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)

The effect of increased doses of Somatostatin-14 (3, 10, 30, 100, 300 micrograms/h) on basal release of insulin, pancreatic glucagon and pancreatic polypeptide (PP) was investigated on eight normal volunteers. Levels of Somatostatin-like immunoreactivity (SLI) was determined in order to correlate the increased SLI levels with the degree of islet hormone inhibition (r = 0.9947, p less than 0.01). By increasing the basal levels of SLI by one-third, a significant inhibition (p less than 0.01) of insulin, glucagon, and PP was noted (78.5, 78.6, 75.2%, respectively, on basal levels). The maximal effect was obtained with 300 micrograms/h for insulin, with 30 micrograms/h for glucagon and 100 micrograms/h for PP. In evaluating the relative inhibitory potency of somatostatin, expressed as ED50, the theoretic potency of somatostatin on each peptide had similar values, ranging from 30 to 10 micrograms/h. The present data show that a minimal peripheric increase in SLI is able to regulate basal islet pancreatic hormones.
Pancreas 1987
PMID:Dose-response effect of somatostatin-14 on human basal pancreatic hormones. 289 Jan 57

In order to investigate the action of somatostatin-28 (SS-28) on the metabolic homeostasis of insulin-dependent diabetics, we compared its effects to those of somatostatin-14 (SS-14) in terms of insulin sparing, changes in dextrose demands, glucose fluctuations and behavior of growth hormone and glucagon secretion. Eight insulin-dependent subjects were connected to Artificial Endocrine Pancreas (Biostator) for 84 hours during which they received intravenous infusions of either SS-14, SS-28 or isotonic saline in a randomized order, after a steady state of metabolism had been achieved. Five of the patients received SS-28 100 micrograms/h and SS-14 250 micrograms/h for 10 hours and three of them SS-28, 50 micrograms/h and SS-14 250 micrograms/h for 12 hours. Identical doses of both peptides were administered as bolus infusions prior to the continuous ones. Under SS-28 100 micrograms/h and SS-14 250 micrograms/h patients required 13.5 +/- 2.3 and 14.5 +/- 1.9 U of insulin respectively vs 40 +/- 5.6 U under isotonic saline infusion (mean +/- SEM, P less than 0.005 and P less than 0.01). At the same period the apparatus delivered 15 times more dextrose under SS-28 and 20 times more under SS-14. The magnitude of glucose fluctuations diminished from 64.6 +/- 2.47 mg% without to 41.4 +/- 2 mg% under SS-14 (P less than 0.01) and 46 +/- 3.8 mg% under SS-28 (P less than 0.02). Similar changes were observed in the remaining three patients who received SS-28 in the dose of 50 micrograms/h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The antidiabetic action of somatostatin-28 as assessed by the artificial endocrine pancreas: greater potency than somatostatin-14. 289 70

It is known that cholecystokinin (CCK) stimulates islet hormone secretion under a variety of experimental conditions. Since CCK occurs in several different molecular forms, with 58, 39, 33, 12, 8, or 4 amino acid residues, the question has evolved as to which is the shortest active form of CCK. We therefore investigated the influences of the C-terminal octapeptide of CCK, CCK-8 (sulfated form) and of the C-terminal tetrapeptide, CCK-4, on the secretion of insulin, glucagon, and somatostatin from the pig pancreas in vivo by infusing each of the two peptides into the superior pancreatic artery. We found that islet hormone secretion increased promptly upon infusion of both CCK-8 and CCK-4. Thus, the secretion of insulin was stimulated from 51 +/- 12 to 295 +/- 70 microU/min during the first 2 min after injection of CCK-8 and from 40 +/- 12 to 240 +/- 78 microU/min after injection of CCK-4. Similarly, the secretion of glucagon was stimulated from 240 +/- 45 to 357 +/- 38 pg/min after CCK-8 and from 282 +/- 44 to 335 +/- 43 pg/min after CCK-4, and somatostatin secretion was stimulated from 112 +/- 7 to 226 +/- 12 pg/min by CCK-8 and from 105 +/- 11 to 246 +/- 16 pg/min by CCK-4. With regard to the efficiency to stimulate the secretion of these three islet hormones, CCK-8 and CCK-4 were equipotent. We conclude that in pigs, CCK-8 and CCK-4 both stimulate the secretion of insulin, glucagon, and somatostatin from the pancreas in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1988
PMID:Cholecystokinin (CCK)-4 and CCK-8 stimulate islet hormone secretion in vivo in the pig. 289 79

