Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PANCREAS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1983

Experimental pancreas imaging study with 13N-glutamate using positron computer tomography.

Accumulation of 13N-L-glutamate in the pancreas was experimentally evaluated by tissue distribution studies and by positron computer tomography imaging studies. The pancreas and salivary gland of Donryu rats exhibited a high rate of 13N-glutamate uptake. The percent administered dose/g of pancreas was 3.8 at 20 min, 4.4 at 30 min after injection, and the pancreas to liver ratio was 1.9 and 2.5, respectively. The same results were obtained with Golden hamsters. The role of the feeding protocols was studied to optimize the technique. The fasting group showed a significantly higher uptake in the pancreas than in the free feeding group. The uptake in the fasting followed by a high protein meal group was higher than fasting only group, but the difference was not significant. Positron emission tomography of a miniature-pig with 13N-glutamate showed a clear image of the pancreas with the highest activity. It was concluded that 13N-glutamate was quite useful in positron imaging of the pancreas.

Animals↗
PubMedDate not supplied

Pancreas-preserving total gastrectomy for proximal gastric cancer.

Lymph node (LN) dissection along the upper border of the pancreas is one of the essential parts of curative surgery for gastric cancer, and the distal portion of the pancreas was frequently resected for complete removal of LNs along the splenic artery. However, pancreatic juice leakage, subphrenic abscess, and postoperative diabetes were common complications in patients treated by pancreatic resection. To avoid these problems a new surgical procedure, the pancreas-preserving operation, was developed by Maruyama in 1979. We found that lymphatic channels from the stomach did not flow into the pancreas parenchyma, and that the spleen, splenic artery, and fatty connective tissue including nodes could be removed completely without dissection of the pancreas parenchyma and splenic vein. The preserved pancreas receives its arterial blood supply through the transverse pancreatic artery, and its preservation prevents postoperative diabetes. A total of 299 patients were treated by this procedure. The operative mortality rate was 0.3%, the hospital death rate 1.6%, and the surgical complications rate 19.6%. The cumulative 5-year survival rate for those with stage II was 70.5% and for those with stage III 54.1%. These results were superior to those of the pancreas resection group.

Gastrectomy↗
PubMed1996

Enhancement of the normal pancreas: comparison of manganese-DPDP and gadolinium chelate.

The purpose of this paper was to compare manganese-DPDP (Mn-DPDP) and gadolinium chelate (Gd-DTPA) contrast agents for enhancement of the normal pancreas. A total of 14 patients with focal liver disease underwent Mn-DPDP- and Gd-DTPA-enhanced 1.5 T MR examinations using spoiled gradient-echo (FLASH) technique at two separate times. Contrast agents were injected according to the currently recommended practices; Gd-DTPA was injected as a rapid bolus injection in a dosage of 0.1 mmol/kg, and Mn-DPDP was injected as a slow IV injection in a dosage of 5 mumol/kg. Quantitative region of interest measurements were made in 11 patients, and percent contrast enhancement of the pancreas and pancreas-fat signal-to-noise ratios (SNR) were determined for each agent. Images were also evaluated qualitatively by consensus reading of two investigators and overall scan quality was rated on a scale from 1 (poor) to 4 (very good). Enhancement of the pancreas immediately post Gd-DTPA was significantly higher than 15 min post Mn-DPDP (73.3 vs 36.3%; p = 0.003). On postcontrast images the pancreas-fat SNR measurements were 7.7 (i.e., pancreas higher in signal than fat) and -6.1 for Gd-DTPA and Mn-DPDP, respectively, which was significantly different (p < 0.001). Image quality was rated as 3.1 and 2.5 for Gd-DTPA- and Mn-DPDP-enhanced images, respectively. The normal pancreas enhances significantly more with Gd-DTPA than with Mn-DPDP administered under the conditions of this study. Overall image quality is also greater on the Gd-DTPA-enhanced images.

