Digestive enzymes considered as pancreatic juice quizlet,greek yogurt probiotics brands available,colon cleanse pills and weight loss of,do probiotics work after expiration date quotes - For Begninners

This seminar text reviews various forms of enzyme supplementation used clinically in digestive and absorption disorders.
Pancreatic exocrine insufficiency is a major consequence of diseases leading to a loss of pancreatic parenchyma (eg, chronic pancreatitis, cystic fibrosis), obstruction of the main pancreatic duct (eg, gallstones, pancreatic and ampullary tumors), decreased pancreatic stimulation (eg, nutricional fibers of cereals and legumes, celiac disease), or acid-mediated inactivation of pancreatic enzymes (microbiota disorders, use of certain medicines, acid based nutrients such as cheese). Lipase also suffers irreversible inactivation at acidic pH, which is frequently present within the duodenum and jejunum in patients with pancreatic exocrine insufficiency due to low pancreatic bicarbonatesecretion [zinc deficiency syndrome]. Gastric lipase activity therefore is capable of compensating for pancreatic lipase deficiency in patients with pancreatic exocrine insufficiency, thus explaining at least in part the absence of steatorrhea in patients with more that 10% of normal pancreatic lipase secretion. The physiological role of these substances is to attack s-adenosylmethionine (SAMe) converting it in spermidine (Kakhi 2007).
The enzymes and the bicarbonate are excreted in the pancreatic ducts, which join the bile duct, reaching the duodenal lumen through the sphincter of Oddi (figure 4, below).
Situations with sphincter spasm has been related with the development of endocrine pancreas insufficiency and pancreatitis (Barreto 2010). Problems can occur when there is a dysfunc¬tion in the ability of the pancreas to produce enzymes or the body’s demand for enzymes exceeds the supply.
Figure 5 shows the chronological production and activation of enzymes and other compounds involved in the digestion of normal food. The activated pancreas enzymes are gradually degraded by deconjugated bilirubin which develops through the deconjugating capacity of another enzyme called beta-glucuronidase (?-GCD); an enzyme normally released by the gut mucosa and certain bacteria belonging to the normal microbiota of the human gut.
Figure 6 shows that trypsin and chymotrypsin are significantly inhibited by free bilirubin, but not conjugated bilirubin or biliverdin (not showed). The amount of digestive proteases secreted by the pancreas largely depends on the amount of protein in the diet.
This happens in animals (including homo sapiens) which ingest a high amount of proteins and animal fat (carnivores).
A meta-anaylisis about the use of probiotics with a high concentration of bifidus bacteria and lactobacillus showed a positive effect for probiotics in people suffering from IBS, UC and MC (Sang 2010).
Carbon anhydrase, expressed in duct cells of the pancreas and responsible for the production of bicarbonate, is dependent on nutritional zinc intake and absorbtion (Lukaski 2005).
Zinc deficiency rate differ from 6 – 73% in selected countries and is often neglected as mayor cause of pathologies and disorders such as growth retardation, male hypogonadism, neuro-sensory changes (abnormal dark adaptation and changes in taste acuity), delayed wound healing, abnormal immune functions, and impaired cognitive functions, all of them reversible with zinc supplementation (Prasad 1998).
Recently, enteropeptidase has been reported to be activated from an inactive precursor (proenteropeptidase) by duodenase, a newly discovered serine protease expressed in the duodenum (Holzinger 2002). Exocrine pancreas insufficiency (EPI) is a syndrome characterized by a lack of active pancreatic enzymes in the duodenal lumen.
Alcohol misuse, tobaco, micronutrient deficiency, high carbohydrate diet, high calorie diet, mayor intake of legumes and cereals, exercise deficit and exercise abundance are factors related with EPI in animal and in human studies (Braganza 2010, Barreto 2010, Taylor 2010, Dominguez-Munoz 2007). EPI is normally characterized by steatorrhea (fatty steaky stool), flatulence, bad breath and inflammation of the upper part of the abdomen (Roxas 2008). EPI can develop in acute and chronic pancreatitis when secretion of the pancreatic juice is impeded by gallstones in the pancreatic duct or by spasm of the sphincter of Oddi (see page 5). The secretion starts almost immediately after the meal with three overlapping phases: cephalic, gastric, and intestinal phases, contributing, respectively, to about 20%, 10%, and 70% of the total postprandial response to a meal. This cephalic phase can be induced by sham feeding in dogs or modified sham feeding in humans, as well as by insulin hypoglycemia or 2-deoxy-D glucose glucocytopenia, which stimulates the bulbar vagal centers with subsequent cholinergic excitation of exocrine pancreas, and GRPergic release of gastrin, which contributes to the activation of pancreatic acinar cells.
