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GI digestion Flashcards

1
Q

Describe the cephalic phase of digestion

A
  • Initiation of GI secretions in preparation of a meal - anticipation, sensory characteristics
  • Vagal stimulation via acetylcholine
    ◦ Accomodative relaxation of proximal gastric smooth muscle
    ◦ Enterochromaffin cells cause release of histamine
    ‣ Acts on histamine receptors on gastric parietal cells
    ‣ Increase gastric HCl secretion
    ◦ G-cells
    ‣ secreation of Gastrin –> gastric acid and pepsin secretion
    ◦ Cholinergic stimulus for release of pancreatic secretions and insulin
    ◦ Increased small intestine mobility
  • Saliva secreted PSNS
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2
Q

What are the hormonal phases in response ot a meal

A

Cephalic
Gastric
Intestinal

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3
Q

What triggers the cephalic hormonal response to a meal?

A
  • Initiation of GI secretions in preparation of a meal - anticipation, sensory characteristics
  • Vagal stimulation via acetylcholine
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4
Q

What are the 3 main actions during the cephalic phase of a meal

A

Vagal stimualtion - accomdative relaxation, increased small intestine mobility and saliva

Enterochromaffin cells –> parietal cells increasing acid secretion

G cells - gastric acid and pepsin secretion

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5
Q

What triggers the gastric phase of hormonal responses to a meal

A
  • Gastric wall stretch –> antral pump activity
  • Peptide content in gastric lumen + gastric stretch –> stimulates G-cells in antrum –> increases secretion of gastrin
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6
Q

What causes the release of gastrin?

A

◦ Peptide hormone released due to
‣ Vagal stimulation
‣ Distension of gastric antrum or duodenum
‣ Amino acids, peptides, alcohol, caffeine

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7
Q

What type of hormone is Gastrin

A

◦ Peptide hormone

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8
Q

What inhibits Gastrin secretion

A

◦ Inhibited by
‣ Aciditiy
‣ Somatostatin
‣ Secretin - stimulated by duodenla acidity
‣ Glucagon

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9
Q

What receptor does gastrin act on

A

CCK B receptors -

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10
Q

Actions of Gastrin

A

enterochromaffin cells increasing histamine release
◦ HCl secretion
◦ Stimulates secretion of pepsinogen by chief cells

◦ Increases antral pump function  
◦ Decreases lower oesophageal sphincter pressure
◦ Promotes gastric emptying
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11
Q

Intestinal phase of digestion triggered by?

A
  • As gastric contents emptied into duodenum, low pH stimulates secretion of secretin by duodenal S cells
  • Protein and FFA content in the duodenum stimulates secretion of cholecystokinin by enteroendocrine cells of the duodenum

Blood glucose following absorption triggering insulin secretion

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12
Q

What triggers S cells

A

As gastric contents emptied into duodenum, low pH stimulates secretion of secretin by duodenal S cells

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13
Q

What type of hormone is Secretin?

A

peptide

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14
Q

What cell releases secretin?

A

S cells

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15
Q

What does Secretin do?

A

◦ Inhibits gastric emptying, inhibbits gastric acid secretion
◦ Increases pancreatic secretion of a bicarbonate rich fluid

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16
Q

What causes release of CCK

A
  • Protein and FFA content in the duodenum stimulates secretion of cholecystokinin by enteroendocrine cells of the duodenum
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17
Q

What releases CCK

A

Enteroendocrine cells

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18
Q

What type of hormone is CCK

A

peptide

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19
Q

What are the actions of CCK

A

◦ Function = GRID
‣ Gall bladder contraction
‣ Relaxation of spincter of oddi - release of bile
‣ Increased pancreatic secretion of enzymes for digestion of fats and proteins
‣ Decreased gastric emptying and gastric acid production

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20
Q

Where does somatostatin come from in the gut?

A

D cells in the stomach due to gastric acidity

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21
Q

What are the actions of somatostatin in the gut?

A

◦ Inhibits gastrin secretion and therefore gastric acid production
◦ Reduces gastric motility
◦ Reduces gastric emptying

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22
Q

What are the actions of motilin in the gut?

