See previous posts:
In this post, we will be focusing on the exocrine pancreas, which is the part that secretes digestive juices. (The endocrine pancreas secretes hormones such as insulin and glucagon.)
Describe the production of alkaline secretions by the
pancreas.
Production of alkaline secretions in the pancreas is actually quite similar to production of acid in the stomach. HCO3- is produced from the reaction of CO2 and H2O, which is catalysed by carbonic anhydrase.
HCO3- is then pumped out of duct cells, and Na+ and H2O follow. To get rid of the H+
also produced during the carbonic anhydrase reaction, there is a H+/Na+ antiport on the side of the cell facing the blood.
List the major pancreatic enzymes and describe their
secretion, activation, & function.
The major pancreatic enzymes include proteases, such as trypsin, chymotrypsin, carboxypeptidase, and elastase; nucleases; carbohydrases, such as pancreatic amylase; and lipases, such as pancreatic lipase, cholesterol esterase, and phospholipase. Proteases are all synthesised in inactive form so that the pancreas doesn't digest itself. For example, trypsin is released as trypsinogen, which is the inactive form of trypsin. The acini also have trypsin inhibitors as an added layer of protection.
Once in the small intestine, proteases become activated. The small intestine has an enzyme called enterokinase, which is held in place by glycosaminoglycans. Enterokinase activates trypsinogen to form trypsin, which can then go around and activate the other proteases.
Inactive proteases are constantly synthesised and stored in secretory vesicles known as zymogen granules. There is a very low amount of constitutive secretion. Secretion of enzymes is increased when CCK (cholecystokinin) and ACh (acetylcholine) bind to their receptors.
The major pancreatic enzymes include proteases, such as trypsin, chymotrypsin, carboxypeptidase, and elastase; nucleases; carbohydrases, such as pancreatic amylase; and lipases, such as pancreatic lipase, cholesterol esterase, and phospholipase. Proteases are all synthesised in inactive form so that the pancreas doesn't digest itself. For example, trypsin is released as trypsinogen, which is the inactive form of trypsin. The acini also have trypsin inhibitors as an added layer of protection.
Once in the small intestine, proteases become activated. The small intestine has an enzyme called enterokinase, which is held in place by glycosaminoglycans. Enterokinase activates trypsinogen to form trypsin, which can then go around and activate the other proteases.
Inactive proteases are constantly synthesised and stored in secretory vesicles known as zymogen granules. There is a very low amount of constitutive secretion. Secretion of enzymes is increased when CCK (cholecystokinin) and ACh (acetylcholine) bind to their receptors.
Describe the control mechanisms regulating
pancreatic secretion.
The most important factors involved in pancreatic secretion are acetylcholine, secretin, CCK, and somatostatin. ACh, released from the vagus nerve, stimulates both bicarbonate and enzyme release. Secretin, secreted from duodenal cells in response to low pH, stimulates bicarbonate production. CCK, secreted in response to duodenal fat and protein, stimulates enzyme production and relaxes the sphincter of Oddi. Somatostatin pretty much just inhibits everything.
In the cephalic phase of secretion, the vagus nerve stimulates some pancreatic secretions, via ACh. (See here if you can't remember the different phases of digestion.) These secretions only account for 10-20% of total secretion. In the gastric phase, gastrin binds loosely to CCK receptors, stimulating a further 5-10% of pancreatic secretions. Finally, in the intestinal phase, large amounts of CCK, secretin and ACh stimulate the bulk of pancreatic secretions.
The most important factors involved in pancreatic secretion are acetylcholine, secretin, CCK, and somatostatin. ACh, released from the vagus nerve, stimulates both bicarbonate and enzyme release. Secretin, secreted from duodenal cells in response to low pH, stimulates bicarbonate production. CCK, secreted in response to duodenal fat and protein, stimulates enzyme production and relaxes the sphincter of Oddi. Somatostatin pretty much just inhibits everything.
In the cephalic phase of secretion, the vagus nerve stimulates some pancreatic secretions, via ACh. (See here if you can't remember the different phases of digestion.) These secretions only account for 10-20% of total secretion. In the gastric phase, gastrin binds loosely to CCK receptors, stimulating a further 5-10% of pancreatic secretions. Finally, in the intestinal phase, large amounts of CCK, secretin and ACh stimulate the bulk of pancreatic secretions.