There is little doubt that CCK plays a crucial role in the overall stimulation of pancreatic secretion as documented by the rise in plasma CCK level and the inhibitory effect of blockade of CCK1 receptors on this secretion, but its major pathways of action appear not to be endocrine, as was proposed in the past, but neural, involving the sensory receptors at afferent nerves and long vagovagal reflexes or short enteropancreatic reflexes, as depicted in figure 10, (Konturek 2003) CCK appears to affect, through the same neural pathway, not only pancreatic secretion, but also bile secretion and gall bladder contraction as well as gastric emptying and pancreatic regeneration (growth). Figure 10 The overall regulation of exocrine pancreatic function through three different pathways; local duodenal liberation of CCK and secretin, stimulation via gastric juice and three, through vagal activity and acetylcholin release in the exocrine pancreas (Konturek 2003). The exocrine pancreas, controlled by these three pathways, influences and is influenced by the endocrine pancreas which produces insulin, glucagon and somatostatine. The development of diabetes greatly influences the prognosis and quality of life of patients with exocrine pancreatic diseases. Table 2 shows the overall influence from different states of insulin on exocrine pancreatic function.
Exocrine pancreas function is influenced by insulin through two pathways; the insulino-acinar pathway (Konturek 2003) and the pathway involving the central nervous system (Pruimboom 2005). These neurons are connected with and activate the nucleus tractus solitaris, which in turn activates the motorneurons of the nervus vagus. Acute and chronic pancreatitis belong to the diseases with the highest morbidity (Saluja 2007).
Exocrine Pancreas Insufficiency is a frequent disorder which can exists as primary disease and a secondary pathology of disorders like cystic fibrosis and NAFLD. People suffering from primary EPI show symptoms such as steatorrhea, abdominal cramps, taste deficiency, abdominal swelling, nutrient intolerance and general malaise. The exocrine pancreas, producing pancreatic enzymes and carbon anhydrase, plays a central role in maintaining human health by digesting food and making nutrients available for the body. Bhardwaj, Payal, Pramod Kumar Garg, Subir Kumar Maulik, Anoop Saraya, Rakesh Kumar Tandon, and Subrat Kumar Acharya.
Cavalot F, Katia Bonomo, Elisa Fiora, Elisa Bacillo, Paola Salacone, Massimo Chirio, Ezio Gaiamariella Trovati.
Dominguez-Munoz JE, Iglesias-Garcia J, Vilarino-Insua M, Iglesias-Rey M: 13C-mixed triglyceride breath test to assess oral enzyme substitution therapy in patients with chronic pancreatitis.
Esposito E, Iacono A, Bianco G, Autore G, Cuzzocrea S, Vajro Probiotics reduce the inflammatory response induced by a high-fat diet in the liver of young rats.
Masamune Atsushi,* Takashi Watanabe,* Kazuhiro Kikuta, Kennichi Satoh, and Tooru Shimosegawa.
Sang LX, Bing Chang, Wen-Liang Zhang, Xiao-Mei Wu, Xiao-Hang Li, Min Jiang Remission induction and maintenance effect of probiotics on ulcerative colitis: A meta-analysis. Solga SF, Buckley G, Clark JM, Horska A, Diehl AM.The effect of a probiotic on hepatic steatosis.
Stewart-Knox BJ *, EEA Simpson, H Parr, G Rae, A Polito, F Intorre, N Meunier, M Andriollo-Sanchez, JM O’Connor, C Coudray and JJ Strain. Also, in rare cases hemorrhagic discoloration of the flanks (Grey Turner sign) or of the umbilicus (Cullen sign) may occur.  Pancreatic pseudocyst, diabetes mellitus or pancreatic cancer can occur as a complication.
Blood investigations: After the physical examination and asking medical history, the doctor will order a blood test. Computerized axial tomography (CAT): The doctor may order an abdominal ultrasound to look for gallstones or look for inflammation or destruction of the pancreas. B) Chronic Pancreatitis: Here the focus is to check whether the pancreas is still making enough digestive enzymes.
A secretin simulation test is considered the most functional test to check if bi-carbonate production is impaired, which would indicate chronic Pancreatitis. In up to 70 percent of adult patients, chronic Pancreatitis appears to be caused by alcoholism.
