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impossible
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Might give you some ideas. I dont buy their stance that they probably dont have an effect on shutting down production, obviously From enzymestuff.com:

What triggers the pancreas to push enzymes into the duodenum?

A number of factors are involved in pancreatic secretion, and is thought to be divided into 3 phases: cephalic (brain), gastric (stomach), and intestinal. The cephalic phase contributes appx. 25% to the pancreatic response, and is controlled by the vagus nerve. The stimulants are sight, smell, taste and eating of food. The gastric phase contributes 10% to the response, and is also via vagal innervation, mainly through stomach distention as it fills with food. The remainder, some 50 – 75% is due to the intestinal phase, mediated by GI hormones (such as secretin and cholecytokinin, aka CCK), and stimulated by amino acids, fatty acids, calcium, and stomach acid. In addition, the pancreas produces a specific peptide known as pancreatic polypeptide (PP), which acts to negatively feedback on pancreatic secretion; that is, it inhibits enzyme secretion. PP is released in response to vagal nerve stimulation.

What is the sequence of biochemical events that regulate pancreatic enzyme secretion?

The pancreas actually is always secreting pancreatic fluid into the duodenum, even between meals. This amount is about 0.2 – 0.3 ml per minute and increases greater than 3 mls per minute in response to a meal. Pancreatic secretion contains proteins in a concentration of about 7 mg/ml during stimulation by secretin and CCK, most of this protein is enzymes. All of the enzymes are secreted as inactive precursors, which are activated by previously activated stomach enzymes.

The most important stimulus for pancreatic stimulation is a meal. The factors controlling the pancreatic response include both chemical composition and physical properties of the meal. The strongest stimulants to pancreatic enzyme secretion are fatty acids and monoglycerides. By themselves they can stimulate maximal enzyme output. Proteins are next, while carbohydrates have little stimulatory action. These nutrients exert their action in the duodenum. The most important factor appears to be the area of contact of nutrient with the mucosa. Therefore, it is the load of nutrient in the case of fat or protein delivered to the duodenum, rather than the concentration, which determines the magnitude of stimulation. Homogenized meals stimulate pancreatic secretion for shorter periods of time, since they leave the stomach more rapidly.

As the acidic chyme, or food mass, enters the duodenum, the acid stimulate the enteroendocrine S cells (specialized endocrine cells in the duodenum) to release a gastrointestinal hormone called secretin, which then stimulates the pancreatic cells to secrete the enzymes and bicarbonate. The presence of partially hydrolysed fat (fatty acids) and protein (amino acids and peptides) in the chyme that enters the duodenum, as well as the acidic pH of the chyme, stimulates enteroendocrine I cells in the upper small intestine to release the hormone cholecystokinin (CCK), which also causes secretion of enzymes and bicarbonate. These same hormones also stimulate bile secretion into the duodenum. Although the digestion of most nutrients in the small intestine is extensively carried out by enzymes secreted by the pancreas, enzymes located at the brush border membrane of the enterocytes are responsible for the completion of this process.

How then is the pancreas regulated?

From the above explanation, there are obviously three areas of potential regulation: cephalic, gastric, and intestinal.

Cephalic regulation is under the control of the parasympathetic nervous system. This system controls salivation which occurs in response to smelling, seeing, and tasting food. The GI tract is connected to the same part of the nervous system, so this stimulation will effect pancreatic secretion. The only way to inhibit pancreatic secretion via this mechanism is to disturb the vagal innervation of the pancreas, which is not easily done in humans.

Gastric regulation plays a minor role, but stomach distention due to food stimulates a vagal response, which in turn stimulates pancreatic secretion. This is not subject to an inhibitory feedback mechanism.

The intestinal response is mainly under the control of GI hormones, namely secretin and CCK. Secretin production occurs when the acidic chyme enters the duodenum. CCK is released in response to the “pre-digestion” that occurs in the stomach from pepsin and lipase enzymes. The resulting amino acids and fatty acids from these enzymes stimulates CCK release, which then stimulates pancreatic secretion and bile production. Obviously, these hormones represent a point of regulation for pancreatic secretion, that is, decreasing the production of secretin and CCK hormones should also decrease pancreatic enzyme secretion. There is data to suggest that bile acids can cause an inhibition of CCK release, which would then effect pancreatic enzyme production.

Does diet effect pancreatic enzyme secretion?

Yes. It has been shown that certain foods have high amounts of enzyme inhibitor, notably soybeans and other legumes. When on a diet of high soy, animals would develop larger pancreases, and their enzyme secretion would increase. Specific inhibitors of pancreatic enzymes, when given to humans, can cause an increase in that specific enzyme by the pancreas. This infers that some type of feedback mechanism exists for pancreatic enzyme secretion. It is also known that the products of proteolysis and lipolysis (amino acids and fatty acids) stimulate the hormones that cause pancreatic secretion to occur. If starch and glucose is placed in the small intestine, one sees less protease produced, but more carbohydrase produced. It is also apparent that adaptation plays a big role in pancreatic secretion. Prolonged intake of certain foods seems to stimulate production of pancreatic enzymes specific for the digestion of that food. Some peptides derived from milk casein seem to also stimulate enzyme production in rats, as does GABA.

Does taking oral enzymes have an inhibitory feedback on pancreatic enzyme secretion?

This has been an area of controversy for some time. Some of this confusion is due to the fact that animal studies don’t often predict what happens in humans. The digestive process is different in rodents than in man, so many of the early studies in animals aren’t applicable to humans. In rodents, enzyme secretion is increased if you quickly remove the pancreatic juice from the intestine. Such a mechanism has not been demonstrated in man.

A Swiss study in 1998 (Friess H. Int. J. Pancreatology 23:115) demonstrated no changes in human pancreatic enzyme secretion after 4 wks of oral pancreatic enzyme therapy at conventional doses. In 1997, a German study (Dominguez-Munoz JE, Aliment Pharmacol. 11:403) indicated a small decrease in pancreatic elastase in human males with a preparation of enteric-coated pancreatic enzyme microtablets, but not with enteric-coated enzyme tablets, indicating that the enzyme preparation or excipients present may have an effect on the study results. The same study showed that the pancreatic effect was not due to inhibition of GI hormones. Another earlier study (Mossner J, Pancreas 6:637, 1991) showed that an extract of pig pancreas placed in the lower small intestine actually increased pancreatic enzyme production, but if pure trypsin protease was used (a pancreatic enzyme) instead, a decrease in pancreatic secretion was observed, but only at very high trypsin levels. Most recently, Walkowiak et al. (Eur J Clin Invest. 33:65, 2003) showed that pancreatic enzymes at very high levels (5 grams per day for 7 days) could decrease pancreatic elastase measured in feces by as much as 50%. This effect was reversed when enzymes were discontinued. Smaller doses of enzyme did not show a significant effect on pancreatic secretion. There is a question as to whether the assays used in that particular study were appropriate for the experimental design, as the oral enzymes interfered with the fecal enzyme testing. Controls for the enteric coatings of the enzymes were not addressed.