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Pancreatic secretions

Pancreatic secretions

These Pancreayic have shaped our current understanding of Pancreatic secretions Benefits of meditation for heart health and hold Pancreatid potential for biomarker discovery and identification of novel Pancreztic Citrus oil for balancing skin tone. Secrerions ligands that eecretions Pancreatic secretions cell surface secgetions, NO penetrates cells and activates guanylate cyclase to generate the second messenger cGMP The biliary juices bile are made in the tissues of the liver hepatic parenchymaand then pass into the biliary ductal system picture. Thus, the protease concentration in the upper small intestine appears to be intimately linked to pancreatic secretion through a negative feedback system in which active proteases within the duodenum limit pancreatic secretion but reduced protease activity stimulates pancreatic secretion. We use cookies to improve your experience on our site and to show you relevant advertising.

Pancreatic secretions -

Key Points Pancreatic fluid or juice contains digestive enzymes that pass to the small intestine where they help to further break down the carbohydrates, proteins, and lipids fats in the chyme. Pancreatic fluid is alkaline in nature due to its high concentration of bicarbonate ions that neutralize the gastric acid and allow effective enzymic action.

Key Terms pancreatic fluid : A liquid secreted by the pancreas that contains a variety of enzymes, including trypsinogen, chymotrypsinogen, elastase, carboxypeptidase, pancreatic lipase, and amylase. Pancreatic Juice Pancreatic juice is a liquid secreted by the pancreas that contains a variety of enzymes, including trypsinogen, chymotrypsinogen, elastase, carboxypeptidase, pancreatic lipase, nucleases, and amylase.

Authored by : Boundless. Provided by : Boundless. Provided by : Wikibooks. Located at : en. License : CC BY-SA: Attribution-ShareAlike Pancreas.

Provided by : Wikipedia. License : CC BY-SA: Attribution-ShareAlike pancreas. Provided by : Wiktionary. Provided by : Wikimedia. This means that normal digestion and absorption of dietary fat is critically dependent on secretions from both the pancreas and liver.

Pancreatic lipase has recently been in the limelight as a target for management of obesity. The drug orlistat Xenical is a pancreatic lipase inhibitor that interferes with digestion of triglyceride and thereby reduces absorption of dietary fat.

Clinical trials support the contention that inhibiting lipase can lead to significant reductions in body weight in some patients. The major dietary carbohydrate for many species is starch , a storage form of glucose in plants.

Amylase technically alpha-amylase is the enzyme that hydrolyses starch to maltose a glucose-glucose disaccharide , as well as the trisaccharide maltotriose and small branchpoints fragments called limit dextrins. The major source of amylase in all species is pancreatic secretions, although amylase is also present in saliva of some animals, including humans.

In addition to the proteases, lipase and amylase, the pancreas produces a host of other digestive enzymes, including ribonuclease, deoxyribonuclease, gelatinase and elastase. Epithelial cells in pancreatic ducts are the source of the bicarbonate and water secreted by the pancreas.

Bicarbonate is a base and critical to neutralizing the acid coming into the small intestine from the stomach. The mechanism underlying bicarbonate secretion is essentially the same as for acid secretion by parietal cells in the stomach and is dependent on the enzyme carbonic anhydrase. In pancreatic duct cells, the bicarbonate is secreted into the lumen of the duct and hence into pancreatic juice.

Sham feeding and electrical vagus nerve stimulation in dogs triggers the release of cholecystokinin CCK although this response may be absent in humans 8, , Endogenous CCK was shown to enhance PP release in humans during sham feeding Therefore, although peptidergic neurotransmitters are released during vagal stimulation, acetylcholine is believed to be the main neurotransmitter which regulates the cephalic phase.

A number of G protein-coupled receptors GPCRs located on acinar cells also mediate the cephalic phase of enzyme secretion. Interaction of CCK with CCK-1 receptors has been shown to induce protein secretion in new born calves This response is possibly dependent upon neural CCK release as cephalic stimulation does not increase blood levels of CCK.