Pancreatitis is usually categorized by the cause as the symptoms and the treatment would differ accordingly.  The Balthazar scoring and necrosis scoring methods can help distinguish each case to identify severity of Pancreatitis. This type of Pancreatitis pertains to sudden inflammation of the pancreas.  It can be further categorized into mild and severe. 1) Mild-acute Pancreatitis: Mild cases can be successfully treated in the common ward by conservative measures like NPO (abstaining from any oral intake) and IV fluid re-hydration. Acute Pancreatitis occurs suddenly and lasts for a short period of time and can be cured easily.  In chronic Pancreatitis there is slow destruction of the pancreas. Posteriorly, the pancreas leans on the superior mesenteric vein, which collects all the venous blood from the bowel directed to the liver, that anatomically merges into the portal vein along with the splenic vein. Because of its particular anatomical position most of the pancreatic diseases become symptomatic when involve the surrounding organs. Considering the fact that traditional radiological imaging is able to diagnose only few diseases in an early stage, the pancreas is still considered difficult to investigate. In addition to the enzyme secretion the pancreas produces also the bicarbonates in order to decrease the gastric acidity and allow digestive pancreatic enzymes to work (because they are not active in an acid environment).
Due to the endocrine activity insulin decreases the sugar blood level of the blood and extra cellular space.
The ductal system is made up of the main pancreatic duct (Wirsung duct) and of an accessory duct (Santorini duct). The main duct goes through the whole pancreas from tail to head and opens onto the duodenal ampulla (Vater ampulla) along with the common bile duct. The Santorini duct originates from the main pancreatic duct in the neck, goes superficially through the head and opens onto the minor ampulla. The bile comes from the liver and carries the biliary secretion (useful, along with the lipase, for fat metabolism) into the duodenum.
It crosses the pancreatic head in the lower part up to join the main pancreatic duct at the Vater ampulla.
The celiac plexus is a very important structure lying underneath the pancreatic body-neck and serves as a crossroad for upper abdominal pain pathway. Cytoplasm is a sticky, semi-fluid material found between the nucleus and the cell membrane. The centrioles are two cylindrical organelles found near the nucleus in a tiny round body called the centrosome.
Endoplasmic reticulum provides passages through which transport of substances occurs in the cytoplasm. Mitochondria are rod-shaped organelles that can be considered the power generators of the cell, converting oxygen and nutrients into adenosine triphosphate (ATP). The main overall function of the Golgi apparatus is to take the proteins that are manufactured in the endoplasmic reticulum, process them according to specific needs and then send them on to their destinations.
Cytoskeleton is the internal framework of the cell which consist of microtubules, intermediate filaments, and microfilaments.
During meiosis the females egg cell is fertilized by the males sperm combining to form a zygote. Diffusion is a physical process whereby molecules of gases, liquids, or solid particles spread or scatter themselves evenly through a medium.
Osmosis is the diffusion of water or any other solvent molecule through a selective permeable membrane (e.g. Filtration is the movement of solutes and water across a semi-permeable membrane from an area of higher pressure to an area of lower pressure. Active transport is a process whereby molecules move across the cell membrane form an area of lower concentration, against a concentration gradient, to an area of higher concentration.
Enzyme supplementation plays an integral role in the management of various digestive disorders, particularly with regard to exocrine pancreatic insufficiency.
In addition, gastrointestinal and pancreatic surgical resection (eg, gastrectomy or duodenopancreatectomy) leading to post-cibal asynchrony, decreased pancreatic stimulation (cereal lectin, soy lectin), and loss of pancreatic parenchyma is a frequent cause of pancreatic exocrine insufficiency. In patients with pancreatic exocrine insufficiency, the reduced luminal action of pancreatic amylase and proteases is compensated for by salivary amylase, intestinal glycosidase, colonic flora, gastric pepsin, and intestinal peptidases.
Despite the proposition by some authors that impairment of lipase secretion occurs earlier than for other enzymes in the context of chronic pancreatitis, which could be an additional factor for fat maldigestion as the major clinical consequence of pancreatic exocrine insufficiency, other authors could not confirm these data; thus, this factor is probably of minor clinical relevance.
SAMe is the universal donor of methyl-groups used by methyltransferases in methylation processes. The acinar cells produce pancreatic enzymes, whereas the islet cells are responsible for the production of insulin (beta cells of Langerhans), glucagon (alpha cells of Langerhans) and somatostatin (delta cells of Langerhans). Cholecystokinin produced by duodenal gut lining cells produces relaxation of the sphincter, facilitating the entrance of bile and pancreatic juice in the duodenal lumen.
The endocrine portion consists of the islets of Langerhans, which are responsible for the secretion of insulin, glucagon, and somatostatin. At the time food reaches the duodenum it will be wrapped in gastric juice and gastric acid.
Free deconjugated bilirubin (in contrast with the conjugated form) can be considered as the mayor protective compound of gut lining against the possible damaging effect of active proteases and lipases in parts of the gut where they not should be active (Qin 2002). The nature of this inhibition and its physiological relevance were further explored for trypsin.
As bilirubin is secreted from the bile to the lumen mainly in the conjugated form, the digestion of dietary proteins in the upper small intestine would proceed smoothly. This would provide an explanation for the observation that bilirubin-predominant species tend to be carnivores or omnivores, while biliverdin-predominant species tend to be herbivores. Heme oxigenase is produced by the so called vitagenes which are under control of indirect anti-oxidants such as curcumin (in turmeric root), resveratrol (in grapes, chocolat) and alliicin (in garlic).