A

◦ Increases gut motility by propelling chyme forware and initiates migrating motor complex (MMC)

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23
Q

Where does motilin come from

A

Enterochromaffin like cells in the small intestine

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24
Q

What stimulates release of motilin?

A

High pH of intestinal chyme

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25
Q

What triggers release of GIP/

A

Jejunal carbs, FFA and amino acids

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26
Q

What does GIP do?

A

‣ Decresed gut motility
‣ Decreased acid secretion
‣ Insulin release

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27
Q

What is GLP? What does it do?

A
  • GLP - glucagon like peptide
    ◦ Stimulated by fat and carbohydrate meals
    ◦ Decreases gastric emptying
    ◦ Promoting satiety
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28
Q

Where does Ghrelin come from? What does it do?

A

Decreased gastric stretch leads to secretion and increased hunger

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29
Q

What stimulates oral secretions?

A

Eating

Markedly decreased if fasted, asleep, sedated or intubated

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30
Q

WHat is the content of oral secretions?

A
  • Content - hypotonic fluid (not an ultrafiltrate of plasma)
    ◦ 99.8% water; low in sodium
    ◦ high in calcium and phosphate to help remineralise tooth enamel
    ◦ Mucin, IgA, amylase, lipase
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31
Q

How much saliva do you make a day?

A

500-1500ml
90% of this requires stimulation

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32
Q

What is the function of oral secretison

A

Lubrication, digestion (amylase), chemically inert carrier fluid to dissolve molecules for taste sensation

Buffering action, barrier function of mucins, maintaining tooth integrity via remineralisation

Antibacterial activity of Immungoolibilin

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33
Q

Exocrine pancreas % of total pancreatic mass?

A

90%

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34
Q

What is the structure of exocrine pancreas

A

Secretory acini and intercalated ducts

Acini secrete enzyme rich fluid resembling plasma

Ducts alkalinise

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35
Q

How large is the main pancreatic duct?

A

3mm

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36
Q

How much pancreatic secretion is made daily?

A

2500ml

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37
Q

What type of enzymes are in pancreatic fluid?

A

‣ Rich in enzymes (amylase, lipase, trypsin, elastase, nucleases) and proenzymes

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38
Q

Describe the electrolyte composition of pancreatic fluid

A

‣ Na 150, K7, Cl 114, Bicarb 38 initially –> Cl reduced to 40mmol/L, bicarb to 90-140mmol/L

39
Q

How is alkalinisation achieved in the pancreas? What pH is reached?

A

◦ Alkaline-isation (pH 8.0)
‣ alkalinised by exchanging chloride for bicarbonate
‣ the chloride is recycled via the CFTR chloride channel –> CL pumped out via cAMP mediated process (triggered by VIP GPCR) and then exchanged for HCO3

40
Q

WHat is the CFTR chloride channel regulated by?

A

◦ Alkaline-isation (pH 8.0)
‣ alkalinised by exchanging chloride for bicarbonate
‣ the chloride is recycled via the CFTR chloride channel –> CL pumped out via cAMP mediated process (triggered by VIP GPCR) and then exchanged for HCO3

41
Q

What are the 2 processes occuring in pancreatic ducts?

A

Alkilinisation and increased voluem through water secretion

42
Q

How is enzyme content related to volume of secretions in the pancreas?

A

◦ Alkalinity and enzyme content increases in proportion to the rate of flow (higher flow produces more enzyme and bicarbonate secretion)

43
Q

What are the roles of pancreatic exocrine secretions?

A

◦ Digest fats, proteins lipids
◦ alkalinise and buffer the acidic gastric contents to moderate their corrosive effects on the duodenal mucosa especially the microvilli
◦ increase the pH of the duodenal lumen to the point where the pancreatic enzymes are activated- amylase and lipase denatured below pH of 4.5; bile function with micelle formation dependent on pH and works better above pH 2 (pKa 1-2)

44
Q

What increases pancreatic secretions/

A

Vagal innervation
CCK
Secretin

45
Q

What decreases pancreatic seceetion

A

‣ Sympathetic stimulus, eg. shock, surgery
‣ Somatostatin, octreotide - by up to 80%

46
Q

WHat % of pancreatic secretion occurs in each phase of digestion?