Thus, both neural and hormonal mechanisms play an important role in regulating the cephalic phase of pancreatic secretion.

Entry of food into the stomach initiates the gastric phase of pancreatic secretion. This phase has been difficult to study in unanesthetized animals because presence of food in the stomach initiates neural reflexes and release of hormones.

Therefore, physiological data regarding this phase has been collected by gastric distention induced either by balloon dilation or instillation of inert substances in the antrum.

Secretions induced during this phase consist mainly of enzymes with minimal release of bicarbonate suggesting that acinar cells are primarily involved in the induction of this phase 8, 37, , The role of gastrin in this phase of pancreatic secretion remains unclear.

It was demonstrated that step-wise alkaline distension of the antrum induced graded release of gastrin and pancreatic enzymes However, when exogenous gastrin was administered to dogs the amount required to stimulate exocrine secretion was much greater than normal postprandial gastrin levels, suggesting that gastrin did not have a physiological role These findings are supported by other studies demonstrating that gastrin release is not required for pancreatic enzyme secretion during this phase.

The vagus nerve plays an important role in the gastric phase of pancreatic secretion. Early experiments in anesthetized cats demonstrated that stimulation of the antrum resulted in vagal stimulation of pancreatic amylase release Antral distension in dogs also increased pancreatic secretion by long route vagal pathways An antropancreatic short reflex pathway which is blocked by hexamethonium and atropine also mediates this phase In addition, atropine and vagotomy block the gastric phase providing further evidence that gastric contributions to pancreatic secretion are mediated by vagovagal cholinergic reflexes that originate in the stomach and terminate in the pancreas , , CCK release plays an important role in antral motility and gastrin release in humans as suggested by sham feeding experiments In the stomach, pepsin and gastric lipases catabolize proteins and fats into peptides and triglycerides plus fatty acids, respectively, while salivary amylase contributes to the continued digestion of carbohydrates.

Peptic digests of proteins are effective in stimulating the intestinal phase Thus when gastric chyme enters the duodenum, it stimulates the intestinal phase of pancreatic secretion. In a clinical setting, surgical procedures that slow the rate of gastric emptying reduce pancreatic secretion , Therefore, the rate of gastric emptying regulates the discharge of nutrients into the intestine and consequently the activation of the intestinal phase through neural and hormonal pathways.

As mentioned above, digestion of food in the stomach is followed by release of acidic chyme into the duodenum which initiates the intestinal phase of pancreatic secretion. By this phase, the pancreas has already been primed by cephalic and gastric influences, which enhance blood flow and initiate exocrine secretion.

The intestinal phase is more easily studied than the gastric phase as food can be instilled directly into the intestinal lumen without concern for gastric emptying.

Stimulation of both acinar and ductal cells results in the production of enzyme and bicarbonate secretion. Pancreatic amylase secretion is stimulated by food molecules such as sodium oleate, monoglycerides, peptides, and amino acids particularly tryptophan and phenylalanine 50, 88, , In the duodenum the high volume of bicarbonate released neutralizes the acidity of gastric chyme, while pancreatic enzymes catabolize partially digested food into molecules that are easily absorbed by intestinal enterocytes.

In the intestinal phase, pancreatic response is regulated primarily by the hormones secretin and CCK, and by neural influences including the enteropancreatic reflex which is mediated by the enteric nervous system and amplifies the pancreatic secretory response.

Entry of low pH gastric chyme into the intestine stimulates release of secretin from S cells into the blood The main action of secretin is to stimulate bicarbonate release from pancreatic duct cells, but it also has a direct effect on acinar cells and potentiates enzyme secretion.

The role of secretin in pancreatic secretion is addressed later in this review. CCK is released by proteins and fats and their partial digestion products: peptides and fatty acids.

