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PubMed2004

A rare diagnosis for a pancreatic mass: splenosis.

Splenosis, the autotransplantation of splenic tissue, has been designed to preserve organ functions after splenectomy. We present the first case of laparoscopic resection of a pancreatic splenosis, in a patient who had undergone a splenectomy 31 years before, complaining of abdominal pain and diarrhea. Abdominal computed tomography (CT) scan showed an enhancing hypervascular 3-cm solid mass in the body of the pancreas, mimicking a pancreatic cancer or a neuroendocrine tumor. A diagnostic laparoscopy was planned, and a 3-cm peripancreatic nodule with a long pedicle was visualized, with many nodules close to the tail of the pancreas and in the greater omentum. They were all resected, and the specimens obtained were immediately sent for frozen-section examination, which confirmed the diagnosis of heterotopic splenic tissue. Splenosis should be included in the differential diagnosis of the pancreatic masses in patients with previous splenic surgery. A hypervascular mass on CT scan should be regarded as an adenocarcinoma of the pancreas until proven otherwise. The possibility of a neuroendocrine tumor mandates an octreotide scan and gastrointestinal hormones dosage. In the unlikely event that all tests may produce equivocal results, a diagnostic laparoscopy is mandatory, in order to obtain an accurate histopathologic diagnosis.

Diagnosis, Differential↗
PubMed2006

Peptide YY attenuates STAT1 and STAT3 activation induced by TNF-alpha in acinar cell line AR42J.

BACKGROUND: STAT1 and STAT3, members of the cytoplasmic family of signal transducers and activators of transcription factors (STAT), have been associated with numerous inflammatory pathologies, including inflammatory bowel disease, hepatitis, and acute lung injury. But little is known about their role in the pancreas. Peptide YY (PYY), an inhibitory gastrointestinal hormone, ameliorates pancreatitis in vivo and in vitro. In addition, we have shown that PYY attenuates transcription factors, such as nuclear transcription factor (NF)-kappaB and Smad3/4, which mediate inflammation. We hypothesized that tumor necrosis factor (TNF)-alpha would induce STAT1 and STAT3, and PYY would attenuate their transcription factor binding. STUDY DESIGN: Rat pancreatic acinar cells were treated with recombinant TNF-alpha (200 ng/mL); PYY (3-36; 500 pM) was added 30 minutes post-TNF-alpha treatment. Cells were harvested at 2 hours, and nuclear protein and conditioned media were extracted. Levels of amylase secretion and cytokine production were measured using commercially available kits. STAT transcription factor binding was determined by protein/DNA array analysis and densitometry; results were verified again by electrophoretic mobility shift assay (EMSA) and ELISA-based assay. RESULTS: Amylase production was considerably increased (p < 0.05) as early as 5 minutes after addition of exogenous TNF-alpha and remained elevated for 24 hours. PYY decreased amylase production to control levels. A notable increase (p < 0.05) in the production of cytokines interleukin (IL)-1beta, IL-4, IL-6, IL-10, and TNF-alpha was observed with TNF-alpha treatment; production was reduced with PYY. TNF-alpha substantially upregulated STAT1 and STAT3 (two-fold or greater); PYY downregulated their binding activity to control levels. Results from both the electrophoretic mobility shift assay- and the ELISA-based assays verified STAT1 and STAT3 responses to TNF-alpha and PYY. CONCLUSIONS: In pancreatic acinar cells, TNF-alpha activated STAT1 and STAT3, known mediators of inflammatory cytokines. Interestingly, PYY attenuated their protein/DNA binding, which may have an impact on development of the disease. Additional investigation of STAT proteins and PYY could provide new therapeutic strategies for pancreatitis.

Amylases↗
PubMed2006

Alcohol ingestion does not affect serum levels of peptide YY but decreases both total and octanoylated ghrelin levels in healthy subjects.