Describe the role of bile and its production and
metabolism
See previous post: Gastrointestinal function part 3
Bile acids can be classified as primary or secondary bile acids. Primary bile acids are those synthesised by hepatocytes, and secondary bile acids are produced when primary bile acids are converted by bacteria in the intestinal lumen.
Bile is formed by hepatocytes secreting stuff into the bile ducts. Some substances, such as bile salts, bilirubin, cholesterol and drugs are actively secreted by specific transporters. Other substances, such as water and glucose, may enter via diffusion through tight junctions.
After leaving the liver and travelling down the bile duct, bile is stored and concentrated in the gallbladder. Concentration of bile occurs via active transport of electrolytes from the gallbladder into the bloodstream. Electrolyte movement is then followed by water movement. One of the consequences of bile concentration is that gallstones can form, mainly from concentrated bilirubin and cholesterol that precipitates out with calcium.
When fats and amino acids enter the duodenum, CCK release is triggered. CCK relaxes the sphincter of Oddi and stimulates gallbladder contraction, pushing bile out of the gallbladder and into the small intestine. ACh from the vagus nerve may also be involved in gallbladder contraction.
When fats and amino acids enter the duodenum, CCK release is triggered. CCK relaxes the sphincter of Oddi and stimulates gallbladder contraction, pushing bile out of the gallbladder and into the small intestine. ACh from the vagus nerve may also be involved in gallbladder contraction.
Discuss haem removal via the bilirubin system
Haem is broken down into bilirubin in the reticuloendothelial system, which includes organs such as the spleen. Heme oxygenase cleaves the haem ring to form biliverdin, and biliverdin reductase reduces biliverdin to form bilirubin. Bilirubin travels around the blood while bound to albumin. When bilirubin reaches the liver, it is released from albumin, and enters the liver via transporters. Once in the liver, two glucose residues are added to form a water-soluble diglucuronide. This diglucuronide is what is pumped into the bile canaliculus.
After being secreted in bile, bilirubin is subjected to one of two main fates. First of all, bilirubin can be pooped out, along with everything else in your intestines. The alternative is that gut bacteria can convert bilirubin into urobilinogens, which the small intestine is permeable to. Urobilinogens can be reabsorbed and essentially recycled.
If bilirubin secretion is not sufficient, jaundice (yellowish tint to the skin) can occur. There are two main types of jaundice: haemolytic jaundice and obstructive jaundice. In haemolytic jaundice, too many red blood cells are broken down, and in obstructive jaundice, bile is unable to leave the bile duct due to an obstruction. The two types of jaundice can be differentiated by looking for conjugated vs. unconjugated bilirubin. Haemolytic jaundice has a large amount of unconjugated bilirubin (since a lot of bilirubin hasn't reached the liver yet), whereas obstructive jaundice has a large amount of conjugated bilirubin (as this is a problem downstream of the liver).
Haem is broken down into bilirubin in the reticuloendothelial system, which includes organs such as the spleen. Heme oxygenase cleaves the haem ring to form biliverdin, and biliverdin reductase reduces biliverdin to form bilirubin. Bilirubin travels around the blood while bound to albumin. When bilirubin reaches the liver, it is released from albumin, and enters the liver via transporters. Once in the liver, two glucose residues are added to form a water-soluble diglucuronide. This diglucuronide is what is pumped into the bile canaliculus.
After being secreted in bile, bilirubin is subjected to one of two main fates. First of all, bilirubin can be pooped out, along with everything else in your intestines. The alternative is that gut bacteria can convert bilirubin into urobilinogens, which the small intestine is permeable to. Urobilinogens can be reabsorbed and essentially recycled.
If bilirubin secretion is not sufficient, jaundice (yellowish tint to the skin) can occur. There are two main types of jaundice: haemolytic jaundice and obstructive jaundice. In haemolytic jaundice, too many red blood cells are broken down, and in obstructive jaundice, bile is unable to leave the bile duct due to an obstruction. The two types of jaundice can be differentiated by looking for conjugated vs. unconjugated bilirubin. Haemolytic jaundice has a large amount of unconjugated bilirubin (since a lot of bilirubin hasn't reached the liver yet), whereas obstructive jaundice has a large amount of conjugated bilirubin (as this is a problem downstream of the liver).
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