Adipose Tissue↗
PubMed1984

Exocrine and endocrine secretion from isolated perfused rat pancreas with islet cell tumors induced by streptozotocin and nicotinamide.

Pancreatic exocrine and endocrine function in the rat with islet cell tumors induced by streptozotocin and nicotinamide was studied in the in vitro isolated perfused pancreas. The tumor-bearing pancreas secreted significant amounts of insulin even at 2.8 mM glucose stimulation. Further, insulin response to 8.3 mM glucose stimulation was greater in the tumor-bearing pancreas than in the control. Not only endocrine, but also exocrine, disorders were found in the rat pancreas bearing islet cell tumors. In contrast to the increased response of insulin, amylase output in response to 0.1 ng/ml cerulein was significantly lower in the tumor-bearing than in the control pancreas, although there was no difference in pancreatic juice flows from both groups. These results suggest that enzyme secretory function of the pancreas with islet cell tumors may be suppressed in the presence of some interrelationship between the exocrine and endocrine portion of the pancreas with islet cell tumors.

Adenoma, Islet Cell↗
PubMed1994

The role of the pancreas in the regulation of zinc status.

A low Zn diet resulted in subacute Zn deficiency in young rats. Thirty minutes after the intubation of a trace 65-Zn we determined the total tissue Zn activity in plasma, erythrocytes, liver, pancreas, bone, muscle, and proximal jejunum. Assuming the body behaved like a closed multicompartmental system in steady state, we estimated the initial Zn exchange between plasma, and the erythrocytes or these tissues. In comparison with control animals the exchanges between plasma and erythrocytes or pancreas increased threefold during subacute Zn deficiency. In the pancreas the ratio also reversed from < 1.0 to > 1.0. This confirmed earlier observations that the specific activity (kBq 65-Zn/mol Zn) increased mostly in the pancreas. By increased net Zn uptake during subacute deficiency, the pancreas Zn content remained constant in chronic Zn deficiency. We discussed the regulation of the Zn status by the pancreas. We hypothesize that the exocrine pancreas modulates Zn absorption by an exocrine ligand that enhances absorption in the jejunum during subacute deficiency: Unsaturated with Zn it binds dietary intraluminal Zn and increases the Zn absorption. The literature provides evidence in confirmation. This hypothesis explains also conflicting data on the inherited Zn malabsorption syndrome Acrodermatitis Enteropathica.

Animals↗
PubMed1986

Ex-vivo isolated perfusion of the pancreas in the Syrian golden hamster.

The technique of ex-vivo isolated pancreatic perfusion has been a valuable method for investigation of the physiology of the exocrine and endocrine pancreas. We have adapted the technique of isolated pancreatic perfusion for use in the Syrian golden hamster, an animal used widely in studies of pancreatic carcinogenesis. The technique involves surgical harvest of the pancreas with its aortic and portal venous blood supply intact and perfusion of the pancreas with a modified Krebs buffer at 37 degrees C. Physiological function of the perfused pancreas system was examined in 27 Syrian hamsters. In tests of endocrine function, the perfused pancreas responded by increasing insulin secretion within 1 min of elevating perfusate glucose concentration, and also secreted insulin promptly in response to 10 mM arginine. In exocrine studies, the flow of pancreatic juice was stimulated by the addition of 0.8 X 10(-9) M secretin to the perfusate, and amylase output was significantly increased by the addition of 0.2 X 10(-9) M cholecystokinin (CCK-8). The ex-vivo isolated perfused pancreas in the hamster thus appears to respond appropriately to physiological stimuli and is a valuable additional tool for studies of the hamster pancreas.

Animals↗
PubMed1986

Resectability of the pancreas without producing diabetes, with special reference to pancreatic regeneration.