The mayor role of bicarbonate in the duodenum is to optimize pH, making pancreatic enzymes capable of executing their digestive role (figure 8 and table 1).
The basic environment of the duodenum is necessary for optimal function of pancreatic enzymes (see table 1). This test, developed in rodents, shows a decreased oral salt sensibility when zin is deficient. A mild deficiency of zinc in pregnant women is associated with increased maternal morbidity, abnormal taste sensation, prolonged gestation, inefficient labor, atonic bleeding, and increased risks to the fetus. It is a mayor consequence of primary pancreatic diseases such as chronic pancreatitis, cystic fibrosis, acute pancreatitis, pancreatic cancer and secundary pancreas disorders including celiac disease, morbus Crohn, lactose malabsorbtion and gastrointestinal – pancreatic surgical resection (Dominguez-Munoz 2007).
The mentioned factors include the mayor intake of legumes (such as soy) and cereals as possible causal factors of EPI. The postprandial phases, especially the cephalic phase, have been attributed mainly to vagal stimulation, with the efferent cholinergic nerves releasing acetylcholine in the pancreas and GRP-releasing neurons releasing gastrin from antral G-cells. Blocking vagal activity reduces the bicarbonate production by over 50%, which means that not only acinar cells are under vagal control, but duct cells as well. In consequence of the close anatomical and functional links between the exocrine and endocrine pancreas, any disease affecting one of these parts will inevitably affect the other. It may cause life threatening complications, such as hypoglycemia, due to the lack of glucagon and the impaired absorption of nutrients, or the micro- and macrovascular complications may impair the organ functions. If the diet proves inadequate to reach the glycemic goals, insulin treatment with multiple injections is required. Hyperinsulinemia (part of the metabolic syndrome) and hyperglicemia inhibit the release of secretin and CCK which can lead to severe lack of activated pancreatic enzymes, maldigestion and malabsorbtion (Pap 2004). Therapy of EPI should therefore not only regulate exocrine function but also the endocrine function of the pancreas (Lam 1999, Lam 1999?, Lam 1997, Berry 1996).
Paradigmatic thinking has ruled medical thinking about interactions between the endocrine pancreas, the liver and the exocrine pancreas for decades. Efferents from these motorneurons innervate the liver and the pancreas, where they respectivily inhibit neoglucogenesis (for the resting 80%) and induce secretion of pancreatic juice of the exocrine part (figure 12). Although there still exist a huge gap in our understanding of pancreatitis, some mechanisms are considered current opinion.
Therapy for pancreatic exocrine insufficiency is based on oral administration of exogenous pancreatic enzymes. Treatment should be based on oral pancreatic enzymes, probiotics and fat soluble vitamins such as vitamin D, vitamin A and vitamin E (Cavelot 2006).
Lipase is the most unstable pancreatic enzyme during gastrointestinal transit most probably due to the high sensitivity of pancreatic lipase to proteolysis and acidic pH.
Disorders of the exocrine pancreas are frequent and can be primary (caused by alcohol abuse, high calorie diet) or secondary to other pathologies (cystic fibrosis, celiac disease).
Insulin inhibits secretin stimulated pancreatic bicarbonate output by a dosedependent neurally mediated mechanism.
Safety and Tolerability of a New Formulation of Pancrelipase Delayed-Release Capsules (CREON(R)) in Children Under Seven Years of Age with Exocrine Pancreatic Insufficiency due to Cystic Fibrosis: An Open-Label, Multicentre, Single-Treatment-Arm Study.
Effect of acute hyperglycemia on basal, secretin and secretin + cholecystokinin stimulated exocrine pancreatic secretion in humans. Effect of acute hyperglycaemia on basal and fat-induced exocrine pancreatic secretion in humans. Effect ofinsulin and glucose on basal and cholecystokininstimulated exocrine pancreatic secretion in humans. Low dietary zinc decreases erythrocyte carbonic anhydrase activities and impairs cardiorespiratory function in men during exercise. Review article: omega-3 fatty acids - a promising novel therapy for non-alcoholic fatty liver disease •Aliment Pharmacol Ther. Inactivation of Digestive Proteases: Another Mechanism That Probiotics May Have Conferred a Protection.
Impaired inactivation of digestive proteases by deconjugated bilirubin: The possible mechanism for inflammatory bowel disease.
I had no idea that zinc was so important, and that a deficiency in it could cause so many issues! This form is more common in men than in women and often develops between the ages of 30 and 40. It has two vital functions: control the activities of the cell and facilitate cell division. During mitosis, or cell division, the two centrioles separate from each other by a thin spindle fiber appartatus. ATP is the chemical energy "currency" of the cell that powers the cell's metabolic activities.