A

‣ 20-25% is released during the cephalic phase due to vagal innervation - rich in enzyme but poor in bicarbonate (acinarcells more stimulated than ductal cells)
* Enteropancreatic reflex managed by dorsal brainstem, CCK on vagal nerve endings
‣ 10% is released during the gastric phase - mainly acinar cell product and due to Vagal
‣ 60-80% is released during the intestinal phase
* Cholecystokinin (mainly increases enzyme secretion and rate of pancreatic secretory flow in aceinar cells) - stimulated by intestinal lipid and protein content
* Secretin (mainly increases the bicarbonate secretion in duct cells) and released due to acidic content in duodenum

47
Q

Which hormone increases bicarbonate content of the pancreatic secretory fluid?

A

Secretin

48
Q

Which hormone mainly increases enzyme secretion into pancratic fluid

A

Vagal
CCK

49
Q

How much intestinal secretion is produced per day?

A

2L

50
Q

How would you describe the contents of intestinal secretions? Mainly secreted form? Stimulated by? Inhibited by?

A
  • 2L
  • Bicarbonate rich mucous
  • pH 7.5-8
  • Mainly from duodenum
  • Stimulated by gastrin, histamine and M3 vagal activity
  • Inhibited by somatostatin, VIP, CCK, and secretin
51
Q

What total volume of fluid is produced by the gut per day?

A

7-9L of which 1200ml reaches the colon

52
Q

Describe the digestion and absorption of protein

A
  • Protein denatured by gastric acid causing unravelling and exposing sites for endopeptidase action in the stomach and degraded further by pepsin
    ◦ Pepsinogen is activated by low pH –> however in vivo the use of PPIs does not appear to reduce the absorption of proteins; similarly for post gastrectomy patients
  • Pancreatic enzymes in the duodenum further breakdown protein into amino acids
    ◦ Only activated in the duodenum by change in pH - trypsin, chymotrypsin etc
  • Absorption in proximal SB as amino acids + di and tripeptides through oligopeptide transporters
    ◦ Often cotransporters with H or Na
53
Q

Describe the mechanisms of absorption fo the fat soluble vitamins

A
  • A (Retinol) is fat-soluble and ends up incorporated into micelles, as well as being generated as the product of carotenoids and retinyl esters which are biotransformed in the enterocytes. Diffusion and protein-mediated transport probably both contribute to its absorption. The most rapid uptake is seen when fat is co-ingested.
  • D (Cholecalciferol) is absorbed by passive diffusion in the duodenum and ileum.
  • E (Tocopherol) is absorbed by passive diffusion in the distal jejunum and ileum.
  • K (Phytomenadione) is absorbed by passive diffusion in the jejunum
54
Q

Describe thaimine absorption

A
  • B1 (Thiamine) is readily absorbed in the proximal jejunum, even though its two transport proteins (THTR-1 and THTR-2) are found in the rest of the gut. The most interesting or examinable aspect of its handling in the gut is the fact that its absorption can be affected by chronic alcohol intake.
  • B2 (Riboflavin) is absorbed in the small and large bowel. The active transport mechanism is not dependent on sodium or pH.
  • B3 (Niacin) is one of those rare substances that can be absorbed through the stomach wall (as well as more conventionally in the small intestine). Nobody seems to have a clear idea as to how exactly it is absorbed, other than that the mechanism seems to be dependent on pH and temperature.
55
Q

Describe riboflavin absorption

A
  • B1 (Thiamine) is readily absorbed in the proximal jejunum, even though its two transport proteins (THTR-1 and THTR-2) are found in the rest of the gut. The most interesting or examinable aspect of its handling in the gut is the fact that its absorption can be affected by chronic alcohol intake.
  • B2 (Riboflavin) is absorbed in the small and large bowel. The active transport mechanism is not dependent on sodium or pH.
  • B3 (Niacin) is one of those rare substances that can be absorbed through the stomach wall (as well as more conventionally in the small intestine). Nobody seems to have a clear idea as to how exactly it is absorbed, other than that the mechanism seems to be dependent on pH and temperature.
56
Q