The exact resectability of the pancreas without producing diabetes was investigated in dogs, with consideration of pancreatic regeneration. Within the first week after major pancreatectomy, acinar cell division occurred, followed by hypertrophy; these changes resulted in an increase in weight of the remnant pancreas. The regeneration rate correlated well with the resection rate, glucose tolerance, and the insulin secretion of the remnant pancreas. Immediately after resection of more than 92% of the pancreas, severe diabetes developed, and the regeneration rate was 29.9 +/- 6.03% three to six weeks after surgery. Twelve weeks after resection of 74-92% of the pancreas, so-called Sandmeyer's diabetes had developed. The regeneration rate was 45.3 +/- 4.22% in the non-diabetic group, but in the diabetic group it proved to be only 15.4 +/- 2.39%. When less than 74% of the pancreas was resected, diabetes did not occur throughout the postoperative observation periods of 3-18 weeks, and the regeneration rate was 5.5 +/- 6.62%. These results suggested that 74% of the pancreas may be removed without producing diabetes.

Animals↗
PubMed1996

[Developmental anomalies and congenital diseases of the pancreas].

Developmental anomalies of the pancreas result from fusion failure between the dorsal and ventral pancreatic ducts (pancreas divisum) or from rotational failure of the ventral bud (pancreas anulare). These variations and anomalies of the ductal anatomy can be asymptomatic throughout life or can cause varying symptoms in different age periods. Pancreas divisum and pancreas anulare can be confirmed exclusively by means of pancreatography. Congenital disorders of the pancreas derive from genetic defects involving different organ systems, which usually dominate the clinical symptoms. Developmental anomalies and congenital disorders of the pancreas lead to varying morphological alterations of the organ which can be assessed by means of modern imaging.

Adult↗
PubMed2006

Alternative splicing of G6PC2, the gene coding for the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP), results in differential expression in human thymus and spleen compared with pancreas.

AIMS/HYPOTHESIS: Autoimmunity to insulin, glutamic acid decarboxylase and the tyrosine-phosphatase-like protein IA-2 is associated with type 1 diabetes. The production of self-molecules in thymus and secondary lymphoid tissues is critical for self-tolerance; reduced levels may impair tolerance and predispose to autoimmunity, as shown for insulin. Alternative splicing causes differential expression of IA-2 gene (PTPRN) transcripts and IA-2 protein in human thymus and spleen compared with pancreas. IA-2 sequences not present in lymphoid tissues become autoimmune targets in type 1 diabetes. The beta cell molecule islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) is an autoantigen in the non-obese diabetic (NOD) mouse, a model of type 1 diabetes. IGRP is a candidate autoantigen in the human disease, but robust assays for IGRP autoantibodies and/or autoreactive T cells are not available. Both full-length and IGRP splice variants encoded by the G6PC2 gene are expressed in the pancreas. In this study we tested the hypothesis that IGRP splice variants could be differentially expressed in thymus and spleen compared with the pancreas. METHODS: We evaluated the expression of G6PC2 transcripts in matched human thymus, spleen and pancreas specimens by RT-PCR. RESULTS: Alternative splicing results in differential expression of G6PC2 transcripts in thymus and spleen compared with pancreas. The full-length transcript is expressed in human pancreas but not in thymus or spleen. Five alternative spliced forms are always expressed in pancreas but those lacking exons 2, 3 and 4, alone or in combination, were rarely detected in thymus or spleen. CONCLUSIONS/INTERPRETATION: Differential tissue expression might favour autoimmune responses to IGRP in humans; target epitopes may be encoded by exons 3 and 4, or at the junctions of the conserved exons in the spliced transcripts. This information may aid in designing synthetic peptides for the identification of IGRP-specific autoreactive T cells in patients with type 1 diabetes.

Alternative Splicing↗
PubMed2006

The pancreas in beta-thalassemia major: MR imaging features and correlation with iron stores and glucose disturbances.

