcoholics and controls during treatment with the inotropic agents, as a result of increases in myocardial oxygen consumption and effects on coronary flow that were similar in both groups of animals. Thus the differences in inotropic responses observed with the alcoholic rat hearts were not primarily the result of compromised oxygen supply. Rather, the decreased stroke work response of the alcoholic hearts which occurred despite an increase in oxygen consumption suggested that the alcoholic rat hearts did not utilize oxygen as efficiently as did control hearts to perform external work. This was reflected in the significant differences between alcoholics and controls in the response of calculated external work efficiency to phenylephrine, glucagon, and dobutamine. Thus, alcohol-induced cardiac hypertrophy was associated with depressed basal left ventricular contractile function and decreased responsiveness to alpha 1-adrenergic, beta 1-adrenergic, and glucagon stimulation, but the responsiveness to ouabain was not significantly affected. These characteristics are similar to those of hearts hypertrophied by other causes.
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PMID:Alcoholic cardiomyopathy in rats: inotropic responses to phenylephrine, glucagon, ouabain, and dobutamine. 343 59

The effect of peroral administration of xylitol (5% or 20% in food) on adrenal function was investigated in thirty-five Long-Evans male rats. The control rats were fed either a non-substituted stock diet or a 20% glucose diet. Glucose elevated and 20% xylitol reduced the growth of the rats (P less than 0.001), but 5% xylitol had no effect on the body weight. The concentrations of serum glucose and lactic acid decreased in rats fed 20% and 5% xylitol, respectively, but those of insulin, glucagon, corticosterone and aldosterone were not affected. In the adrenal glands, 20% xylitol loading was associated with increased epinephrine (P less than 0.05) and norepinephrine (P less than 0.001), but with decreased aldosterone (P less than 0.001) concentrations. The weights and histological picture of adrenal glands were normal. The urinary pH of xylitol-fed rats decreased significantly (P less than 0.01). Although peroral xylitol affected the levels of aldosterone and catecholamines, a normal glucocorticoid metabolism was permitted. The reduced aldosterone levels were regarded as secondary reactions, possibly resulting from alterations in electrolyte and/or acid-base balance. The increased catecholamine synthesis may be associated with the promoting effect of xylitol on intestinal calcium absorption.
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PMID:Adrenal function of the rat in relation to peroral administration of xylitol: depression of aldosterone. 363 Jul 41

1. Inflammatory responses were induced by the injection of carrageenin into the rat paw and lymph was collected by cannulation of the thoracic duct. Cell-free lymph samples were intracutaneously injected into a second group of rats to measure vascular permeability activity by local exudation of Evans blue. 2. The vascular permeability activity in lymph samples draining inflamed tissue was consistently higher than in lymph from normal controls. Activity increased with the development of inflammation, attaining maximum values 2 to 2.5 h after the injection of carrageenin. 3. The activity was reduced by pretreatment of lymph donors with indomethacin or soybean trypsin inhibitor. Pretreatment of the animals used to measure vascular permeability activity with diphenhydramine or methysergide attenuated their responses to the permeability factors present in lymph. Thus prostaglandins, kinins, vasoactive amines or their generating systems may have contributed to the total activity detected. 4. Pretreatment of lymph donors with corticosterone or glucagon, whose anti-inflammatory action is mediated by the release of endogenous corticosteroids, did not alter the amount of activity in lymph. 5. These data suggest that the formation of the permeability factors present in lymph draining inflamed tissue was not affected by corticosteroids. We conclude that corticosteroids do not exert their anti-inflammatory activity at this level.
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PMID:Permeability factors in lymph draining inflamed tissues: effect of anti-inflammatory drugs. 730 23