Experiments in dogs with chronic pancreatic fistulae have shown that CCK antagonism diminishes pancreatic protein response to a meal and duodenal perfusion suggesting that CCK plays an important role in this phase Similar results were also obtained in humans, where CCK receptor antagonism reduced pancreatic enzyme secretion during the intestinal phase 85, Cholinergic regulation plays a critical role during this phase of pancreatic secretion.

In the absence of secretin, atropine partially inhibits pancreatic bicarbonate secretion stimulated by low pH due to acidic chyme in the duodenum , In addition, the amount of bicarbonate produced by infusion of secretin is lower than that released by entry of food into the duodenum suggesting that other factors contribute to meal-stimulated pancreatic bicarbonate secretion Atropine inhibited pancreatic enzyme secretion from 30 minutes following meal ingestion, implicating cholinergic mechanisms Vagovagal enteropancreatic reflexes mediated by M1 and M3 muscarinic receptors and CCK receptors play an important role in the intestinal phase of secretion , These vagovagal enteropancreatic reflexes are modulated by input from the dorsal motor nucleus of the vagus projecting into the pancreas.

Thus, vagal stimulation activates pancreatic bicarbonate secretion through both cholinergic muscarinic and noncholinergic transmission. The physiological effects of acid on pancreatic secretion have been evaluated by various methods such as diversion of gastric and pancreatic contents with fistulae, and instillation of acidic solutions into the duodenum.

Both gastric acid and exogenous HCl are powerful regulators of postprandial pancreatic bicarbonate secretion and their effects are potentiated by intrapancreatic and vagovagal neural pathways as well as by hormones such as secretin and CCK indicating that the physiological effects of gastric acid are due to its pH.

Intraduodenal infusion of hydrochloric acid elicited a concentration-dependent increase in both the amount of bicarbonate and volume of pancreatic secretion.

Secretion was similar to that attained with intravenous infusion of exogenous secretin suggesting that pH changes resulting from entry of acidic contents into the duodenum are important in inducing pancreatic secretion.

Administration of a peptone meal of varying pH pH 1 to 5 produced a maximal secretory response at pH 3. Acid infusion in both the duodenum and upper jejunum elicited pancreatic secretion suggesting that the proximal small intestine responds to this stimulus Entry of gastric contents into the duodenum creates an acidic environment with a pH of 2.

This difference in pH is due to pancreatic bicarbonate release, which is augmented in large part by gastric acid-induced secretin release from the intestinal mucosa. In conscious rats with gastric and pancreatic fistulae, diversion through a gastric fistula produced a small increase in pancreatic secretion.

However, instilling hydrochloric acid into the duodenum with an open gastric fistula augmented pancreatic secretion 22, In addition, pancreatic bicarbonate secretion was much greater when pancreatic juice was diverted from the intestine signifying a correlation between intestinal pH and quantity of pancreatic bicarbonate release 48, The pancreatic bicarbonate response is dependent on the concentration of free unbuffered hydrogen ions and not on the total load of buffered acid entering the duodenum.

This evidence implies that gastric acid is an important regulator of pancreatic bicarbonate secretion which neutralizes the acid to create an alkaline environment optimal for the action of pancreatic enzymes and continued digestion of food.

Dietary fats stimulate pancreatic enzyme and bicarbonate secretion. Perfusion of monoolein stimulated pancreatic enzyme secretion in humans and this effect was similar in potency to that observed with intravenous CCK injection In contrast, triglycerides administered directly into the duodenum in the absence of endogenous lipase were unable to induce pancreatic secretion.

However, following lipase digestion of fatty acids, monoglycerides stimulated pancreatic secretion but glycerol was ineffective indicating that fatty acids are the major component of ingested fats that stimulate pancreatic secretion , There is some evidence to suggest that both free and saponified fatty acids induce pancreatic secretion, while other experiments suggest effectiveness only in a micellar form.