Describe niacin absorption

A
  • B1 (Thiamine) is readily absorbed in the proximal jejunum, even though its two transport proteins (THTR-1 and THTR-2) are found in the rest of the gut. The most interesting or examinable aspect of its handling in the gut is the fact that its absorption can be affected by chronic alcohol intake.
  • B2 (Riboflavin) is absorbed in the small and large bowel. The active transport mechanism is not dependent on sodium or pH.
  • B3 (Niacin) is one of those rare substances that can be absorbed through the stomach wall (as well as more conventionally in the small intestine). Nobody seems to have a clear idea as to how exactly it is absorbed, other than that the mechanism seems to be dependent on pH and temperature.
57
Q

Describe folate absorption

A
  • B9 (Folate) is present in the diet in the form of a polymer, which needs to be hydrolysed in the proximal half of the small bowel. It is then absorbed in the proximal half of the small bowel by a proton-coupled pH-dependent mechanism, through several different transport proteins.
  • B12 (Cobalamin) comes in a complex with dietary protein, and is usually liberated by the action of pepsin in the stomach. It is then protected by being bound to Intrinsic Factor, a glycoprotein that protects it from the lytic activity of upper GI enzymes. That is how it makes its way to the terminal ileum, where it is absorbed (the whole IF-cobalamin complex is entrained by the absorption mechanism).
58
Q

Describe B12 absoroption

A
  • B9 (Folate) is present in the diet in the form of a polymer, which needs to be hydrolysed in the proximal half of the small bowel. It is then absorbed in the proximal half of the small bowel by a proton-coupled pH-dependent mechanism, through several different transport proteins.
  • B12 (Cobalamin) comes in a complex with dietary protein, and is usually liberated by the action of pepsin in the stomach. It is then protected by being bound to Intrinsic Factor, a glycoprotein that protects it from the lytic activity of upper GI enzymes. That is how it makes its way to the terminal ileum, where it is absorbed (the whole IF-cobalamin complex is entrained by the absorption mechanism).
59
Q

Describe vitamin C absorption

A
  • C (Ascorbic acid) is actively co-transported with sodium by a brush border transport protein SVCT1. The transport is saturable, or at least regulated in a way that ensures that excess ingestion does not translate into dangerously high blood levels. The site of absorption is distal ileum and jejunum`
60
Q

How is water absorbed in the gut

A

Water absorption is near-complete, rapid, and mainly occurs in the proximal small bowel. Most of the diffusion is transcellular. It is driven by osmotic mechanisms: an osmotic gradient is generated by the active absorption of other electrolytes, especially sodium.

61
Q

Describe sodium reabsorption in the gut

A

Sodium absorption is coupled to the transport of other substances, as one might have noticed from the above. Virtually everything is co-transported with sodium in the jejunum. In the ileum and colon, there are other mechanisms, including transport by sodium/proton transporters (NHE2, NHE3, and NHE8) as well as the aldosterone-responsive ENac channels.

62
Q

Describe chloride absorption in the gut?

A

Chloride absorption and sodium absorption are linked in order to maintain electroneutrality. Chloride is usually absorbed as the net result of the balance between channel-mediated absorption and cAMP/ATP-gated channel-mediated secretion. The latter is the work of the CFTR protein, the same chloride channel affected by cystic fibrosis and the toxin of Vibrio cholerae.D

63
Q

Describe K absorption in the gut

A

Potassium absorption in the small intestine occurs by passive paracellular diffusion, which is completely unregulated. Absorption is purely driven by the concentration gradient.

64
Q

Describe magnesium absorption in the gut

A

Magnesium absorption is 90% by passive paracellular mechanisms, and the rest is subject to some sort of saturable transcellular facilitated transport. This mainly happens in the distal small bowel (jejunum and ileum).

65
Q

Describe calcium absorption in the gut

A

Calcium absorption occurs in the duodenum by some active transcellular process, and passively along the rest of the gut. When calcium uptake is high or normal, it is the paracellular passive uptake that accounts for the majority of the gastrointestinal absorption.

66
Q

How are carbohydrates absorbed?

A

x ◦ Carbohydrates on ingestion broken down to monosaccharides and disaccharides within intestinal lumen and by brush border enzymes and intestinal mucosal cells (maltase, lactase and sucrase) cleaved disaccharides into hexoses
◦ Absorbed to portal veinous system - active, energy dependent process

67
Q

What are the monosacchardides

A
  • Only monosaccharides are absorbed from the bowel therefore all dietary carbohydrates need to be converted to either glucose, galactose, fructose
68
Q

What are the dietary carbohydrates?