Alcohol has been reported to have appetite-stimulating properties in humans. The underlying mechanism is unknown. Gastrointestinal hormones, such as ghrelin and peptide YY (PYY), could be involved as mediators of the alcohol effect because ghrelin stimulates the appetite and PYY appears to induce satiety. This investigation was undertaken with the intention to study that issue. Twelve young and healthy volunteers of both sexes participated in 2 experiments (experiments A and B), which were performed in random order 1 week apart. Alcohol (0.55 g ethanol per kilogram) was ingested in experiment A, drinking water in experiment B. Venous blood samples were collected before and repeatedly after the drinks. Serum concentrations of total ghrelin, octanoylated ghrelin (the bioactive form of the hormone), PYY, and ethanol were determined over a period of 5 hours. In experiment A, the ethanol level increased from 0 to 12.5 +/- 0.7 mmol/L in 1 hour (P < .001), and then began to decrease. In experiment B, the ethanol level remained at zero throughout the entire experiment. Alcohol induced significant declines in total and octanoylated ghrelin concentrations from 30 minutes on. The total ghrelin level reached its lowest point 5 hours after the alcohol intake (36% +/- 4% below the basal level; P < .001). The octanoylated ghrelin level fell 48% +/- 5% below the basal level in 2 hours (P < .001) and then tended to level out. Drinking water left both total and octanoylated ghrelin levels unaffected. The PYY level remained unchanged after both alcohol and water ingestion. Alcohol has a strong inhibitory influence on human ghrelin secretion, but has no effect on circulating PYY levels. This makes it unlikely that the orexigenic effect of alcohol is mediated by either of these 2 hormones.

Adolescent↗
PubMed2003

Glucose-dependent insulinotropic polypeptide (GIP): anti-diabetic and anti-obesity potential?

Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a gastrointestinal hormone, which modulates physiological insulin secretion. Due to its insulinotropic activity, there has been a considerable increase of interest in utilising the hormone as a potential therapy for type 2 diabetes. One of the difficulties in attempting to harness the insulinotropic activity of GIP into an effective therapeutic agent is its short biological half-life in the circulation. However, recent years have witnessed the development of a substantial number of designer enzyme-resistant 'super GIP' molecules with potent insulinotropic and anti-diabetic properties. In addition, observations in transgenic GIP receptor deficient mice indicate that GIP directly links overnutrition to obesity, therein playing a crucial role in the development of obesity and related metabolic disorders. The present review aims to highlight the rapidly emerging potential therapeutic applications of GIP, and especially, enzyme-resistant GIP analogues.

Amino Acid Sequence↗
PubMed2004

Expression, purification, and C-terminal amidation of recombinant human glucagon-like peptide-1.

Human glucagon-like peptide-1 (hGLP-1) (7-36) amide, a gastrointestinal hormone with a pharmaceutical potential in treating type 2 diabetes mellitus, is composed of 30 amino acid residues as a mature protein. We report here the development of a method for high-level expression and purification of recombinant hGLP-1 (7-36) amide (rhGLP-1) through glutathione S-transferase (GST) fusion expression system. The cDNA of hGLP-1-Leu, the 31st-residue leucine-extended precursor peptide, was prepared by annealing and ligating of artificially synthetic oligonucleotide fragments, inserted into pBluescript SK (+/-) plasmid, and then cloned into pGEX-4T-3 GST fusion vector. The fusion protein GST-hGLP-1-Leu, expressed in Escherichia coli strain BL21 (DE3), was purified by affinity chromatography after high-level culture and sonication of bacteria. Following cleavage of GST-hGLP-1-Leu by cyanogen bromide, the recombinant hGLP-1-Leu was released from fusion protein, and purified using QAE Sepharose ion exchange and RP C(18) chromatography. After purification, the precursor hGLP-1-Leu was transacylated by carboxypeptidase Y, Arg-NH(2) as a nucleophile, to produce rhGLP-1. Electrospray ionization mass spectrometry showed the molecular weight was as expected. The biological activity of rhGLP-1 in a rat model demonstrated that plasma glucose concentrations were significantly lower and insulin concentrations higher after intraperitoneal injection of rhGLP-1 together with glucose compared with glucose alone (P < 0.001).

Animals↗
PubMed2004

Effect of GIP, GLP-1, insulin and gastrin on ghrelin release in the isolated rat stomach.

Ghrelin release in man depends on the macronutrient composition of the test meal. The mechanisms contributing to the differential regulation are largely unknown. To elucidate their potential role, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP), insulin, gastrin and somatostatin were examined on isolated rat stomach ghrelin secretion, which offers the advantage of avoiding systemic interactions. Basal ghrelin secretion was in a range that did not permit to consistently evaluate inhibiting effects. Therefore, the effect of gastrointestinal hormones and insulin was analyzed during vagal prestimulation. GLP-1(7-36)amide 10(-8) and 10(-7) M decreased ghrelin secretion significantly. In contrast, GIP 10(-8) and 10(-7) M augmented not only prestimulated, but also basal ghrelin secretion (p<0.05). Insulin reduced ghrelin at 10(-10), 10(-8) and 10(-6) M (p<0.05). Both gastrin 10(-8) M and somatostatin 10(-6) M also significantly inhibited ghrelin secretion. These data demonstrate that GLP-1(7-36)amide, insulin, gastrin and somatostatin are potential candidates to contribute to the postprandially observed inhibition of ghrelin secretion with insulin being the most effective inhibitor in this isolated stomach model. GIP, on the other hand, could attenuate the postprandial decrease. Because protein-rich meals do not effectively stimulate GIP release, other as yet unknown intestinal factors must be responsible for protein-induced stimulation of ghrelin release.