Secretion has been shown to be dependent on fatty acid chain length, with C4 being least effective and C18 being most effective Although the reason for this difference in potency is not entirely clear, it is not believed to be related to the efficiency of absorption Other studies have demonstrated that intraduodenal administration of propionate C3 was more effective than oleate C18 in stimulating acinar cell secretion The reason for the differences between the two studies is not entirely clear but could be species related as these experiments have been performed in humans, rats, and rabbits.

Both oleate and neutral fats stimulate bicarbonate and fluid secretion, whereas only neutral fats stimulate pancreatic enzyme secretion.

In dogs, oleic acid was shown to potentiate acidified protein-meditated pancreatic enzyme and bicarbonate secretion Fat emulsions given to conscious rats produced a 3-fold increase in pancreatic protein secretion.

The route of fat administration also has an impact on pancreatic secretion. Intravenous administration of fat did not produce pancreatic secretion, whereas intraduodenal administration led to elevated protein, bicarbonate, and fluid secretion , Administration of fat emulsions increases plasma CCK and secretin levels.

Fat-mediated pancreatic secretion was blocked by proglumide, a CCK receptor antagonist, implicating the importance of CCK in stimulating pancreatic secretion Both C12 and C18 fatty acids augment the effects of secretin-induced bicarbonate secretion In humans, introduction of different concentrations of oleic acid into the duodenum induce pancreatic secretion, although the threshold for CCK stimulation is much lower than for secretin Secretin release is physiologically important since injection of anti-secretin antibodies in conscious rats greatly reduce fat-mediated protein and bicarbonate secretion A critical fatty acid chain length of C12 was required for CCK release from STC-1 cells, a neuroendocrine tumor cell line.

Fatty acids with less than ten carbon atoms did not augment secretion. This dependence on fatty acid chain length is similar to that observed previously for in vivo CCK release in humans.

In addition to the fatty acid carbon chain length, a free carboxyl terminus is also important as esterification of the carboxylic terminus abolished CCK secretion, while modification of the methyl terminus had no effect Two cell surface receptors have been identified and demonstrated to promote fat-mediated CCK release.

Mice with global deletion of GPR40 show partial reduction in CCK secretion following fatty acid administration The recently discovered immunoglobulin-like domain containing receptor ILDR is expressed in I cells of the duodenum. ILDR appears to play an essential role in fat-stimulated CCK release as deletion of ILDR in mice completely eliminates fatty acid-stimulated CCK secretion Thus fats and fatty acids are important regulators of pancreatic secretion.

Experimental evidence suggests that the degree and extent of acinar and ductal cell activation may vary depending on the animal species and the route of fat administration.

Studies performed in dogs, rats, and humans have shown that proteins, peptides, and amino acids stimulate pancreatic secretion while the magnitude of this effect may be dependent on the species being evaluated In dogs, intact, undigested proteins such as casein, albumin, and gelatin did not stimulate pancreatic secretion, whereas protease digests of these proteins were very effective In contrast, studies in rats suggested that intestinal administration of hydrolyzed casein produced a smaller response than some of the other proteins which potently stimulated pancreatic enzyme secretion, suggesting that the amino acid composition of a protein is relevant in determining the extent of stimulation 96, Although intravenous infusion of amino acids in humans stimulated pancreatic enzyme and bicarbonate secretion, a mixture of L-amino acids when infused intravenously in dogs was not effective.

In contrast to intravenous infusion, intraduodenal delivery of amino acids in dogs induced pancreatic fluid, bicarbonate and protein secretion which was comparable to an elemental diet suggesting the importance of the route of administration on pancreatic secretion , Only L-amino acids stimulate pancreatic secretion which is consistent with the overall physiological importance of these stereoisomers.

Of all the amino acids, aromatic amino acids such as phenylalanine and tryptophan have the greatest potency 76, , Although aromatic amino acids are highly effective in stimulating pancreatic secretion, peptides may be more physiologically relevant as they are more abundant than amino acids in the intestinal lumen Oligopeptides and longer peptides containing the amino acids phenylalanine and tryptophan are effective stimulants of pancreatic secretion , Acidification of amino acid , and peptide 76 preparations with hydrochloric acid potentiates the bicarbonate response but pancreatic enzyme secretion is not influenced beyond that observed in the absence of acid.

