Insufficient acid production in stomach. Cystic Fibrosis (of the pancreas). Acute pancreatitis. Steatorrhea. Lactose intolerance. Celiac disease (gluten).
Major component for energy metabolism. Provide sugars than can eventually be stored as Glycogen.
High carbohydrate diet
Can lead to increased fatty acid synthesis in the liver and eventually to increased fat deposits.
Sucrose, Lactose, maltose
Cleaved by sucrase, lactase and maltase.
Common and normal in most adults and leads to bloating and diarrhea after ingestion of milk. Exception are societies who use dairy products as food source.
Dietary Protein Digestion
Important because it does not only provide amino acids, but also delivers the dietary essential amino acids which can not be synthesized in humans.
Diseases due to insufficient protein in diet. Causes edema and plump belly. Albumin is synthesized in the liver and needed in the blood for specific transport and also for the regulation of osmolality.
Activated to pepsin in the stomach. Need a high proton concentration (low pH) which can not be synthesized in humans. Antacids interfere with protein degradation by increasing pH.
Can be dangerous to the body. Proteases and phospholipases can digest cell membranes. Meant to be active only in the lumen of intestines.
Abnormal and premature proteolytic activation of pancreatic enzymes.
Nucleic acid digestion
Dietary purine and pyrimidine bases are mostly degraded. They are not used to a large extent for the re-synthesis of nucleic acids in tissues. Dietary purines are mainly degraded in the intestinal mucosal cells and lead to uric acid. Uric acid is released into the blood and is then excreted by the kidney into the urine.
Patients suffering from this disease should eat a diet low in purine nucleotides.
Important for energy metabolism and dietary essential fatty acids, linoleic acid (18:2, w6) and alpha-linoleic acid (18:3, w3). Needs conjugated bile salts which are also important for the solubility of cholesterol in bile (together with PC).
Dietary essential Fatty acids and Fat soluble vitamins
Taken up via chylomicrons.
Released into the lymph and join the blood circulation at the thoracic duct.
Can lead to the lack of dietary essential fatty acids and fat soluble vitamins.
Caused by lack of fat-soluble vitamin A.
Start of digestion of carbohydrates and of triacylglycerols (TAG) with medium chain fatty acids.
Homogenization and acidification (the hormone gastrin induces gastric acid secretion). Stop of carbohydrate digestion. Start of digestion of proteins and continuation of digestion of TAGs with medium-chain fatty acids.
Leads to increase of proton concentration in the stomach.
Cleaves alpha alpha(1-4) bonds of starch and glycogen. Leads to branched oligosaccharides. Is inhibited in the acidic stomach lumen.
Linqual lipase and gastric lipase
Degrade human milk triacylglycerides which contain medium-chain fatty acids.
Synthesized in the stomach cells and released into the lumen of the stomach (normal pH 1-2). Cleaved to pepsin when it comes into contact with strong acid (below pH 5).
Can cleave pepsinogen to generate more pepsin. Optimal activity at pH 2.
Endopeptidase that cleaves peptide bonds inside of proteins. Produces smaller proteins or peptides that are released with the acid stomach content into the small intestine.
Acidic stomach contents. When in intestines, leads to the release of hormones secretin and cholecystokinin (CCK) from intestinal endocrine cells.
Activates secretion of water and bicarbonate from the pancreas. Action allows to neutralize the pH so that the pancreatic enzymes can act.
Inhibits gastric mobility. Activates enteropeptidase and secretion of enzymes from the pancreas. Activates secretion of bile from the gallbladder (contraction)
glucagon from alpha cells and insulin from beta cells and also somatostatin from the delta cell.
An inhibitory hormone that suppresses the releases the GI hormones like gastrin, CCK, secretin and others.
Acts on oligosaccharides and forms disaccharides (sucrose, lactose, maltose and isomaltose)
Synthesized from zymogens and need to be proteolytically activated to trypsin, chymotrypsin, elastase and carboxypeptidases and pancreatic phospholipase A2.
Once reaching the intestines cleaved by enteropeptidase into trypsin.
Acitvates more tyrpsinogen and also chymotrypsinogen, proelastase and procarboxypeptidase and for lipid digestion procolipase and prophospholipase A2.