The filaments provide support for the cells; the microtubules are thought to aid in movement of substances through the cytoplasm. The process of meiosis involves reproduction The process of mitosis involves growth or maintenance of cells in the human body. The physical processes that control the passage of materials through the cell membrane are diffusion, osmosis, filtration, active transport, phagocytosis, and pinocytosis.
Generally, molecules move from an area where they are greatly concentrated to an area where they are less concentrated. If the pattern is interrupted by an abnormal and uncontrolled growth of cells, the result is a tumor. However, application of enzymes may also be beneficial for other conditions associated with poor digestion including lactose intolerante and coeliac disease.
The main clinical consequence of pancreatic exocrine insufficiency is fat maldigestion and steatorrhea (Dominguez-Munoz 2007).
However, it has been generally accepted that digestive action of pancreatic lipase is hardly compensated by extrapancreatic mechanisms.
Together with abdominal cramps and the typical characteristics of fatty stools associated with steatorrhea (loose, greasy, foul-smelling voluminous stools that are difficult to flush), which are not always evident because patients tend to limit fat ingestion, fat maldigestion causes important clinical problems. An excess of the protein based putrifactors could produce a lack of SAMe and therefore deficient methylation of certain monoamines such as serotonin with decreased production of essential melatonin in the gut.
Pan¬creatic exocrine tissues (the acini) produce digestive enzymes that are mixed with sodium bicarbonate from the ductules connecting the acini to the pancreatic duct. A deficiency of pancreatic enzymes could potentially contribute to the development of numerous illnesses and degenerative conditions (Roxas 2008). The acid will lower duodenal pH which induces the production of secretine releasing peptide (SLP) by glandular pancreas cells. Beta-glucuronidase is produced in high amounts in the healthy large intestine by Escherichia coli and Streptococcus pyogenesis, which can only do so in a relative acid environment (pH 4 – 5); An environment based on the production of lactic acid by bifidobacteria (Qin 2007).
Important is the fact that the inhibition is non-competitive, suggesting that free bilirubin can inactivate the enzyme.
Deconjugation of bilirubin by beta-glucuronidase from the mucosal cells would form a protective layer on the surface of the gut. Large amounts of bilirubin exist in the bile of cats, dogs, opossums, armadillos, alligators, African clawed toads, bullfrogs, mudpuppies, sharks (spiny dogfish), small skates, trout, goosefish, perch and humans, while biliverdin is the main bile pigment of rabbits, nutrias (rodents that eat water plants), sloths (leaf eaters), birds and tilapia (fish that eat algae).
These substances are recognized for their protecting effect of the digestive system probably through upregulation of the production of (free) bilirubin (Calabrese 2006). Schepovalnikow in 1899, as a factor that is contained in the duodenum and that is capable of activating pancreatic juice to digest fibrin. Exocrine pancreas insufficiency syndrome (EPI) can be caused by a variety of etiological factors.
Studies published already in the nineties and eighties of last century showed that cereal fibers and so called protease-inhibitors in legumes are able to inhibit the production and activation of pancreatic enzymes (Hendrick 1991, Jacobs 1983, Dunaif 1981). HCHD seems to diminish the volume of the gall-bladder, augment cholesterol-gallstone formation and increases the cristal mass (Mathur 2007). During the intestinal phase, the major role has been attributed to CCK and secretin, released from endocrine I and S-cells by protein and fat digestion products and by gastric acid entering the duodenum, respectively, but the relative contribution of these hormones and their potentiating interaction on postprandial pancreatic secretion has not been fully elucidated.
Pancreatic conditions which might cause diabetes mellitus include acute and chronic pancreatitis, pancreatic surgery, cystic fibrosis and pancreatic cancer.
Diabetes mellitus is an independent risk factor of mortality in those with exocrine pancreatic diseases. Impairments of the exocrine pancreatic function and morphology in diabetic patients are frequent and well known.
People with acute or chronic pancreatitis express a higher activity of amylase enzymes, leading to a faster digestion of polysaccharides and a secular increase in blood glucose. Insulin resistance and fatty liver (NAFLD and AFLD) disease can disturb the function of this so called pancreas-liver-brain axis (Lustig 2006). Risk factors such as smoking, alcohol abuse, high calorie diet, but also several chemicals (e.g. In addition, dietary modifications have classically played an important role that should probably be reconsidered.