A
  • Dietary carbohydrates
    ◦ Starches - mostly as amylopectin a branched polyglucose contains alpha- 1,4 and alpha 1,6 linkages (all plant starches are polymers of glucose, polysaccharide storage in animals is glycogen a glucose polymer)
    ◦ Oligosaccharides - mostly disaccharides sucrose and lactose
69
Q

Describe early digestion of carbohydrates

A
  • Salivary alpha amylase
    ◦ Produced in the mouth
    ◦ Digestion sites - primarily in the stomach at higher pH or the intestine (pH 4-7)
    ◦ Inactivated by low pH of the stomach (optimal pH for activity 6.7)
  • Pancreatic alpha amylase
    ◦ Pancreatic origin, Important for starch digestion in small intestine
    ◦ Cannot act on alpha 1,6 or terminal alpha 1,4 bonds (or ones adjacent to alpha 1,6 bonds) therefore cannot produce monosaccharides instead producing
    ‣ Maltose
    ‣ Maltotriose
    ‣ Alpha limit dextrins - amylopectin end product of amylase digestion (glucose polymers)
70
Q

What is the role of salivary amylase in carbohdyrate digestion

A
  • Salivary alpha amylase
    ◦ Produced in the mouth
    ◦ Digestion sites - primarily in the stomach at higher pH or the intestine (pH 4-7)
    ◦ Inactivated by low pH of the stomach (optimal pH for activity 6.7)
  • Pancreatic alpha amylase
    ◦ Pancreatic origin, Important for starch digestion in small intestine
    ◦ Cannot act on alpha 1,6 or terminal alpha 1,4 bonds (or ones adjacent to alpha 1,6 bonds) therefore cannot produce monosaccharides instead producing
    ‣ Maltose
    ‣ Maltotriose
    ‣ Alpha limit dextrins - amylopectin end product of amylase digestion (glucose polymers)
71
Q

What is the role of pancreatic alpha amylase in carbohydrate digestion

A
  • Salivary alpha amylase
    ◦ Produced in the mouth
    ◦ Digestion sites - primarily in the stomach at higher pH or the intestine (pH 4-7)
    ◦ Inactivated by low pH of the stomach (optimal pH for activity 6.7)
  • Pancreatic alpha amylase
    ◦ Pancreatic origin, Important for starch digestion in small intestine
    ◦ Cannot act on alpha 1,6 or terminal alpha 1,4 bonds (or ones adjacent to alpha 1,6 bonds) therefore cannot produce monosaccharides instead producing
    ‣ Maltose
    ‣ Maltotriose
    ‣ Alpha limit dextrins - amylopectin end product of amylase digestion (glucose polymers)
72
Q

What can pancreatic amylase not act on? Therefore cannot produce what?

A
  • Salivary alpha amylase
    ◦ Produced in the mouth
    ◦ Digestion sites - primarily in the stomach at higher pH or the intestine (pH 4-7)
    ◦ Inactivated by low pH of the stomach (optimal pH for activity 6.7)
  • Pancreatic alpha amylase
    ◦ Pancreatic origin, Important for starch digestion in small intestine
    ◦ Cannot act on alpha 1,6 or terminal alpha 1,4 bonds (or ones adjacent to alpha 1,6 bonds) therefore cannot produce monosaccharides instead producing
    ‣ Maltose
    ‣ Maltotriose
    ‣ Alpha limit dextrins - amylopectin end product of amylase digestion (glucose polymers)
73
Q

Brush border carbohydrate metabolism is done by?