Animals↗
PubMed1998

Multiple neuroendocrine tumors of the pancreas in von Hippel-Lindau disease patients: histopathological and molecular genetic analysis.

Although pancreatic neuroendocrine tumors (NETs) in von Hippel-Lindau (VHL) disease have been reported, their pathological features have not been characterized. In addition, it is unknown whether alterations of the VHL gene are responsible for pancreatic NET development. To evaluate NETs in VHL patients, we performed histopathological analysis of 30 pancreatic tumors in 14 patients. In addition, DNA from NETs and normal pancreatic tissue from 6 patients with documented germ-line VHL gene mutations was studied for allelic deletions of the second copy of the VHL gene by fluorescence in situ hybridization and polymerase chain reaction-based single-strand conformational polymorphism analysis. Morphologically, the tumors were characterized by solid, trabecular, and/or glandular architecture and prominent stromal collagen bands. Sixty percent of the tumors revealed at least focally clear-cell cytology. All tumors were positive for panendocrine immunohistochemistry markers (chromogranin A and/or synaptophysin); 35% of NETs demonstrated focal positivity for pancreatic polypeptide, somatostatin, insulin, and/or glucagon; and no immunostaining for pancreatic and gastrointestinal hormones was observed in 65% of tumors. Dense core neurosecretory granules were evident by electron microscopic examination, and the clear cells additionally revealed abundant intracytoplasmic lipid. All NETs that were subjected to genetic analysis showed allelic loss of the second copy of the VHL gene. We conclude that multiple, nonfunctional pancreatic NETs occur in VHL patients. Stromal collagen bands and clear-cell morphology are important histological features of VHL-associated NETs. The presence of allelic deletions of the VHL gene in pancreatic NETs provides direct molecular evidence for a role of the gene in their tumorigenesis and establishes NET as an independent tumor type of VHL disease.

Adolescent↗
PubMed2002

(13)C-(1)H NMR relaxation and fluorescence anisotropy decay study of tyrosine dynamics in motilin.

Tyrosine ring dynamics of the gastrointestinal hormone motilin was studied using two independent physical methods: fluorescence polarization anisotropy decay and NMR relaxation. Motilin, a 22-residue peptide, was selectively (13)C labeled in the ring epsilon-carbons of the single tyrosine residue. To eliminate effects of differences in peptide concentration, the same motilin sample was used in both experiments. NMR relaxation rates of the tyrosine ring C(epsilon)-H(epsilon) vectors, measured at four magnetic field strengths (9.4, 11.7, 14.1, and 18.8 Tesla) were used to map the spectral density function. When the data were analyzed using dynamic models with the same number of components, the dynamic parameters from NMR and fluorescence are in excellent agreement. However, the estimated rotational correlation times depend on the choice of dynamic model. The correlation times estimated from the two-component model-free approach and the three-component models were significantly different (1.7 ns and 2.2 ns, respectively). Various earlier studies of protein dynamics by NMR and fluorescence were compared. The rotational correlation times estimated by NMR for samples with high protein concentration were on average 18% longer for folded monomeric proteins than the corresponding times estimated by fluorescence polarization anisotropy decay, after correction for differences in viscosity due to temperature and D(2)O/H(2)O ratio.

Animals↗
PubMed1976

Diagnosis of chronic pancreatic disease.