This study was performed to assess the relationships between prohormone transport and processing in separate cell types in pancreatic islet tissue. Anglerfish islets were subjected to pulse-chase incubation with [3H]tryptophan and/or [35S]cysteine. Tissue and media were removed at specific time points during the incubation and prepared for electron microscopic examination or biochemical analysis. Specific islet cell types were identified ultrastructurally using protein A gold immunocytochemistry. Transport of newly synthesized peptides through specific subcellular compartments was monitored using electron microscopic autoradiography. Prohormone-product ratios were established by gel filtration and high-performance liquid chromatography analyses of tissue extracts. Complete analyses were performed on A-cells (source of proglucagon-II, glucagon-II, and glucagon-like peptide-II), B-cells (proinsulin and insulin), D-cells (prosomatostatin-II and somatostatin-28), and S-cells (prosomatostatin-I and somatostatin-14). Transport of newly synthesized peptides proceeded from rough endoplasmic reticulum (RER) to Golgi complex and then to mature secretory granules in all cell types. The transport rate was most rapid in A- and B-cells, slower in S-cells, and slowest in D-cells. The T1/2 for conversion of prohormone to product(s) was shortest in S-cells (150 min), slightly longer in B-cells (155 min), much longer in D-cells (259 min), and greater than 300 min in A-cells. These results demonstrate that the transport/prohormone conversion relationships are unique in each of the islet cell types monitored.
Pancreas 1988
PMID:Simultaneous assessment of prohormone transport and processing in four separate islet cell types: a combined autoradiographic and biochemical study. 290 25

The proliferative capacity of individual immunocytochemically identified islet beta cells was investigated in tissue culture. The pancreatic digest was filtered through a 20-micron filter to eliminate partially digested tissue fragments and islets; it was then cultured at low density to allow assessment of single cells. The type of cell was identified immunocytochemically by reaction with antibody to insulin or glucagon, and DNA synthesis was estimated from autoradiographs after incorporation of tritiated thymidine. Single immunocytochemically reactive beta or alpha cells attached to the culture substratum and then proliferated, directly proportional to time in culture. Single beta cells did not incorporate thymidine after 1 day in culture; nonendocrine cells, presumed to be mainly fibroblasts, readily incorporated thymidine. Beyond the first day, about 10% of the beta cells incorporated thymidine. The number of radioactively labeled, immunocytochemically reactive beta cells increased for 5 days in culture and then remained at the elevated level until experiments were terminated at 12 days. DNA synthesis in beta cells occurred in two waves separated by about 3 days, suggesting a generation time of about 3 days for immunocytochemically identified beta cells. Fetal calf serum was found to be an essential culture medium ingredient to sustain thymidine incorporation; horse serum was found to be an unsuitable substitute. Mitotic figures were recorded in differentiated beta and alpha cells. These studies conclusively show that differentiated beta and alpha cells can proliferate in culture.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1988
PMID:Clonal growth of immunocytochemically identified islet beta and alpha cells in culture. 305 Sep 77

Periodic oscillation of insulin and glucagon by isolated mice islets has been studied. Pulsatile secretion of insulin and glucagon was observed at all glucose concentrations tested. The frequency of oscillation per 20 min for glucagon was 5.0 +/- 0.26 and for insulin 4.0 +/- 0.26 (n = 6), approximating to periodicities of 4 and 5 min, respectively. These did not change by increasing the glucose concentration to 11.1 or 22.2 mM from 5.5 mM (basal). The maximal amplitude of glucagon secretion was not altered by raising the glucose concentration to 11.1 mM from basal. However, 22.2 mM glucose significantly suppressed the amount of glucagon released when compared with glucagon secretion in the presence of 5.5 mM glucose. In contrast, the maximal amplitude of insulin increased from 444.2 +/- 37.7 to 777.2 +/- 61.4 and from 271.8 +/- 35 to 701 +/- 26.5 pg/min (p less than 0.01, n = 6) by switching from basal to 11.1 and 22.2 mM glucose, respectively. We conclude from this study that the pacemaker controlling pulsatile secretion of insulin and glucagon is within the islet. Although the amplitude of secretion of these hormones is regulated by the ambient glucose concentration, the frequency of their pulsatile secretion is not.
Pancreas 1988
PMID:Characterization and control of pulsatile secretion of insulin and glucagon. 305 Sep 80

