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 pancreatin on insulinopenic diabetes was studied in 10 patients with chronic pancreatitis and exocrine function impairment. All patients were treated for 4 days in a randomized crossover trial with either pancreatin (6 x 2 capsules, 6 x 300 mg/d) or placebo. Blood glucose levels were determined 7 times every day and night. On day 5, the patients were studied by a glucose sensor with adjustment of blood glucose to 120 mg/dl until 8.00 in the morning. A test meal was applied with 2 capsules pancreatin or placebo. Blood glucose and plasma levels of C-peptide, glucagon and pancreatic polypeptide (PP) were determined in regular intervals for 4 hours. Blood glucose levels were not significantly altered by pancreatin. As shown by M-value according to Schlichtkrull (21.6 +/- 2.9 versus 32.4 +/- 7.4), there was a tendency towards smaller oscillations of blood glucose with pancreatin treatment. C-peptide levels (basal 0.081 +/- 0.008 ng/ml; postprandial 0.119 +/- 0.013 ng/ml) were not significantly altered by the administration of pancreatin. Basal and postprandial glucagon and PP plasma levels were not influenced by pancreatin. From these results, we conclude that pancreatic enzyme supplementation does not significantly alter the requirement of insulin in patients with diabetes mellitus secondary to chronic pancreatitis. Possible disturbances of the enteroinsular axis are discussed in this paper.
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PMID:[Effect of pancreatin on diabetes mellitus in chronic pancreatitis]. 223 55

Pharmacological, percutaneous celiac plexus blockade is often inefficient in the treatment of pain in chronic pancreatitis. Lack of efficiency could be due to incomplete denervation of the plexus; however, a method for measuring the completeness of celiac plexus blockade is not yet available. We have, therefore, monitored the physiological completeness of pharmacological percutaneous celiac blockade with 40 ml 25% ethanol by measuring the effect of posture on heart rate, blood pressure, hepato-splanchnic vascular resistance, and pancreatic hormone concentrations before and after celiac plexus block in 6 patients with chronic pancreatitis. Blood pressure decreased and heart rate increased after the block (P less than 0.025), whereas no significant change was found in hepato-splanchnic vascular resistance nor in the change of these parameters during transition from the supine to standing position. Pancreatic hormones (C-peptide, free insulin, glucagon, pancreatic polypeptide and somatostatin) did not change in response to standing, either before or after the block. The cardiovascular variables were normalized the day after the block, and all the patients were in their habitual state regarding pain after 1 week. In conclusion, pancreatic hormone concentrations in response to standing are not useful for monitoring celiac plexus block, whereas heart rate, blood pressure and hepato-splanchnic blood flow may yield useful information. From such measurements it was concluded that permanent denervation of the celiac plexus was not achieved in our patients after injection of 40 ml 25% ethanol.
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PMID:Monitoring of celiac plexus block in chronic pancreatitis. 213 12

S-100 protein-containing cells were demonstrated by immunogold silver staining in human islets of Langerhans from patients with chronic pancreatitis (CP) with (n = 6) (Group I) or without (n = 6) (Group II) diabetes mellitus, (DM) and from nondiabetic, non-pancreatic controls (n = 6) (Group III). In all three groups S-100 protein containing cells were observed in all islets of Langerhans throughout the pancreas. Quantitative analysis of cell composition of islets did not reveal significant differences in S-100 protein cell content between the three groups. When double immunohistochemical staining was used to demonstrate different endocrine cell types (insulin, glucagon and pancreatic polypeptide) and S-100 protein immunoreactive cells, the latter proved to be a distinct cell type. Somatostatin-producing cells and S-100 protein-containing cells were usually also present as two distinct cell populations, but positive staining for both S-100 protein and somatostatin was occasionally observed within the same cells.
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PMID:S-100 protein immunoreactivity in human islets of Langerhans. 251 43

Pancreatojejunal anastomosis disruption still represents the main postoperative complication after pancreatoduodenectomy. In this study, a technique of occlusion of the residual pancreatic stump instead of pancreatojejunal anastomosis is proposed. Between March, 1981 and August, 1987, we performed 51 pancreatoduodenectomies, using Neoprene injection in the Wirsung duct, for carcinoma of the pancreatic head (28 cases), ampullary carcinoma (12 cases), islet cell carcinoma (5 cases), and chronic pancreatitis (6 cases). We observed a 33.3% overall morbidity, with a 5.8% operative mortality. The complications observed seemed not to be related to the technique of pancreatic stump occlusion, except for 2 pancreatic fistulas which spontaneously resolved. Abdominal ultrasound and computed tomography scan performed during the follow-up did not show any significant morphological alteration of the residual stump. Pancreatic endocrine function was assessed in 10 patients by evaluating blood glucose, plasma insulin and plasma glucagon levels both fasting and after oral glucose, and intravenous arginine infusion. These tests were performed before surgery and 15 days, 6 months, 1, 2, and 3 years after surgery. The results showed that 60% of the patients had impaired glucose tolerance before surgery and the percentage did not significantly change up to 3 years later (75%). No patient developed diabetes mellitus, and only 1 patient progressed from a normal to an impaired glucose tolerance. In conclusion, intraductal injection of Neoprene after pancreatoduodenectomy seems to be a safer procedure compared to pancreatojejunal anastomosis and does not induce a post-surgical diabetes.
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PMID:Pancreatoduodenectomy with occlusion of the residual stump by Neoprene injection. 254 44