We investigated the influence of and interactions among pancreatic hormones on the secretion of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IG-FBPs) by treating primary hepatocytes from young male Long-Evans rats with insulin or glucagon in combination with rat GH (rGH). The concentration of IGF-I secreted into the medium was estimated by radioimmunoassay after formic acid-acetone cryoextraction, and secreted IGFBPs were analysed by Western ligand blot and immunoblot; accumulation of IGF-I mRNA was analysed by Northern blot. Both insulin (0.1-100 nmol/l) and rGH (0.5, 5 and 50 pmol/l) produced a dose-dependent stimulation of IGF-I secretion over a 24-h incubation period. In contrast, glucagon (0.1-100 nmol/l) inhibited IGF-I production in a dose-related manner. Glucagon (10 nmol/l) also inhibited IGF-I secretion stimulated by rGH (5 pmol/l) and insulin (10 nmol/l). Northern blot analysis of total RNA isolated from rat hepatocytes revealed that rGH (5 pmol/l) elevated IGF-I mRNA levels, glucagon (10 nmol/l) alone had no effect on this parameter, but glucagon significantly reduced IGF-I transcript accumulation in response to rGH. IGFBPs secreted by rat hepatocytes run in two molecular weight ranges on SDS-PAGE: approximately 25 kDa (IGFBP-4) and approximately 29-31 kDa (IGFBP-1 and -2); the predominant hormonally regulated IGFBP was identified as IGFBP-1. Insulin produced a dose-dependent inhibition of production of IGFBP-1, while glucagon was stimulatory; when given together at an equivalent concentration (1 nmol/l), the effects of insulin were dominant to glucagon on IGFBP-1. These observations provide support for significant opposite roles for the pancreatic hormones, insulin and glucagon, in the regulation of liver IGF-I and IGFBP-1 production. As the production of pancreatic hormones is influenced by nutritional status, these polypeptides may mediate the effects of changing nutritional state on the hormonal control of protein anabolism and glucose homeostasis by directly influencing the circulating level of liver-derived IGF-I and its binding proteins.
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PMID:Pancreatic hormones differentially regulate insulin-like growth factor (IGF)-I and IGF-binding protein production by primary rat hepatocytes. 752 61

To identify the primary disorder causing diabetes mellitus in a model rat (Otsuka Long-Evans Tokushima Fatty [OLETF]) with non-insulin-dependent diabetes mellitus (NIDDM), we studied the temporal relationship between insulin resistance and impairment of pancreatic beta-cell function. Groups of 28 male OLETF rats and male nondiabetic control Long-Evans Tokushima Otsuka (LETO) rats were given an intravenous (i.v.) glucose and glucagon tolerance test (IVGTT) and hyperinsulinemic euglycemic clamp tests at 10, 16, 24, and 40 weeks of age. After the euglycemic clamp test, abdominal fat was measured and the pancreas was examined histologically. At 16 weeks of age, insulin-mediated whole-body glucose uptake as measured by the hyperinsulinemic euglycemic clamp technique was significantly reduced in OLETF rats (glucose infusion rat [GIR], 40.9 +/- 4.2 mumol/kg.min) as compared with LETO rats (78.4 +/- 6.9). On the other hand, plasma insulin responses to glucose and glucagon in OLETF rats were higher than those in LETO rats at 16 and 24 weeks of age, but clearly decreased at 40 weeks of age (sigma immunoreactive insulin [IRI] to glucagon, 8.81 +/- 1.81 v 27.32 +/- 4.59 nmol.min in OLETF and LETO rats, respectively, P < .01). Abdominal fat deposition was significantly greater in OLETF rats than in LETO rats at all ages tested except 10 weeks. Pancreatic islets of OLETF rats became enlarged and fibrotic. These results demonstrated that insulin resistance preceded impairment of pancreatic beta-cell function in OLETF rats, and that insulin resistance seemed closely related to fat deposition in the abdominal cavity.
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PMID:Which is the primary etiologic event in Otsuka Long-Evans Tokushima Fatty rats, a model of spontaneous non-insulin-dependent diabetes mellitus, insulin resistance, or impaired insulin secretion? 761 55

Pancreatic A-cell function in the newly developed Otsuka Long Evans Tokushima Fatty (OLETF) strain of non-insulin-dependent diabetes mellitus (NIDDM) rats was examined in relation to the morphological changes in their islets and the plasma glucagon responses to insulin-induced hypoglycemia and an arginine test by chronological studies in seven male OLETF and seven male non-diabetic control Long Evans Tokushima Otsuka (LETO) rats each at 10, 16 and 24 weeks of age and eight male OLETF rats that were placed in a cage with a wheel for exercising from 5 to 24 weeks of age. The hormonal contents and morphological features of the pancreas of these rats were examined. After iv injection of insulin, the plasma glucagon level rose significantly from the basal level in OLETF rats at 10 weeks old, but little if at all in those of 16 and 24 weeks old. The pancreatic A cells of LETO rats of all age groups responded equally well to glucopenia. The areas under the response curves of plasma glucagon (sigma delta IRG) during the 90 min of insulin-induced hypoglycemia were 14496 +/- 7860 vs 9588 +/- 3930, 2257 +/- 3018 vs 9235 +/- 5447 (p < 0.05) and 826 +/- 985 vs 9707 +/- 2510 (p < 0.01) ng.min-1.l-1 in OLETF rats vs LETO rats of 10, 16 and 24 weeks old, respectively. The plasma glucagon responses during the arginine test were higher in OLETF rats than in LETO rats at 10 and 16 weeks but not at 24 weeks of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma glucagon responses to insulin-induced hypoglycemia and arginine in spontaneous non-insulin-dependent diabetes mellitus (NIDDM) rats, Otsuka Long Evans Tokushima Fatty (OLETF) strain. 810 92


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