It has been shown that the large bowel contains substances with a potential to inhibit exocrine pancreatic function. Following large bowel removal in rats, there is an increase of pancreatic weight, digestive enzyme concentration, and secretion capacity in vitro. To evaluate the role of various GI hormones in the exocrine pancreatic adaptation following colectomy, we measured plasma cholecystokinin (CCK), neurotensin, glucagon, and insulin after meal stimulation. The test meal was applied via a transabdominal gastric tube in eight colectomized Wistar rats after a median of 18 days following surgery. Ten rats with a gastric tube without previous bowel surgery served as controls. After large bowel removal, there was impaired glucose tolerance and attenuated plasma insulin secretion. Baseline plasma glucagon levels were increased after colon removal, whereas the total postprandial glucagon release was decreased. Baseline and postprandial neurotensin values were comparable in both the experimental and control animals. Baseline and postprandial CCK plasma levels were intensely increased in the colectomized rats. It is assumed that the baseline and postprandial CCK pattern in rats after subtotal colectomy is responsible for exocrine pancreatic adaptation.
Pancreas 1988
PMID:Pancreatic trophism following colectomy in rats: the potential role of gastrointestinal hormones. 305 Sep 79

A new technique to obstruct the pancreatic ducts was developed by injecting zein solution into the common bile duct of the rat. Four weeks after the injection, the fate of the endocrine pancreas was investigated by studying (a) pancreatic content of four pancreatic hormones, (b) histology and immunohistochemistry of the pancreas, (c) i.v. glucose tolerance and i.v. insulin tolerance tests for monitoring plasma glucose, insulin, and pancreatic polypeptide (PP) levels in vivo, and (d) in vitro perifusion of pancreatic tissue slices to assess insulin and PP secretion. In zein-injected rats, the total pancreatic content of insulin, glucagon, PP, and somatostatin was reduced to 80, 70, 40, and 20%, respectively, of the corresponding controls. In response to insulin-induced hypoglycemia, the plasma PP levels rose to about one-half that of the controls. By contrast, perifused zein-injected rat pancreases released several times more PP than the controls in response to carbachol stimulation. In zein-injected rats, total pancreatic protein was reduced to 20% of the controls and pancreatic amylase was almost absent, reflecting practically complete loss of acinar tissue. Thus, this experimental model appears to be suitable for producing chronic pancreatic insufficiency in the rat and provides a useful model for studying both endocrine and exocrine functions in the small rodent.
Pancreas 1988
PMID:Endocrine pancreas in the rat model of exocrine pancreatic insufficiency. 305 70

This study examines the endocrine function of duct-obliterated canine segmental autografts for periods up to 5 years posttransplant. Overall the response profile of autografted animals was subnormal. After intravenous glucose tolerance tests K-values in transplanted animals (2.8 +/- 0.9%/min) were significantly lower than normal (4.6 +/- 1.2% min, p less than 0.001). After oral glucose stimulation, blood glucose in the autografted dogs reached a mean peak of 10.6 +/- 2.8 mmol/L whereas in normal dogs the peak value was 6.0 +/- 1.0 mmol/L (p less than 0.002). The mean insulin response in autografted dogs showed lower insulin concentrations in the early stages of the test, whereas insulin secretion after glucagon stimulation was significantly reduced in autografted dogs. Intravenous glucose tolerance tests were analyzed by calculating K value or measuring a single blood glucose concentration 40 min after glucose injection. This value had a high correlation with the K value (r = 0.967). No progressive deterioration of graft function up to 5 years was found. Glycosylated hemoglobin levels were measured in autografted (646 +/- 59 pmol/mg) and normal dogs (620 +/- 85 pmol/mg) and no significant difference was found. In conclusion, duct-occluded segmental pancreatic autografts were shown to have a reduced functional capacity but there was no deterioration of function up to 5 years after duct-occlusion and grafting. The degree of metabolic control may be sufficient to prevent diabetic complications.
Pancreas 1988
PMID:Long-term canine duct-occluded segmental pancreatic autografts: endocrine function. 306 74

Ultrasonic monitoring of the pancreas following secretin stimulation has shown to cause a marked dilatation of Wirsung duct; whether this phenomenon is due to the stimulation of pancreatic secretion and/or to the effect of secretin on the sphincter of Oddi (SO) motility is unknown. In the present study pancreatic scan after secretin was performed in 11 patients with nonpancreatic diseases after premedication with glucagon (inhibition of both pancreatic secretion and SO motility) or tyropramide (inhibition of SO motor function) and in patients with different degrees of pancreatic insufficiency. Serum immunoreactive trypsinogen (IRT) levels were measured in all the subjects during the test. Premedication with glucagon completely abolished both Wirsung enlargement and serum IRT increase, while tyropramide significantly reduced, but did not abolish, the response to secretin. These results suggest that both stimulation of pancreatic secretion and the increase of SO pressure are prerequisites for a full-blown occurrence of the secretin-induced modifications of Wirsung. Within chronic pancreatitis patients, the response to secretin was exaggerated in those with a still preserved pancreatic function and it was lacking in those with severe pancreatic insufficiency.
Pancreas 1987
PMID:Ultrasonic monitoring of Wirsung duct following secretin in controls and in chronic pancreatitis patients. 330 64


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