In pancreatitis

AQP10 has only been identified in the small intestine so far and is thought to play a role in hormonal secretion. AQP11 is expressed in kidney, liver, testis and brain, but no function has been found so far. AQP12 has been identified in pancreatic acinar cells, where it is thought to facilitate the release of digestive enzymes into the pancreatic duct. 

Incretin Hormones. Figure 3 Processing of the proglucagon. The proglucagon peptide is synthesized in pancreatic cells and cells from the gastrointestinal (Gl) tract and the brain. Different proconvertases process the peptide so that in the pancreas the glucagon is produced whereas in the Gl tract and the brain, the GLP-1 and GLP-2 peptides are mainly released. 

On the other hand, EFN-a may also be involved in the activation of autoreactive T-cells as has been proposed for type I diabetes. An DFN-a inducible superantigen, encoded by the truncated envelope gene of a human endogenous retrovirus and specifically activating V 37 T-cells, has been detected in pancreatic lesions from type I diabetes patients, infiltrated by V 37 T-cells. Since IFN-a expression could be detected in pancreatic (3 cells in conceit with persistent viral infections, there is a clear link between viral infections and autoimmunity via IFN-a-stimulated superantigen expression. 

The hormone pancreatic polypeptide (PP) is a 36 amino acid peptide, which is closely related to neuropeptide Y and peptide YY PP is mainly found in pancreatic cells distinct from those storing insulin, glucagon or somatostatin. It acts on receptors that belong to the family of neuropeptide Y receptors, particularly on the Y4 subtype. 

TRPV5 and TRPV6, also known as the epithelial Ca2+ channel or ECaC (TRPV5) and Ca2+transporter 1 or Ca2+ transporter-like (TRPV6), are the only two Ca2+-selective TRP channels identified so far. They may function in vitamin D-dependent transcellular transport of Ca2+in kidney, intestine and placenta. TRPV6 is also expressed in pancreatic acinar cells, and in prostate cancer, but not in healthy prostate or in benign prostate hyperplasia. 

Self-Test 10.5B The pH of pancreatic fluids, which help to digest food once it has left the stomach, is about 8.2. What is the approximate concentration of H30+ ions in pancreatic fluids ... 

Sparmann G, Behrend S, Merkord J, Kieine HD, Grasser E, Ritter T, Liebe S, Emmrich J (2001) Cytokine mRNA ieveis and iymphocyte infiitration in pancreatic tissue during experimentai chronic pancreatitis induced by dibutyitin dichioride. Digestive Diseases and Sciences, 46 1647-1656. 

Lenzen S Hexose recognition mechanisms in pancreatic B-cells. Biochem Soc Trans 1990 18 105. 

Newgard CB, McGarry JD Metabolic coupling factors in pancreatic beta-cell signal transduction. Annu Rev Biochem 1995 64 689. 

The rate of urine amylase excretion is a sensitive reflection of the amylase released into the blood. The urine amylase remains abnormal 1-2 weeks after the serum returns to normal because the renal clearance of amylase rises 3-fold in acute pancreatitis and takes 1-2 weeks to return to normal. In pancreatitis, a number of investigators have reported a higher percentage of urinary amylase elevations, as contrasted with serum amylase elevations, particularly when the urinary amylase output over an interval is measured. Random urine collections for one, two and 24 hours are 792-4264 (2926 1074 S.D.) units per 24 hours. However, the wide range of normals make interpretation of results difficult. Of 107 patients with elevated serum or urine amylases, 16 were found to have a normal pancreas at operation (78). 

CP-channels with smaller conductance have first been noted in the rectal gland of Squalus acanthias by ourselves and in the colonic carcinoma cell line HT29 [61,73]. Later these types of 5-15 pS CP-channels were also found in pancreatic ducts, A6-cells and many other cells [74,75]. It is now claimed that this kind of channel is much more relevant than the ICOR for the pathophysiology of cystic fibrosis [12]. 

Studies of both acute and chronic pancreatitis in humans and in animals support the hypothesis that free radicals are involved in the pathogenesis of pancreatitis. There is some conflicting data from the animal work, which may in part be due to differences in the models used. It does also indicate that free radicals are not the only factors involved and su ests that activation of pancreatic enzymes are also imprortant, particularly in the development of haemorrhagic pancreatitis (Sanfey, 1991). The findings of decreased antioxidant defences and the success of treatment reported in chronic pancreatitis with a cocktail of antioxidants and with allopurinol surest further studies are required to establish the role of antioxidants in pancreatic disease and its prevention. 

Dabrowski, A., Gabryelewicz, A. and Chwiecko, M. (1991). Products of lipid peroxidation and changes in sulphydryl compounds in pancreatic tissue of rats with caerulein-induced acute pancreatitis. Biochem. Med. Metab. Biol. 46, 10-16. 

Sanfey, H. (1991). Free radicals and antioxidants in pancreatic inflammation. In Pancreatic Disease (eds. C.D. Johnson and C.W. Imrie) pp. 241-250. Springer-Verlag, London. 

Recurrent pancreatitis (usually in pancreatic-sufficient patients) may present with episodes of epigastric abdominal pain, persistent vomiting, and fever. 

Fat-soluble vitamin supplementation is usually required in pancreatic insufficiency. Specially-formulated products for CF patients (ADEKs and Vitamax ) are usually sufficient to attain normal serum vitamin levels at a dose of 1 tablet daily for younger children and 2 tablets daily for teenagers and adults. Additional supplementation may be needed in uncontrolled malabsorption or for replacement of severe vitamin deficiency.5,15 Appetite stimulants such as cyproheptadine may be an option for promoting nutrition and weight gain, but efficacy has not been established. 

Agents targeting the excessive immune response or cytokines involved in IBD are potential treatment options (Table 16-3). Azathioprine and its active metabolite 6-mercaptopurine (6-MP) are inhibitors of purine biosynthesis and reduce IBD-associated GI inflammation. They are most useful for maintaining remission of IBD or reducing the need for long-term use of corticosteroids. Use in active disease is limited by their slow onset of action, which may be as long as 3 to 12 months. Adverse effects associated with azathioprine and 6-MP include hypersensitivity reactions resulting in pancreatitis, fever, rash, hepatitis, and leukopenia.25,26... 

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