Aromatic amino acids are capable of inducing maximal secretory response as potentiation of pancreatic enzyme secretion is not observed when amino acids or peptides are administered concomitantly with lipid molecules such as oleate or monoolein 75, The pancreatic secretory response to intraduodenal administration of amino acids appears to be concentration dependent.

A minimal concentration of 8 mM is necessary for stimulation by most amino acids although the more potent aromatic amino acids such as tryptophan stimulate secretion at concentrations as low as 3 mM The length of the intestine exposed to amino acids also plays a critical role in pancreatic secretion.

In dogs, exposure of the first 10 cm was least effective, while perfusion of the whole intestine produced significant enzyme output suggesting that the pancreatic response was dependent upon the entire load of nutrients, not just their concentration.

The majority of stimuli responsible for pancreatic stimulation originate in the proximal small intestine. In humans, amino acids stimulated pancreatic secretion only when perfused into the duodenum and no response was observed upon perfusion in the ileum Therefore, similar to fats, the primary mechanisms that stimulate pancreatic secretion are limited to the proximal regions of the small intestine.

The amount of bicarbonate released by intraluminal administration of tryptophan is similar to that produced by maximal doses of exogenously infused CCK indicating that release of CCK by tryptophan leads to pancreatic secretion 52, , Similarly, intraduodenal administration of liver extracts in dogs mediated CCK release along with pancreatic enzyme and bicarbonate secretion, both of which were blocked by CCK receptor antagonists Bile acids released from the gallbladder can significantly inhibit pancreatic stimulation induced by intraluminal amino acids.

This inhibition of pancreatic secretion by bile acids appears to be due to inhibition of CCK release and serves as a feedback mechanism in regulating pancreatic and gallbladder function By using a sensitive bioassay for CCK measurement, it was shown that one of the pathways by which proteins stimulate CCK release is by their ability to inhibit intraluminal trypsin activity Another mechanism by which aromatic amino acids mediate CCK release is by activation of the calcium sensing receptor CaSR , a known nutrient sensor , , , In addition to stimulating the release of hormones such as CCK and secretin, amino acids also activate cholinergic neural mechanisms which regulate pancreatic bicarbonate secretion Hence proteins, peptides, and amino acids stimulate pancreatic secretion but the magnitude of stimulation depends upon the mode of administration and the species being evaluated.

Bile is produced by hepatocytes as a complex mixture of bile acids, cholesterol, and organic molecules. It is stored and concentrated in the gall bladder and released into the duodenum upon entry of chyme. Bile acids such as cholate, deoxycholate, and chenodeoxycholate are conjugated with glycine or taurine amino acids which increase their solubility.

In the intestine, bile acids assist in the emulsification and absorption of fatty acids, monoacylglycerols, and lipids and stimulate lipolysis by facilitating binding of pancreatic lipase with its co-lipase.

Under basal conditions, intraduodenal administration of physiological concentrations of bile or the bile salt sodium taurocholate, elevated plasma secretin and stimulated pancreatic fluid secretion in cats , Secretin was released only in response to perfusion of sodium taurocholate in the duodenum.

Perfusion in the upper jejunum produced a significantly diminished pancreatic response, while no response was observed upon ileal perfusion Pancreatic fluid secretion was stimulated by the free ionized form of taurocholate and was not dependent on its detergent properties In humans, infusion of bovine bile augmented secretin release along with pancreatic exocrine secretions of fluid, bicarbonate, and enzymes , In addition to secretin, infusion of bovine bile and bile acids in humans and dogs was shown to stimulate the release several hormones and neuropeptides such as CCK, neurotensin, VIP, gastric inhibitory peptide GIP , PP, and somatostatin 34, 42, , Fluid and bicarbonate release was enhanced when elevated levels of VIP were present in the plasma, suggesting that bile activates peptidergic nerves resulting in pancreatic secretion.