The study aims at describing the MR features of pancreas in beta-thalassemia major, investigating the relations between MR findings and glucose disturbances and between hepatic and pancreatic siderosis. Signal intensity ratios of the pancreas and liver to right paraspinous muscle (P/M, L/M) were retrospectively assessed on abdominal MR imaging studies of 31 transfusion-dependent patients with beta-thalassemia major undergoing quantification of hepatic siderosis and 10 healthy controls, using T1- (120/4/90), intermediate in and out of phase - (120/2.7, 4/20), and T2*-(120/15/20) weighted GRE sequences. Using the signal drop of the liver and pancreas on opposed phase images, we recorded serum ferritin and results of oral glucose tolerance test (OGTT). Decreased L/M and P/M on at least the T2* sequence were noticed in 31/31 and 30/31 patients, respectively, but no correlation between P/M and L/M was found. Patients with pathologic OGTT displayed a higher degree of hepatic siderosis (p < 0.04) and signal drop of pancreas on opposed phase imaging (p < 0.025), implying fatty replacement of pancreas. P/M was neither correlated with glucose disturbances nor serum ferritin. Iron deposition in the pancreas cannot be predicted by the degree of hepatic siderosis in beta-thalassemia major. Fatty replacement of the pancreas is common and may be associated with glucose disturbances.

Adolescent↗
PubMed1999

Orthotopic pancreas transplantation with portal venous drainage in rats. Surgical technique and metabolic effects(*).

Heterotopic pancreas transplantation in type I diabetic patients does not correct hyperglucagonemia, which is thought to be due to insufficiently suppressed glucagon release by the host pancreas. The diabetogenic effects of glucagon then have to be corrected by higher than normal insulin secretion from the transplant, with the attendant risk of earlier loss of islet cell function, and development of atherosclerosis. To establish whether this situation can be prevented, we investigated glucose homeostasis and blood lipids, as well as fecal fat and chymotrypsin as indicators for pancreatic exocrine function 14 weeks after orthotopic pancreas transplantation in inbred rats. The pancreas was resected before orthotopic transplantation of the donor pancreas with portal venous drainage (n=8). Laparotomized animals served as controls (n=8). Basal plasma glucagon, basal plasma insulin to glucagon molar ratio, and basal and integrated incremental responses of plasma glucose, insulin, and C-peptide after an oral glucose load (2 g/kg body weight) were similar in both groups. However, hepatic insulin clearance was slightly but significantly lower in the transplanted group (1.1+/- 0.1 vs 1.6+/-0.2; P<0.05). Basal plasma levels of free fatty acids, phospholipids, triglycerides, cholesterol, low-density lipoproteins, and high-density lipoproteins were unchanged after transplantation. Also unchanged were fecal fat and chymotrypsin levels, thus indicating preserved pancreatic exocrine function. We concluded that orthotopic pancreas transplantation with portal venous drainage achieves almost optimal metabolic control with respect to endocrine and exocrine pancreatic function as well as blood lipids. This technique could therefore be used to treat combined endocrine and exocrine insufficiency in chronic pancreatitis and thus enlarges the spectrum of indications for pancreas transplantation.

Animals↗
PubMed2000

Postabsorptive muscle protein metabolism in type 1 diabetic patients after pancreas transplantation.

Insulin was shown to induce protein anabolism in vivo mainly by inhibiting proteolysis. Heterotopic pancreas transplantation in type 1 diabetes mellitus is characterized by peripheral hyperinsulinemia due to systemic rather than portal insulin delivery. Therefore, we studied the postabsorptive muscle protein metabolism in type 1 diabetic patients with or without pancreas transplantation. The forearm balance technique was performed in 9 type 1 diabetic patients on exogenous insulin treatment, in 4 type 1 diabetic patients following successful pancreas transplantation and in 6 healthy volunteers. Labelled leucine and phenylalanine were infused to quantify whole-body and muscle protein synthesis, respectively. In the postabsorptive state, whole-body protein synthesis (leucine kinetics) was similar in pancreas-transplanted patients and controls. In contrast, muscle protein synthesis tended to be less negative in pancreas-transplanted patients with respect to type 1 diabetic patients and healthy volunteers. The present data suggest that recipients with peripheral insulin delivery and chronic hyperinsulinemia are characterized by a preferential stimulation of protein synthesis in muscle rather than in the splanchnic district. When insulin was infused acutely, while maintaining euglycemia, the whole-body and muscle protein synthesis rates were approximately halved in type 1 diabetic patients with and without pancreas transplantation. We conclude that pancreas transplantation is able to normalize basal and insulin-stimulated protein metabolism. Chronic hyperinsulinemia counteract steroid-induced protein degradation by means of a mild, but persistent stimulation of muscle protein synthesis.