The diagnosis of pancreatic disease is difficult. The first step is clinical suspicion, based on the symptoms and signs. If pancreatic disease is suspected, investigation is necessary to prove this diagnosis. Investigation aims to answer two questions: a) is there pancreatic disease and b) if so, what type? The first question may be answered by demonstrating abnormal pancreatic function, using pancreatic function tests, whereas the second is answered by using techniques to demonstrate structural (anatomical) abnormalities of the pancreas. a) The methods to establish abnormal pancreatic function consist of 1. tests to demonstrate abnormal digestive capability, 2. tests to study pancreatic exocrine secretion, and 3. tests to study endocrine secretion. The tests of group 1 are: chemical fat balance study before and during enzyme replacement therapy, faecal nitrogen balance study, and the demonstration of either the malabsorption of vitamins A, D and K or the sequelae of their malabsorption (low serum calcium, high alkaline phosphatase, prolonged prothrombin time, etc.). Abnormal vitamin B12 absorption also may be present. 2. The tests designed to study pancreatic exocrine secretion are determination of the presence or absence of proteolytic enzymes in the stool, the secretion test, the pancreozymin stimulation test and the Lundh test. The serum amylase and lipase values are of little help in assessment of pancreatic function. 3. The tests to study endocrine function are the glucose tolerances test (which frequently gives abnormal results in pancreatic disease), and radioimmunoassays for insulin and gastrointestinal hormones (which may be increased in patients with functioning tumours of the islet cells). b) The techniques used to establish structural abnormalities of the pancreas are: duodenal cytology (during secretin tests), radiological techniques (abdominal survey films, barium meal, hypotonic duodenography, roentgenography of the biliary tract, barium enema, and angiography,) gastroscopy, duodensocopy, endoscopy and retrograde pancreatography, echography, scan and laparotomy. The relative value of these tests is discussed.

Amylases↗
PubMed1985

Effect of a meal on human whole blood serotonin.

Levels of whole blood serotonin and tryptophan were measured in 11 human subjects after the consumption of a meal. Blood samples were obtained at 30 and 15 min before the meal and at 15, 30, and 60 min postcibal. One-hour urine specimens were collected for 5 subjects at 0, 60, and 120 min. Whole blood serotonin and tryptophan and urinary 5-hydroxyindoleacetic acid were measured using specific high-performance liquid chromatographic methods. A precibal mean (+/- SEM) serotonin level of 136 +/- 8 ng/ml (n = 22) was observed; means at 15, 30, and 60 min after the meal were 138 +/- 20 ng/ml (n = 9), 145 +/- 18 ng/ml (n = 11), and 138 +/- 16 ng/ml (n = 11), respectively. At no time were postcibal levels of whole blood serotonin significantly higher than baseline levels (paired t-test). Urinary excretion of 5-hydroxyindoleacetic acid also was unchanged; mean hourly rates were 230 +/- 23 micrograms/h before the meal, and 196 +/- 17 micrograms/h and 190 +/- 33 micrograms/h (n = 5) during the first and second hour postcibal, respectively. The absence of a postcibal increase of serotonin in circulating whole blood indicates that serotonin is probably not a human gastrointestinal hormone in the usual sense.

Adult↗
PubMed1988

Gastrointestinal dysfunction in systemic mastocytosis. A prospective study.

In 16 consecutive patients with systemic mastocytosis, we prospectively evaluated a variety of gastrointestinal functions and examined how they relate to the occurrence of gastrointestinal symptoms. Nine patients had either a duodenal ulcer or duodenitis. Hypersecretion of gastric acid was present in 6 patients, and in these patients the mean basal acid output was 20.7 +/- 4.1 mEq/h (range 14-39 mEq/h). Impaired small intestinal absorption occurred in 5 patients, although this was usually mild. The mean fractional emptying rate of liquids for all patients (14.7% +/- 2.3% per minute) did not differ from that for controls (10.7% +/- 0.6% per minute). Mean mouth-to-cecum transit time measured by breath hydrogen testing was the same among patients (87.7 +/- 6.7 min) and controls (86.7 +/- 8.0 min). Plasma histamine concentrations were increased in all patients (mean 1886 pg/ml, range 480-7450) and correlated with the basal acid output (r = 0.64, p less than 0.02) but not maximal acid output or the presence or absence of pain or diarrhea. Mean fasting plasma concentrations of motilin, substance P, and neurotensin from 6 patients did not differ significantly from controls, whereas gastrin and vasoactive intestinal peptide were significantly less than in controls (p less than 0.01). Gastrointestinal symptoms, consisting of abdominal pain or diarrhea, occurred in 80% of patients. Abdominal pain classified as dyspeptic was usually associated with acid-peptic disease of the duodenum and hypersecretion of gastric acid, whereas abdominal pain of a nondyspeptic character was not. Only in those cases of diarrhea consisting of greater than 200 g stool/day was gastric acid hypersecretion frequently found. Neither fecal urgency nor nondyspeptic pain could be accounted for by alterations of gastrointestinal transit. These results demonstrate that gastrointestinal symptoms, peptic disease, and mild malabsorption are much more common than described previously in patients with systemic mastocytosis. Furthermore, the results provide no evidence for the contention that altered gastrointestinal transit is involved in the pathogenesis of these symptoms.