Omega 3 fatty acids are needed for recovering of pancreas lipase transport and need to be supplemented. Due to proteolytic degradation, most amylase activity and more than 20% of trypsin activity but only 1% of lipase activity produced by the pancreas and secreted into the duodenum after a pure carbohydrate meal, are still present within the terminal ileum. Various Dietary Fibers Have Different Effects on Lipase-Catalyzed Hydrolysis of Tributyrin in Vitro. Oysters are great too, as long as they are sustainably sourced, but not many people enjoy them. All living things whether plant or animal, unicellular or multicellular, large or small are composed of cells. The cell membrane separates the cell from its external environment and from the neighboring cells.
The spindle fibers attach themselves to individual chromosomes to help in the equal distribution of these chromosomes to two daughter cells.
These organelles are abundant in the cells of gastric glands, salivary glands, and pancreatic glands.
Blood-forming cells in the bone marrow, cells of the skin, and cells of the intestinal tract reproduce continuously.
The molecules will eventually distribute themselves evenly, they are then said to be in a state of equilibrium.
A selective permeable membrane is any membrane through which some solutes can diffuse, but others cannot. Historically, porcine and bovine pancreatic enzymes have been the preferred form of supplementation for exocrine pancreatic insufficiency. Steatorrhea does not develop until pancreatic lipase output is below 10% of normal, which has been classically interpretedas the consequence of a very large reserve capacity of the exocrine pancreas for enzyme secretion. Fat maldigestion can cause deficiency of vitamin D, vitamin A and vitamin E (Dominguez-Munoz 2007?).
Melatonin has been proven to regulate the production of insulin and pancreatic enzymes, as does its precursor triptophane (Jaworek 2007). This pancreatic “juice” flows through the pancreatic duct, connecting with the hepatic duct, and ultimately empty¬ing into the duodenum via the sphincter of Oddi.
SLP will consequently stimulate S cells in the so called crypts of Lieberkuhn in the duodenum, responsible for the production of secretin. The effect of free bilirubin on protein digestion by trypsin was further investigated using chymotrypsinogen as the substrate.
A more dramatic deconjugation of bilirubin by the high amounts of beta-glucuronidase from gut bacteria would further cause a prompt and effective inactivation of these digestive proteases in the lower intestine. Heme oxygenase catalyzes heme(from hemoglobin, cytochrom enzymes, cyclo-oxygenase) in biliverdin, which is further metabolized in bilirubin by biliverdin reductase. Evidence in vitro and vivo shows that deficiency of beta-glucuronidase and the subsequent lack of free bilirubin can be responsible for the development of irritable bowel syndrom (IBS), colitis ulcerosa (CU) and morbus Crohn (MC, Qin 2007). Zinc supplementation can recover salt-sensibility through upregulation of carbon anhydrase production (Prasad 1998).
Enteropeptidase acts as a sequence-specific protease activating trypsinogen by cleaving off an inhibitory portion. The most investigated factors are genetical ones, relating recurrent EPI with cystic fibrosis and the Schwachman-Diamond syndrome.

The cientific excellent cereal paper of Cordain (Cordain 1999) adds to the fiber influence of legumes and cereals, the effects of lectins, saponins and protease-inhibitors (such as Bowman-Birk factors in legumes and Kunnitz factors in potato) on the exocrine pancreas. This is the reason for the fact that people suffering from EPI almost always have steatorrhea. The combined production of secretin and CCK activates the pancreas and opens the sphincter of Oddi through three pathways (Konturek 2003). The treatment of pancreatic diabetes, a distinct metabolic and clinical form of diabetes, requires special knowledge.
Atrophy of the exocrine tissue may be caused by the lack of trophic insulin, whereas pancreatic fibrosis can result from activation of stellate cells by hyperglycemia, or from microangiopathy and neuropathy. The resulting chronic hyperglicemia seems to exhaust beta cells of the pancreas with a subsequent loss of insulin signalling. Postprandial pancreatic insulin is secreted in the portal vein and arrives for the fully 100% in the liver where neoglucogenesis is inhibited for just 20%. Deficiency of central insulin signalling decreases activity of the vagus motorneurons; liver neoglucogenesis will be desinhibited, pancreatic output of enzymes decreased and EPI will be a logical consequence. Indications for therapy, the role of dietary modifications, the basis and critical aspects of enzyme substitution therapy, factors inhibiting normalization of fat digestion despite correct enzyme substitution therapy, ways to improve the efficacy of enzyme therapy, and future developments are discussed in the last part of this seminar text.
Lipase also suffers irreversible inactivationat acidic pH, which is frequently present within the duodenum and jejunum in patients with pancreatic exocrine insufficiency due to low pancreatic bicarbonate secretion. It also regulates the passage or transport of certain molecules into and out of the cell, while preventing the passage of others.