Additionally, cholinergic mechanisms are also important as atropine blocked bile- and taurocholate-stimulated exocrine pancreatic secretion The composition of bile is important in mechanisms regulating this secretory response as some differences in hydrokinetic and ecbolic responses were observed with administration of bile versus various bile acids However, a stimulatory effect of bile acids on pancreatic fluid secretion was not observed in the presence of digestive intraluminal contents In some studies where bile acids were administered concomitantly with amino acids or fat, an inhibition of pancreatic enzyme secretion was observed.

The mechanism underlying this observation is not completely understood, although it is possible that bile acids inhibit CCK release by a negative feedback mechanism which helps to relax and refill the gallbladder 24, , , Chemical sequestration of bile acids in dogs augmented the release of CCK and pancreatic enzyme secretion in response to amino acids and addition of taurocholate reversed this effect Long term diversion of bile in dogs also augmented basal and oleate-stimulated pancreatic fluid, bicarbonate, and enzyme secretion along with plasma CCK levels, further supporting the role of bile acids in inhibiting CCK release Other studies have shown that the bile salt chenodeoxycholate when infused in humans, inhibited bombesin- and CCK-stimulated gallbladder emptying along with elevation of plasma CCK levels.

These results led the authors to hypothesize that chenodeoxycholate, by a yet unknown mechanism, reduced the sensitivity of the gall bladder to stimulation by bombesin and CCK In contrast to many species including mice and humans, rats do not possess a gallbladder and multiple pancreatic ducts join the lower end of the common bile duct.

In rats, diversion of bile and pancreatic juice stimulates the release of pancreatic enzymes. This augmentation of enzyme secretion has been suggested to compensate for the increased degradation of proteolytic enzymes in the absence of bile.

Thus exocrine secretion in rats is regulated by a luminal feedback mechanism 93, Additional experiments have shown that certain bile salts stimulate bicarbonate secretion via CCK release whereas other bile salts inhibit exocrine secretion , , Two inhibitory mechanisms have been proposed — one dependent on the stabilization of luminal proteases and the other independent of protease activity The physiological role of bile and bile salts in regulating pancreatic secretions is not completely understood and appears to be dependent on multiple factors, including the chemical properties of bile salts, the animal model being evaluated, and prandial status of the animal being studied Once nutrients are absorbed from the intestinal lumen, they may directly stimulate pancreatic secretion leading to the absorbed nutrient phase.

Nutrients can either directly stimulate pancreatic acinar cells, or they may indirectly activate hormonal and neural pathways to further regulate exocrine secretion. Little conclusive evidence is available for intravenous lipids and glucose in stimulating pancreatic secretion However, intravenous administration of amino acids increases the amount of trypsin and chymotrypsin secretion, but not lipase or amylase Amino acids appear to have a substantial indirect effect on pancreatic secretion, since intraduodenal administration of amino acids produces large increases in pancreatic secretion , , The role of nutrients after absorption on pancreatic secretion is not well understood and additional studies are needed to fully investigate these effects.

One effect is to stimulate synthesis of new digestive enzymes to replenish the pancreatic supply. Feedback Regulation of Pancreatic Secretion.

The concept of feedback regulation of pancreatic secretion emanated from a series of studies demonstrating that 1 instillation of trypsin inhibitor into the upper small intestine or 2 surgical diversion of the bile-pancreatic duct removing bile and pancreatic juice from the duodenum of rats stimulated pancreatic enzyme secretion Conversely, infusion of trypsin into the duodenum during bile-pancreatic juice diversion suppressed pancreatic enzyme release.

Thus, the protease concentration in the upper small intestine appears to be intimately linked to pancreatic secretion through a negative feedback system in which active proteases within the duodenum limit pancreatic secretion but reduced protease activity stimulates pancreatic secretion.