Adult↗
PubMed1996

Development of morphological changes and ileal glucagon gene expression in the small intestine of lambs infected with Trichostrongylus colubriformis.

To investigate the consequences of subclinical Trichostrongylus colubriformis infection on the intestinal mucosa and the associated changes in entero-glucagon gene expression, sheep were infected with 30000 larvae and killed 5, 10, 15 or 20 days after infection. Histological and cytological changes were examined. In the main site of infection, the upper duodenum, villous atrophy associated with crypt hyperplasia developed gradually. Cytological changes in the enterocytes appeared concurrently, characterized by a progressive reduction in brush border and in the number of ribosomes in the cytoplasm, changes in the internal structure of mitochondria, and enlargement of the intercellular spaces. Neither histological nor cytological modifications were found before day 15. At the same time, villous hypertrophy developed distally, beyond the main site of infection; this was interpreted as an adaptive response to parasitism. Enteroglucagon gene expression in the ileum was measured in parallel with the mucosal changes but did not reveal any difference between infected and control sheep. The results indicate that this gastrointestinal hormone does not have a major role in the response to nematode parasitism.

Animals↗
PubMed1992

Effect of early feeding on maturation of the preterm infant's small intestine.

To determine the response of the preterm infant's intestine to entire feedings at different postnatal ages, we recorded results of manometry of the gastroduodenum and determined fasting plasma concentrations of gastrin, gastric inhibitory peptide, neurotensin, and peptide YY three times in each of two groups: 27 preterm infants were randomly assigned to receive hypocaloric enteral nutrition on postnatal days 3 to 5 (early feeding) or on days 10 to 14 (late feeding). Initial observations (study 1) were performed by the fifth postnatal day; study 2 was performed on days 10 to 14, and study 3 on days 24 to 28. Early-fed infants received hypocaloric feedings immediately after study 1; late-fed infants did not receive enteral feedings until the completion of study 2. Although motor activity and fasting gastrointestinal peptide concentrations did not differ between groups at study 1, at study 2 early-fed infants had significantly more mature motor patterns than did babies not being fed. Early-fed infants also had significantly higher plasma concentrations of gastrin and gastric inhibitory peptide than did late-fed infants; neurotensin and peptide YY values were similar in both groups. By the time of study 3, when late-fed infants had also received enteral feedings, gut development was not different in the two groups. However, early-fed infants were able to tolerate full oral nutrition sooner, had fewer days of feeding intolerance, and had shorter hospital stays. Thus the provision of early hypocaloric nutrition was associated with earlier nutrition of preterm infants' intestinal function and resulted in improved feeding tolerance. These findings support the use of early feedings in preterm infants.

Energy Intake↗
PubMed1992

Selective 5-hydroxytryptamine type 3 receptor antagonism with ondansetron as treatment for diarrhea-predominant irritable bowel syndrome: a pilot study.

Serotoninergic innervation may contribute to the control of colonic motility and to visceral sensation from the large bowel. Indeed, ondansetron hydrochloride, a selective 5-hydroxytryptamine type 3 receptor antagonist, has been shown to slow colonic transit in healthy volunteers. Thus, we wished to determine whether 5-hydroxytryptamine type 3 receptor blockade slows colonic and small bowel transit in patients with diarrhea-predominant irritable bowel syndrome (IBS) and whether symptoms would be ameliorated with drug therapy. Of 14 patients with well-established IBS who entered a randomized, double-blind, placebo-controlled crossover pilot trial of 4 weeks of treatment with ondansetron, 16 mg three times daily, 11 completed the study. A minimal "washout period" of 4 weeks (median, 7 weeks) separated the two phases of the trial because patients were required to have similar symptoms before both periods of the study. Colonic transit tended to be longer during drug therapy than during the placebo trial, but this difference was not significant. Small intestinal transit and orocecal transit were unchanged by the drug. The integrated and peak postprandial increases in neurotensin, peptide YY, and human pancreatic polypeptide in serum were not significantly different in the drug and placebo periods. After treatment with ondansetron, stool consistency improved significantly; however, stool frequency, stool weight, abdominal pain, and the symptom criteria for IBS were not significantly altered by the drug. The results of this pilot study suggest that the motor effects expected with 5-hydroxytryptamine type 3 receptor blockade (namely, slowed colonic transit) may be diminished in some patients with IBS. The subjective improvement in stool consistency may reflect changes in the perception of defecation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