Adult↗
PubMed2001

L-arginine stimulates insulin secretion from the pancreas of normal and diabetic rats.

Several reports have shown that nitric oxide (NO) stimulates glucose-induced insulin secretion in the pancreas of normal rat but the effect of L-arginine (a NO donor) on insulin secretion from the pancreas of diabetic pancreas is unknown. Fragments of pancreatic tissue from normal and diabetic rats were incubated for 45 min in Krebs solution containing 100mM L-arginine. The supernatant was subsequently analyzed for the insulin content using radioimmunoassay technique. L-arginine evoked large increases in insulin secretion from the pancreas of diabetic rat. The insulin secreted from the pancreas of diabetic rat was numerically but not significantly lower compared to that of normal rat pancreas. In conclusion, L-arginine, a nitric oxide donor stimulates insulin secretion from the pancreas of diabetic rats.

Animals↗
PubMed2004

Evolving surgical strategies for pancreas transplantation.

Pancreas transplant has become a reliably predictable treatment and cure for patients with type 1 diabetes mellitus and hypoglycemic unawareness or renal failure. During the past 2 years, the use of enteric drainage has been shown to decrease morbidity over traditional bladder drainage, and the use of the portal system for venous drainage continues to be explored. Technically, the use of circular staplers, over a hand-sown anastomosis for duodenal drainage, has gained popularity, and alternative arterial reconstruction methods have been developed. Living donor pancreas and kidney transplants are also becoming more common throughout the world. In the area of immunosuppression, steroid-free protocols, now commonplace in kidney transplants, are being applied successfully to pancreas transplantation. Finally, the benefit of solitary pancreas and pancreas after kidney transplantation has been questioned, and a more complete analysis of pancreas alone and pancreas after kidney transplants is anticipated in the near future.

Diabetes Mellitus, Type 1↗
PubMed1984

DNA damage in isolated hamster and rat pancreas cells by pancreatic carcinogens.

N-Nitrosobis(2-oxopropyl)amine (BOP), N-nitrosobis(2-hydroxypropyl)-amine (BHP) and N-nitroso(2-hydroxypropyl-2-oxopropyl)amine (HPOP) are pancreatic carcinogens in the Syrian golden hamster (SGH) but do not cause pancreatic tumors in rats. In this study, the ability of these three compounds to induce DNA damage in isolated pancreas cells from both species was determined by alkaline elution analysis. BOP was highly potent in SGH cells, causing DNA damage at concentrations as low as 0.5 micrograms/ml, and HPOP, although less potent than BOP, also caused considerable damage. Isolated SGH pancreas cells are thus able to metabolize BOP and HPOP to DNA-damaging species. Of the three compounds tested, only HPOP at higher doses (25-100 micrograms/ml) induced DNA damage in isolated rat pancreas cells. BHP did not damage rat or SGH pancreas cell DNA at concentrations up to 100 micrograms/ml, apparently due to lack of uptake of this compound by the cells. The observed insensitivity to DNA damage in rat cells is consistent with the resistance of the rat pancreas to carcinogenesis by these three compounds. The sensitivity of SGH pancreas cells to BOP- and HPOP-induced DNA damage correlates with the high carcinogenicity of these compounds for the SGH pancreas.