When assays for CCK became available, it was shown that CCK mediated the effects of proteases on pancreatic secretion through protease-sensitive CCK releasing factors , see Figure 1. In the absence of proteases, CCK releasing factor can stimulate CCK cells, but in the presence of proteases, the releasing factors are inactivated and CCK secretion is low.

Negative feedback regulation of pancreatic secretion has been shown to exist in many species although other proteases such as elastase may be more important in regulating pancreatic secretion in humans.

Figure 1. Feedback regulation of pancreatic exocrine secretion is mediated by positive and negative mechanisms. Positive feedback: Monitor peptide is secreted by acinar cells and directly stimulates CCK cells in the small intestine and amplifies pancreatic secretion once it has been initiated. Pancreatic exocrine secretion is also influenced through a positive feedback mechanism.

Monitor peptide is a 61 amino acid peptide produced by pancreatic acinar cells and possessing CCK releasing activity. Although monitor peptide has modest trypsin inhibitor capability, its ability to stimulate CCK is independent of this action because monitor peptide can directly stimulate CCK secretion from isolated CCK cells in vitro 28, Monitor peptide is secreted in pancreatic juice, therefore, it does not stimulate CCK secretion unless pancreatic secretion is underway.

Thus, monitor peptide cannot account for the increase in CCK in during bile-pancreatic juice diversion, but it may serve to reinforce pancreatic secretion once the process has been initiated.

The exocrine pancreas delivers its secretions of digestive enzymes, fluid, and bicarbonate ions to the duodenum following ingestion of food. The pancreas is composed of both endocrine and exocrine components. The endocrine pancreas is comprised of α, β, δ, ε, and PP F cells, which.

are located in the islets of Langerhans. These specialized cells secrete the hormones insulin, glucagon, somatostatin, ghrelin, amylin, and pancreatic polypeptide into the blood, which exert endocrine and paracrine actions within the pancreas.

Ninety percent of the pancreas is composed of acinar cells which secrete digestive enzymes such as trypsin, chymotrypsin, and amylase for digestion of food in the small intestine.

The acinar cells are triangular in shape and arranged in clusters with the apex of the cell opening into a centrally located terminal duct. The terminal or intercalated ducts merge to form interlobular ducts, which in turn congregate to form the main pancreatic duct. The pancreatic duct delivers exocrine secretions into the duodenum.

The ductal cells secrete fluid and bicarbonate ions, which neutralize acinar cell secretions, as well as the acidic gastric contents entering the duodenum The pancreas is heavily innervated by sympathetic and parasympathetic peripheral nerves and contains a dense network of blood vessels which regulate blood flow and modulate pancreatic secretion.

Pancreatic Carbohydrate metabolism and intestinal absorption contains digestive enzymes that help to Secregions break down the Pancreqtic, proteins, and lipids in Glycogen replenishment for swimmers chyme. The pancreas is a glandular organ in the digestive system secretoins endocrine system Pancrdatic Citrus oil for balancing skin tone. It is both seecretions Pancreatic secretions gland Pancrreatic produces several secretkons hormones—including insulin, glucagon, somatostatin, and xecretions polypeptide—and a digestive organ that secretes pancreatic juice that has digestive enzymes that assist the absorption of nutrients and digestion in the small intestine. These enzymes help to further break down the carbohydrates, proteins, and lipids in the chyme. Pancreatic juice is a liquid secreted by the pancreas that contains a variety of enzymes, including trypsinogen, chymotrypsinogen, elastase, carboxypeptidase, pancreatic lipase, nucleases, and amylase. Pancreatic fluid : A schematic diagram that shows pancreatic acini and the ducts where fluid is created and released. Pancreatic juice is alkaline in nature due to its high concentration of bicarbonate ions that neutralize the gastric acid and allow effective enzymic action. Pancreatic secretions

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