This study includes nine patients with diabetes mellitus (DM) and chronic pancreatitis (CP) (group I); 11 patients without DM and with CP (group II); and a control group (group III) consisting of five autopsy cases with neither DM nor CP. These groups were evaluated by routine histologic stains and immunocytochemical stains for insulin, glucagon, and somatostatin. Semiquantitative assessment of the degree of exocrine pancreatic atrophy and of two endocrine features (diffuse endocrine proliferation and ductoendocrine proliferation) was performed for each pancreas. Quantitative determination of the cell composition was carried out in three kinds of islets (parenchymal, sclerosis, and newly formed). The mean percentages of the insulin-producing B cells were significantly lower in the parenchymal (44.5%) and new (34.3%) islets of diabetic patients than in the controls (67.8%) and parenchymal (59.4%) islets of nondiabetic patients. The mean percentages of glucagon-producing A cells revealed significant increases in the parenchymal (43.0%) and new (55.7%) islets of diabetic patients as compared with the controls (24.3%) and parenchymal (32.2%) islets of nondiabetic patients. The mean percentage of somatostatin-producing D cells was significantly increased in the parenchymal islets (12.4%) of diabetic patients as compared with the parenchymal islets (8.2%) of nondiabetic patients and controls (7.5%). These findings correlate with clinical data of frequent DM in CP, but are partly in contrast with previous immunohistochemical analysis findings in CP.
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PMID:Endocrine pancreas in chronic pancreatitis. A qualitative and quantitative study. 256 17

The immunohistochemical features of pancreatic grafts in eight patients with pancreatic transplants were analyzed and compared with pancreases from five patients with chronic pancreatitis and with three pancreatic tissues without histological abnormalities. There was a significant increase in glucagon producing cells in patients with transplanted pancreases compared with those with chronic pancreatitis (P less than 0.05). A significant decline in insulin-producing cells was seen in the transplanted pancreases with rejection in comparison with normal pancreatic tissue. Immunohistochemical staining for HLA-DR (Ia) antigens revealed expression of HLA-DR by endothelial cells, mononuclear cells, and by some ductal epithelial cells, but not by the endocrine islet cells. These results suggest that significant changes in insulin and glucagon production occur in the transplanted pancreas with rejection and that HLA-DR is not expressed by islet cells during graft rejection or with chronic inflammation.
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PMID:Pancreas transplantation: an immunohistochemical analysis of pancreatic hormones and HLA-DR expression. 256 35

In vitro isolated liver perfusion in a rat model of chronic pancreatitis (CP) has been shown to demonstrate hepatic resistance to insulin. The ability of pancreatic polypeptide (PP) to reverse the resistance to insulin on glucagon-stimulated hepatic glucose production was therefore investigated in this model. CP was induced in 250 to 300 gm Sprague-Dawley rats by infusion of 50 microliters of 99% oleic acid into the pancreas via the common bile duct. After 6 to 8 weeks, isolated liver perfusion was performed on livers from both CP rats and sham-operated control animals (n = 12, 14), both with and without PP administration. Glucagon infusion (100 pg/ml for 30 minutes) produced a five- to sixfold increase in hepatic glucose production. The integrated hepatic glucose output (IHGO) response to glucagon alone was comparable in pancreatic and sham-operated animals; during period 1 (0 to 10 minutes) IHGO was 7.1 +/- 0.5 mg/gm-min for sham-operated controls (n = 8) and 7.1 +/- 0.4 mg/gm-min for pancreatitic animals (n = 6) without PP treatment. Animals that received PP (100 ng intraperitoneally 5 hours before liver harvest and perfusion with 4.2 ng/ml from 10 to 30 minutes) demonstrated an IHGO for period 1 for the sham (n = 6) and pancreatitic animals (n = 6) of 5.6 +/- 0.6 and 4.8 +/- 0.8 mg/gm-min, respectively. Insulin infusion (100 microU/ml added to perfusate from 10 to 30 minutes) in CP livers without PP revealed impaired responsiveness to insulin; the ratio of period 3 (20 to 30 minutes)/period 1 IHGO was 110% +/- 5% in CP livers compared with 77% +/- 5% in sham controls (p less than 0.01). In contrast, PP treatment restored hepatic responsiveness to insulin to control levels; the period 3/period 1 IHGO was 75% +/- 13% in CP livers treated with PP, which was indistinguishable from the 67% +/- 9% response seen in sham-operated control animals. These data provide the first in vitro evidence of a primary hepatic glucoregulatory role of PP. Therefore PP deficiency may contribute to altered glucose metabolism through the induction of a reversible hepatic resistance to insulin.
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PMID:Reversal of in vitro hepatic insulin resistance in chronic pancreatitis by pancreatic polypeptide in the rat. 258 16

