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)

Antibodies were readily produced in three rabbits to unconjugated pure natural porcine secretin, and in two rabbits to synthetic porcine secretin conjugated to BSA. The final dilutions of the antisera to bind 50% of 1 fmol 125-i-labeled secretin prepared by the Chloramine-T method and purified on a Sephadex G-15 and a SP Sephadex C-25 column varied between 1:14,500 and 1:245,000. The effective equilibrium constants (Keff) according to Scatchard varied between 0.8 x 10(11) and 3.4 x 10(11), the average equilibrium constants (Ko) according to Sips varied between 0.8 x 10(11) and 3.6 x 10(11), and the indices of heterogeneity (alpha) according to Sips were 1.00 or close to 1.00. None of the antisera showed any cross reactivity to gastrin, glucagon or insulin. There was no differences in any of the preceding parameters between the antisera produced to the two immunogen preparations. It is suggested that the immunogenicity of secretin may be related to its basic charge, and to the possibility that secretin may circulate bound to certain plasmafactors or in a polymerized form. The two antisera with the highest equilibrium constants, which also allowed the highest working dilution to be applied, allowed measurements of fasting plasma secretin levels in the low pmol/1 range in all acidified plasmas examined.
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PMID:Production and evaluation of secretin antibodies. 65 47

The release of pancreatic polypeptide (PP) by gut hormones, acetyl choline and adrenaline was investigated in an isolated perfused pancreas preparation. PP was potently released by 1 nmol/1 caerulein (186 +/- 12%, p is less than 0.001) and gastric inhibitory peptide (GIP) (211 +/- 31%, p is less than 0.005) as well as by 1 mumol/1 acetyl choline (1097 +/- 59%, p is less than 0.001). A significant two-fold release of PP was also evoked by 1 nmol/1 vasoactive intestinal peptide (VIP) (129 +/- 38%, p is less than 0.02 and gastrin (108 +/- 25% p is less than 0.01). Insulin release, induced by high glucose concentration was enhanced by both GIP (210 +/- 38%, p is less than (0.01) and VIP (48 +/- 5%, p is less than 0.001). In addition GIP enhanced the release of glucagon by 179 +/- 18% (p is less 0.001) at 1.4 mmol/1 glucose and by 127 +/- 24% (p is less than 0.005) at 8.3 mmol/1 glucose. Thus no simple inter-relationship appears to exist between the control of the three circulating islet hormones.
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PMID:Pancreatic polypeptide, glucagon and insulin secretion from the isolated perfused canine pancreas. 66 4

Both vagal and sympathetic innervation been have described as influencing hormone release from the gastrointestinal tract and pancreas. The role of neural influences on the release of gastrin, glucagon, and secretin has been studied using the potent autonomic nerve stimulus of hypoglycaemia. Healthy subjects were each rendered hypoglycaemic by insulin 0.2 units/kg on three occasions: after atropine 20 microgram/kg: after propranolol 160 mg orally, and without prior drug administration. Adequate beta-blockade was confirmed by observation of the pusle rate response to a standard exercise at the end of the experiment, and by measurements of plasma propranolol levels. Hypoglycaemia failed to produce a rise in plasma gastrin under either propranolol or control conditions but a significant rise was noted with prior atropinisation. The glucagon response to hypoglycaemia, when measured with either the C- or N-terminal reactive antibodies, was found not to be influenced to any significant extent by either beta-blockade or atropinisation. No alteration in plasma secretin levels was noted during hypoglycaemia. It therefore appears that neural influences are relatively unimportant in the release of gastrin, glucagon, and secretin in man.
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PMID:Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man. 68 May 95

1. The effect of alpha- and beta-adrenoceptor blockade on the release of pancreatic glucagon, in response to stimulation of the peripheral ends of the splanchnic nerves has been examined in adrenalectomized calves 3-5 weeks after birth. In addition, the effects of insulin, atropine and somatostatin on the glucagon response to splanchnic nerve stimulation have been assessed in adrenalectomized dogs. 2. In calves release of pancreatic glucagon in response to splanchnic nerve stimulation was not suppressed by phentolamine at a dose that effectively abolished alpha-adrenergic inhibition of insulin release, or by propranolol, at a dose that completely eliminated the chronotropic action of the cardiac sympathetic innervation. 3. In dogs release of pancreatic glucagon in response to splanchnic nerve stimulation was not suppressed by atropine (0.2 mg/kg) or somatostatin, at a dose that caused a steady fall in the concentration of gastrin in the circulating plasma (0.5 microgram-kg-1 min-1). Glucagon release was apparently potentiated by exogenous insulin (4.0 u./kg). 4. The results are discussed in relation to the findings of other workers and it is concluded that the precise mechanism whereby stimulation of the sympathetic innervation to the pancreas leads to secretion of glucagon merits more detailed investigation.
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PMID:Certain pharmacological characteristics of the release of pancreatic glucagon in response to stimulation of the splanchnic nerves. 69 Aug 73