It serves as the brain for the control of the cells metabolic activities and cell division. Lysosomes are also known as suicide bags because if the lysosome ruptures, it will start to digest the cells proteins, causing it to die. When the cell dies the lysosmes work swiftly with their chemicals and digest the dead cell. Use of microbe-derived lipase has shown promise with studies indicating benefit similar to pancreatic enzymes, but at a lower dosage concentration and with a broader pH range. Due to proteolytic degradation, most amylase activity and more than 20% of trypsin activity but only 1% of lipase activity produced by the pancreas and secreted into the duodenum after a pure carbohydrate meal, are still present within terminal ileum. In contrast, more recent studies have demonstrated a rather linear correlation between inhibition of duodenal lipolysis and fatexcretion levels.
Maldigestion of protein and carbohydrates is able to induce the production of methylmercaptane, putrescine and cadaverine which are responsible for the bad odor of stool, breath and sometimes vagina in people suffering from exocrine pancreas insufficiency (Lewis 1998). Triptophan and melatonin are able to increase the production of pancreas enzymes in exocrine pancreas deficiency syndrome and protect the pancreas against chronic stimulation (figures 1 and 2).
Free radicals play an essential role in the development of exocrine pancreas insufficiency and pancreatitis, mainly by upregulation of the enzym complex NADPH oxidase (Masumane 2008). The digestive enzymes in the pancreatic juice break down carbohydrates, proteins, and fats (Table 1). At the same time cholecystokinin (CCK) is liberated by I-cells in the duodenal lining as a response of entering proteins and fat-rich chyme in the duodenum.
Here we can see the wonderful design of nature that turns a waste byproduct into a precious treasure.
Trypsin, in turn, releases chymotrypsin, carboxypeptidases, elastases, and also lipases from their inactive pancreatic precursors.
The EPI syndrome in these disorders are very frequent and results of different human trials concerning the efficacy of use of pancreatic enzyme formulas make this intervention evidence based (Graff 2010).
Diet and pancreatic enzyme replacement therapy, together with substances which improve insulin sensitivity may be sufficient in the early stages.
The regulation of the exocrine pancreatic function is also damaged because of the impaired effect of islet hormones. Insulin is necessary for pancreas regeneration after an pancreatic insult leading to pancreatitis, which means that a lack of insulin could impede pancreas recovery, produce multiple organ disorder, multiple organ failure and in the end death (Pap 2004).
The final conclusion is that chronic insulin resistance can be considered exocrine pancreas toxic through direct effects (insulino-acinar connection) and through long vagal reflex deficiencies. The consequence is that pancreatic enzymes are not excreted in the duodenum lumen and stay in the pancreatic duct or in the acinar cells. This can lead to multiple organ disorder, involving organs such as the liver and the kidneys. Disorders of insulin signalling can cause (severe) malfunction of the exocrine pancreas, multiple organ failure and death.
High dietary carbohydrates decrease gallbladder volume and enhance cholesterol crystal formation.
Oxygen diffuses from the bloodstream (greater concentration) to the cell (lesser concentation). Safety and efficacy of enzymes derived from microbial species in the treatment of conditions such as malabsorption and lactose intolerance is promising. This finding is also supported by the fact that human pancreatic lipase-specific activity on meal triglycerides is three orders of magnitude lower than the very high specific activity usually measured under experimental conditions in aspirated duodenal juice. The use of exogenous triptophan in patients suffering from exocrine pancreas insufficiency syndrome has been proven effective in vitro and in vivo (Jawrok 2007, Leja-Szpac 2004), while human trials still lacking. NADPH oxidase activity converts oxigen in the superoxid radical which possibly damages the cell membrane of the pancreas cells and the lysosomes in which inactive pancreas enzymes are embedded; Acute pancreatitis could therefore develop. Sodium bi¬carbonate neutralizes the acidic chyme that will make its way from the stomach to mix with the juice in the duodenum and start the enzyme-activating process.
Secretin induces bicarbonate (HCO3) production by duct cells which neutralizes the gastric acid and optimizes the duodenal pH (8) for consequent enzyme activation. Intestinal activation of pancreatic precursors is the physiologic mechanism preventing the damage that proteases would cause if they were active within the pancreatic-duct system.
In the event of a proven impairment of the pancreatic exocrine function in diabetes mellitus, pancreatic enzyme replacement therapy is indicated.
Figure 11 shows the possible interaction between diabetes and pancreatitis; a situation which can be considered a devils vicious circle. Activation by a lysosomal enzyme called cathepsin beta can actually activate trypsin in the pancreas itself, producing activation of proteases, lipases and amylases in acinar cells, through which these cells will be damaged. Exocrine pancreas insufficiency is often not recognized while the incidence of people suffering from this disorder increases continously.