Animals↗
PubMed1988

Effects of L-364,718, a new cholecystokinin receptor antagonist, on camostate-induced growth of the rat pancreas.

Chronic feeding of rats with camostate results in pancreatic hypertrophy or hyperplasia, or both. Previous studies suggest that this effect of camostate occurs via an increase in endogenous cholecystokinin due to an enteral feedback mechanism involving the inhibition of trypsin in the duodenum. Studies employing proglumide, a weak and relatively nonspecific cholecystokinin antagonist, have failed to fully abolish camostate-induced pancreas growth. We examined the effects of L-364,718, a new and highly potent cholecystokinin receptor antagonist, on camostate-induced pancreas growth in rats. The pancreas weights and the concentrations of ribonucleic acid, protein, and chymotrypsinogen in the pancreas of rats treated with camostate alone were significantly elevated over those of controls. These effects of camostate were completely abolished in rats treated with camostate + L-364,718. The pancreas weights and the concentrations of deoxyribonucleic acid and ribonucleic acid in the pancreas of rats treated with L-364,718 alone were significantly lower than values in control rats. These data indicate that camostate-induced pancreas growth in rats appears to be dependent on the actions of endogenous cholecystokinin and that cholecystokinin may play a role in the maintenance of pancreatic growth in normal rats.

Animals↗
PubMed1993

NADPH-diaphorase activity in neurons of the mammalian pancreas: coexpression with vasoactive intestinal polypeptide.

BACKGROUND: To provide a morphological basis for understanding the role of nitric oxide in the pancreas, the present study was designed to clarify the localization and distribution of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) activity, a marker of NO synthase, in the pancreas of several mammalian species, including humans. METHODS: NADPH-d activity was examined in the rat, guinea pig, dog, and human pancreas by histochemistry. In addition, the possibility of coproduction of NO and vasoactive intestinal polypeptide (VIP) was investigated by a combined use of histochemistry and immunohistochemistry. RESULTS: In the pancreas, NADPH-d activity was localized in nerve fibers, nerve cell bodies, and the vascular endothelium. Nerve fibers with the enzyme activity were chiefly distributed in the exocrine pancreas and showed species differences in the distribution. Nerve fibers stained for NADPH-d were also observed in the endocrine pancreas, but the enzyme activity was not detected in the islet cells. Part of the nerve fibers and nerve cell bodies coexpressed NADPH-d activity and VIP-immunoreactivity. CONCLUSIONS: These results suggest that NO may act as a neuronal mediator and an endothelium-derived relaxing factor and may physiologically interact with VIP in the mammalian pancreas.

Amino Acid Oxidoreductases↗
PubMed1994

Altered expression of MUC2, MUC4, and MUC5 mucin genes in pancreas tissues and cancer cell lines.

BACKGROUND/AIMS: Neoplastic transformation of epithelial cells is commonly associated with altered synthesis and structure of mucin glycoproteins. The aim of the study was to determine if altered mucin gene expression takes place in pancreas cancer. METHODS: To examine mucin gene expression in normal pancreas and pancreas cancer, antibodies detecting the MUC1, MUC2, MUC5B, and MUC5C apomucins were used in immunohistochemical techniques and complementary DNA probes specific for the MUC1-MUC5 genes were used in Northern blots. RESULTS: MUC1 is the major apomucin expressed in normal pancreas, whereas MUC2-MUC5 are weakly expressed or undetectable. In pancreas cancer tissues and cell lines, increased expression of MUC2, MUC4, and MUC5C is shown. The cytoplasmic expression of MUC2 and MUC5C in tumor cells suggests that these apomucins are underglycosylated and abnormally compartmentalized. CONCLUSIONS: Enhanced expression of MUC2, MUC4, and MUC5C genes is a frequent event in pancreas cancer and may contribute to the alterations in the biochemical structure of pancreas cancer mucins.

Cell Division↗