1. Pancreatic endocrine responses to ingestion of milk have been investigated in conscious unweaned calves, 3-5 weeks after birth. Passage of gastric content from abomasum to small intestine was prevented by means of a cannula placed in the duodenum adjacent to the pylorus and food was witheld for at least 22 h in order to deplete liver glycogen. 2. Under these conditions ingestion of milk was followed by a prompt rise in the concentrations of pancreatic glucagon, PP and gastrin in the arterial plasma but the usual rises in plasma glucose and insulin concentration were absent. 3. Evidence was obtained to show that absorption of glucose from the small intestine occurs sufficiently rapidly to account for the initial rise in plasma glucose concentration after feeding in normal animals. However, the rise in plasma glucagon concentration was sufficient to contribute to alimentary hyperglycaemia by promoting hepatic glycogenolysis in calves with abundant liver glycogen. 4. None of the neuroendocrine responses to ingestion of milk was affected by prior section of the splanchnic nerves whereas each was blocked by atropine (0.2 mg/kg), showing that all depend upon muscarinic, parasympathetic rather than sympathetic activity, in the absence of extraneous stress.
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PMID:The role of the autonomic nervous system in the control of pancreatic endocrine responses to milk ingestion in the calf. 69 Aug 86

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15

The first feed of breast milk given to a group of 12 term infants was previously shown to increase the levels of blood glucose and plasma insulin, growth hormone (GH), gastrin, and enteroglucagon. We have now studied the effects of the first feed of breast milk in two similar groups of preterm infants, to compare the results with those obtained for the term infant. One group of 8 preterm infants received a bolus (2.5 ml/kg) of breast milk via a nasogastric tube; the other group of 5 infants received a continuous intragastric infusion (2.5 ml/kg per hour) of breast milk. No change occurred in the concentrations of blood glucose, lactate, pyruvate, or ketone bodies, or in plasma insulin, GH, pancreatic glucagon, or enteroglucagon in either the 'bolus fed' or the 'infusion fed' group of preterm infants. Thus the marked metabolic and endocrine changes in term infants after the first feed do not occur in preterm infants with standard methods of feeding.
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PMID:Metabolic and endocrine events at the time of the first feed of human milk in preterm and term infants. 71 42

The effect of intravenous infusion of glucagon (300 ng x kg(-1) x h(-1)), 1-arginine (0.6 g x kg(-1) x h(-1)) and of saline on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Infusion of glucagon and 1-arginine enhanced plasma concentrations of pancreatic glucagon to 65--85 pmol/l, a level similar to that seen after a normal protein-rich meal. Both infusions significantly inhibited the acid response to the meal, most pronounced after 1-arginine. The difference in acid inhibition could not be ascribed either to differences in plasma glucagon concentrations or to differences in serum gastrin concentrations. The study supports the concept that pancreatic glucagon is a physiological inhibitor of gastric acid secretion.
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PMID:Inhibition of meal-stimulated gastric acid secretion in man by exogenous and endogenous pancreatic glucagon. 72 1

Antibody was readily produced in a rabbit against synthetic porcine secretin coupled to BSA. The final dilution of the antiserum to bind 50% of 1 fmol 125I-labeled secretin was 1 : 150,000. The effective equilibrium constant (Keff) according to Scatchard was 3.4 X 10(11) l/mol, the average equilibrium constant (Ko) according to Sips 3.5 X 10(11) l/mol, and the index of heterogeneity (alpha) according to Sips 1,00. No cross reactivity was found for gastrin, glucagon and insulin. 125I-labeled synthetic porcine secretin was prepared by the Chloramine-T-method, and the label purified on a Sephadex G-15 column followed by a SP Sephadex C-25 column had a specific radioactivity of 1.150 muCi/nmol. The radioimmunoassay method described has a detection limit of 1.6 pmol/l with 95% confidence limit, a within assay precision of 9,6%, and a between assay precision of 12.8%. It allows detection of fasting plasma secretin in the low pmol/l range, and the rather sharp rise and fall in plasma secretin subsequent to a brief period of duodenal acidification. The problem involved in measuring plasma secretin have been overcome by acidification of the plasma, and by subtracting the "apparent" secretin concentration in corresponding secretin-free plasma prepared by incubation at 37 degrees C for 96 h for each subject.
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PMID:Radioimmunoassay of secretin in acidified plasma. 72 17

Fasting levels of 5 gut hormones were studied in 30 patients with advanced uraemia (CRF), 40 undergoing regular dialysis (RD) and 555 renal transplant patients (RT). Mean values of gastrin and total glucagon were markedly elevated in CRF and RD patients compared with 20 normal subjects; there were lesser elevations in pancreatic glucagon, insulin and vasoactive intestinal peptide (VIP). Secretin levels were unchanged. In RT patients, fasting levels of VIP and pancreatic glucagon had returned to normal, while levels of gastrin, total glucagon and insulin remained slightly elevated compared with controls. Food stimulated hormone levels were measured in 18 RD patients and compared with 18 controls. After eating, RD patients failed to show the late increase in total glucagon, or the suppression of VIP and secretin seen in normal subjects; the pattern of gastrin and insulin response was similar to controls, but after the initial increase plasma levels in RD patients tended to show a slower decline. Thus involvement of the gastrointestinal tract in uraemia is associated with functional disturbance of the endocrine system of the gut.
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PMID:Elevations of gastrointestinal hormones in chronic renal failure. 74 Jun 78


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