To investigate the effect of chronic pancreatitis (CP) on in vitro hepatic sensitivity to insulin, the suppression of glucagon-stimulated hepatic glucose production (HGP) by insulin was examined during isolated liver perfusion (ILP) in CP and sham-operated rats. CP was induced at laparotomy by infusion of 50 microliters 99% oleic acid into the common bile duct during temporary occlusion of the proximal hepatic duct in 250- to 350-g Sprague-Dawley rats. Eight to sixteen weeks later, single-pass ILP was performed on fed animals. Glucagon (100 pg/ml) was infused for 30 min; the final 20 min of perfusion was performed with (a) no insulin, (b) 25 microU/ml insulin, or (c) 100 microU/ml insulin. CP and sham rats demonstrated comparable HGP responses to glucagon during the 0- to 10-min period (5.2 +/- 0.5 vs 5.9 +/- 0.5 mg/g/min, P = NS). CP rats demonstrated an HGP response to glucagon alone more evanescent than that in sham rats (20-30 min of HGP, 6.6 +/- 0.6 vs 9.5 +/- 0.4 mg/g/min, P less than 0.05). Sham rats showed a dose-dependent inhibition of HGP by insulin, however (percentage 20-30 min of HGP/0-10 min of HGP for 0, 25, and 100 microU/ml insulin: 166 +/- 12, 125 +/- 7, and 101 +/- 5%, P less than 0.01), whereas CP rats showed no effect of insulin (130 +/- 6, 123 +/- 7, 134 +/- 7%, P = NS). Pre- and postperfusion liver glycogen contents revealed comparable decreases in liver glycogen in both groups: insulin inhibition of HGP in sham rats was accompanied by higher postperfusion glycogen content. These data demonstrate a loss of insulin-mediated suppression of hepatic glucose production in livers obtained from pancreatitic rats. We conclude that CP is accompanied by a primary hepatic resistance to insulin; this defect may play a role in the etiology of pancreatogenic diabetes.
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PMID:In vitro hepatic insulin resistance in chronic pancreatitis in the rat. 265 78

The B-cells of patients with recently diagnosed Type 1 (insulin-dependent) diabetes may have no response to glucose when the response to glucagon is present but attenuated. This observation suggests that the recognition of glucose is more severely affected than that for non-glucose stimulants. To determine whether a similar selective decrease in glucose response was present before the onset of diabetes we studied two groups of non-diabetic identical twins of patients with recently diagnosed Type 1 diabetes: one group with complement-fixing islet cell antibodies who were at high risk of developing diabetes (four of the five have already developed diabetes) and a group without such antibodies at low risk of developing diabetes. In addition, a group of patients with chronic pancreatitis were studied to control for non-specific damage to the B-cell. Responses to i.v. glucose and i.v. glucagon were compared. Patients with chronic pancreatitis has similar responses to both glucose and glucagon and the responses did not differ from control subjects. The B-cells of the immune positive group showed evidence of pathology because the insulin and C-peptide responses to both stimuli were reduced when compared to either their control subjects or the immune negative twin group. However, the B-cell response to both glucose and glucagon in the immune positive twins was similar. Because the B-cell response to glucose was not less than that to glucagon, a selective destruction of the glucose recognition system cannot be a characteristic of all twins throughout the period before they develop Type 1 diabetes.
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PMID:B-cell responses to intravenous glucose and glucagon in non-diabetic twins of patients with type 1 (insulin-dependent) diabetes mellitus. 268 66

Diabetes mellitus caused by pancreatic exocrine disease is a unique clinical and metabolic form of diabetes. The diagnosis of pancreatic diabetes caused by chronic pancreatitis may be elusive because it is occasionally painless and often not accompanied by clinical malabsorption until after hyperglycemia occurs. Diabetic patients with pancreatic calcification or clinically demonstrable pancreatic exocrine dysfunction will manifest the unique aspects of pancreatic diabetes described herein. Like other forms of diabetes, the primary hormonal abnormality in pancreatic diabetes is decreased insulin secretion. Patients with this disorder are unique in that they have low glucagon levels that respond abnormally to several physiological stimuli, blunted epinephrine responses to insulin-induced hypoglycemia, and malabsorption. In addition, they often have concomitant alcohol abuse with hepatic disease and poor nutrition. These characteristics result in increased levels of circulating gluconeogenic amino acids, decreased insulin requirements, a resistance to ketosis, low cholesterol levels, an increased risk of hypoglycemia while on insulin therapy, and the clinical impression of brittle diabetes. Retinopathy occurs at a rate equal to that of insulin-dependent diabetes but may be less severe in degree. Other complications of pancreatic diabetes have been less well studied but may be expected to be seen more frequently as these patients survive longer. The characteristics of pancreatic diabetes suggest that a conservative approach be taken in regard to intensive insulin therapy and tight blood glucose control.
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PMID:Pancreatic diabetes mellitus. 269 11


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