Arg or Lys residues (long, narrow pocket)
Specific cleavage sites for trypsin
Cleavage sites for chyomotrypsin
Bulky and aromatic residues (wide and large pocket)
Cleavage site for elastase
glycine, alanine, serine (small pocket).
Cleave from the carboxyl-end.
Proteolytic activation of Trypsin
Should happen normally only in the lumen of the intestines performed by enteropeptidase.
Trypsin inhibitor protein
A secretory peptide, travels as protection with the zymogens from the pancreas to the intestines.
Can be caused by a blockage of pancreatic duct. Serum injury markers are pancreatic lipase and alpha-amylase.
Patients with this have dried mucus that blocks the pancreatic duct and leads to less pancreatic enzymes for digestion of mainly proteins and lipids. Carbohydrates can still be digested with even only 10% of normal amounts of pancreatic alpha-amylase.
cystic fibrosis diet
Calorie rich. Preferably a diet that is rich in milk or generally TAG's with medium-chain fatty acids which do not need pancreatic enzyme digestion. This can provide some more nutrients for energy metabolism. in addition, modified pancreatic enzymes can be ingested.
Pancreatic Phospholipase A2
Cleaves dietary phospholipids to lysophospholipids and fatty acids
Forms cholesterol and fatty acids from cholesterylesters.
Cleaves dietary triacylglycerols. Secreted together with procolipase and reaches the intestine.
Needed for both, lipase and phospholipase A activities. Emulsify the dietary lipids and form mixed micelles for the uptake of digested lipids into the mucosal cells. Conjugated bile acids.
Are hydrophobic and hydrophilic. Have a pH of 6 and are at pH 6 in the duodenum 50% charged. In order to improve this in favor of more charged molecules, conjugation with glycine leads to a pK of 4 and conjugation with taurine even leads to a pK of 2!
Conjugated bile salts and lysophosphatidylcholine
Emulsify dietary lipids.
Primary bile acids
Formed in the liver from cholesterol.
Secondary bile acids
Formed from primary bile acids by intestinal bacteria.
Digestion of Triacylglycerols
Trypsin cleaves pro-colipase to colipase which anchors now pancreatic lipase on the water-lipids interface. The purpose of pancreatic lipase is to form molecules (monoacylglycerol and fatty acids) that can enter the intestinal mucosal cells which are monoacylglycerol and fatty acids.
Cholesterol hallstone disease, often due to decrease of bile salts and phosphatidylcholine in bile, or due to increased biliary cholesterol secretion.
Primarily due to reduced lactase activity with age or secondary due to intestinal injury from severe diarrhea or gastroenteritis due to rotavirus. Celiac disease is immune-mediated damage in response to gluten (protein in grains). Lactose reaches the large intestines. Colonic bacteria degrade lactose to lactic acid and short chain fatty acids. This fermentations leads to hydrogen gas, carbon dioxide and methane. H2 can be measured in the breath. Incomplete digestion leads via the osmotic effect to uptake of water into the intestine, bloating and diarrhea. This leads to dehydration.
Primary lactose intolerance
Very common in individuals of Asian, African or Native american heritage. Much less common in societies that use milk as major nutrition for adults like Northern Europe.
Activity of Lactase
Highest in infants and decline by about 90% at the average human age of seven in the majority of humans.
Congenital lactase deficiency
Rare autosomal recessive disorder which was life-threatening in the past. Affected baby need early on special formula without lactose that can substitute human milk.
Leads to fatty feces and shows the loss of lipid soluble vitamins and essential fatty acids. Strong smell of feces.
Possible causes of Steatorrhea
Lack of conjugated bile salts. Can be due to liver or bile duct damage, or liver cirrhosis.
Possible causes of Steatorrhea
Defects related to pancreatic juice. Deficiency of enzymes, lack of transport of enzymes into the intestines like seen in CF, lack of bicarbonate secretion which would impair the adjustment of the pH in the duodenum.
Possible causes of Steatorrhea
Defective mucosal cells related to uptake of nutrients. A shortened bowel could also lead to this disease.