Alcohol Use and Cigarette Smoking as Risk Factors for Post–Endoscopic Retrograde Cholangiopancreatography Pancreatitis. Plant-based enzymes, such as bromelain from pineapple, serve as effective digestive aids in the breakdown of proteins. Finally, human gastric lipase output is increased three- to fourfold in patients with pancreatic exocrine insufficiency, which can be responsible for a relevant proportion of dietary triglyceride digestion in these patients. CCK receptors on acinar cells sense CCK and secrete chymotrypsin in the pancreatic duct which is then transported to the duodenal lumen. Consequently, protein digestion is expected to be largely dependent on enteropeptidase activity. This may improve the nutritional condition of the patient and decrease the metabolic instability (Czako 2009). The damaged cells attract neighbouring immune cells which infiltrate the pancreas and produce pro-inflammatory cytokines (IL1beta, TNF, IL6). Many people suffer from helicobacter pylori and pH disorders, which means that oral enzyme therapy efficacy could be less than expacted. EPI is characterized by steatorrhea, abdominal swelling and cramps, bad breath and flatulence. Synergistic effects have been observed using a combination of animal-based enzymes and microbe-derived enzymes or bromelain. Enteropeptidase is exclusively expressed in the brush border of the proximal small intestine. The pancreas will now suffer a inflammation which can lead to multiple organ disorder, multiple organ failure and death (figure 13, Saluja 2007).
If so, dosis should be raised and anti-acids (such as magnesium) should be added to the treatment. Lipase deficiency, the most vulnerable enzyme of the total pancreatic juice, is responsible for the mayority of symptoms.
Mutations in the Proenteropeptidase Gene Are the Molecular Cause of Congenital Enteropeptidase Deficiency.
Until you are sure of your specific zinc needs, be sure to consume zinc-rich foods through a nutrient-dense diet (refer to the list above). Pancreatic enzyme activity depends on different pathways including local duodenal mechanism and central parasympathetic (acetylcholinergic) signalling.
The active trypsin is capable of hydrolizing peptides and thus produce amino acids which can be absorbed.
Pancreatic enzyme therapy seems to be the only valuable intervention together with withdrawal of alcohol, low carbohydrate diet, rest, direct and indirect antioxidants (Lieb 2009, Bhardwaj 2009). Oral pancreatic enzyme therapy can be very effective and relieve a great variety of disorders. Lipase deficiency further causes malabsorbtion of fat soluble vitamines (vitamin A, D, E) and omega 3 fatty acids.
You may find if you have picky eaters that they are low in zinc (they may have elevated copper). Trypsin further activates other digestive enzymes such as pre-amylases and pre-lipases which become carbohydrate and fat digesting enzymes. RDA is likely too low of a recommendation for optimal health in light of soil depletion and excess stored copper ( a very common problem today).
Cholecystokinin is considered an anorexigenic compound and is produced by duodenal gut lining cells. Proteins, carbohydrates and fat are converted in respectively amino acids, monosaccharides and fatty acids by this pathway making food available for the human body (figure 5). The skin also has a high concentration of zinc and can be a sensitive indicator of an individual’s zinc status, since the body will often draw the mineral from peripheral tissues when needed elsewhere by the body. Once pancreatic enzymes are activated, they degrdadate fats, proteins and carbohydrates in absorbable microsubstances.
Non-responding patients should be tested on bacterial overgrowth and possibly a carcinogenic proces.
Gallstones can block the sphincter of Oddi through which pancreatic juice and bile should be excreted in the duodenal lumen. Zinc is found in the adrenal glands, bone, brain, heart, kidneys, liver, muscles, prostate gland, spleen, and testes. Insufficiency of the exocrine pancreas could therefore produce malabsorbtion syndrome, nutritional deficiency (vitamin A, vitamin D and vitamin E), steatorrhea and multiple organ disorder. Obstruction can lead to acute and chronic pancreatitis and is considered one of the most frequent detah causes in developing and developed countries.
Melatonin precursor, l-tryptophan protects the pancreas from development of acute pancreatitis through the central site of action. Testing is key, and a hair tissue mineral analysis is a great test to get started with, and then if needed, a comprehensive copper panel so you can see your ceruloplasmin levels and the current balance of copper to zinc. Free bilirubin is formed through activation of mucosal and bacterial produced beta-glucuronidase.
A lack of this enzyme can cause IBS, CU and MC; one of the mayor causes of beta-glucuronidase deficiency is the intake of saccharin (Qin 2002). Zinc is critical for the thyroid, as it is needed for thyroid stimulating hormone to work.  Zinc deficiency will impair your ability to convert T4 to T3 in the liver and kidneys.
Also, zinc can be lost in the sweat, if you have a job or lifestyle where you sweat profusely you likely are losing a lot of zinc that needs to be replaced. Conditions associated with relative zinc deficiency: AIDS, Autism, Candida, Depression, Eclampsia, Fungus, Gastric Ulcers, PMS, PPD, Pregnancy, Viruses, Immune Deficiency.

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