A
  • Contain 5 oligosaccharidases converting digestible oligosaccharides to monosaccharides for absorption - 80% glucose
    ◦ Sucrase - produces fructose and glucose from sucrose,also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Lactase - produces galactose and glucose from lactose
    ◦ Alpha limit dextrinase - produces glucose from alpha limit dextrins, also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Maltose - glucose from maltose and maltotriose
    ◦ Trehelase proudcing glucose from the haloes (1:1alpha glucose dimer)
74
Q

What is sucrose made up of

A
  • Contain 5 oligosaccharidases converting digestible oligosaccharides to monosaccharides for absorption - 80% glucose
    ◦ Sucrase - produces fructose and glucose from sucrose,also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Lactase - produces galactose and glucose from lactose
    ◦ Alpha limit dextrinase - produces glucose from alpha limit dextrins, also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Maltose - glucose from maltose and maltotriose
    ◦ Trehelase proudcing glucose from the haloes (1:1alpha glucose dimer)
75
Q

What is lactose made up of

A
  • Contain 5 oligosaccharidases converting digestible oligosaccharides to monosaccharides for absorption - 80% glucose
    ◦ Sucrase - produces fructose and glucose from sucrose,also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Lactase - produces galactose and glucose from lactose
    ◦ Alpha limit dextrinase - produces glucose from alpha limit dextrins, also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Maltose - glucose from maltose and maltotriose
    ◦ Trehelase proudcing glucose from the haloes (1:1alpha glucose dimer)
76
Q

What is dextrin made up of

A
  • Contain 5 oligosaccharidases converting digestible oligosaccharides to monosaccharides for absorption - 80% glucose
    ◦ Sucrase - produces fructose and glucose from sucrose,also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Lactase - produces galactose and glucose from lactose
    ◦ Alpha limit dextrinase - produces glucose from alpha limit dextrins, also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Maltose - glucose from maltose and maltotriose
    ◦ Trehelase proudcing glucose from the haloes (1:1alpha glucose dimer)
77
Q

What is maltose made up of

A
  • Contain 5 oligosaccharidases converting digestible oligosaccharides to monosaccharides for absorption - 80% glucose
    ◦ Sucrase - produces fructose and glucose from sucrose,also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Lactase - produces galactose and glucose from lactose
    ◦ Alpha limit dextrinase - produces glucose from alpha limit dextrins, also important for hydrolysis of maltose and maltotriose to glucose
    ◦ Maltose - glucose from maltose and maltotriose
    ◦ Trehelase proudcing glucose from the haloes (1:1alpha glucose dimer)
78
Q

How is glucose absorbed from the gut

A
  • Glucose and sodium cotransported at the luminal/apical membrane - secondary active transport
    ◦ Energy provided by low intracellular sodium concentration produced from the sodium/potassium cotransporter
    ◦ Glucose concentration may be higher or lower in the cell than the lumen but does not affect transport
    ◦ Activity increased by increased sodium in the bowel (i.e. this is the basis for sodium containing glucose electrolyte solutions in infantile diarrhoea)
    ◦ Galactose competes with glucose for the same cotransporter
  • GLUT 1-5 - membrane sodium independent transporters
    ◦ Fructose is absorbed across the apical membrane by GLUT5
    ◦ Glucose and fructose both use GLUT2 to cross the basso lateral membrane
  • Both galactose and fructose can be converted to glucose to enter the glycolytic pathway
  • Pentose sugars e.g.ribose absorbed by simple diffusion
  • Insulin plays NO role in this
79
Q

How are galactose and fructose utilised?

A
  • Both galactose and fructose can be converted to glucose to enter the glycolytic pathway
80
Q

How does fructose get absorbed

A
  • GLUT 1-5 - membrane sodium independent transporters
    ◦ Fructose is absorbed across the apical membrane by GLUT5
    ◦ Glucose and fructose both use GLUT2 to cross the basso lateral membrane
81
Q

How is galactose absorbed

A
  • Glucose and sodium cotransported at the luminal/apical membrane - secondary active transport
    ◦ Energy provided by low intracellular sodium concentration produced from the sodium/potassium cotransporter
    ◦ Glucose concentration may be higher or lower in the cell than the lumen but does not affect transport
    ◦ Activity increased by increased sodium in the bowel (i.e. this is the basis for sodium containing glucose electrolyte solutions in infantile diarrhoea)
    ◦ Galactose competes with glucose for the same cotransporter
82
Q

How is glucose absorption optimised from the gut?

A

Activity of glucose absorptino increased by increased sodum delivery in the bowel as this increases the concentration gradient for sodium/glucose cotransport

83
Q

What are the 3 main dietary fats

A

Dietary fat
* Triglyceride esters - the dominant form of ingested dietary fat
* Cholesterol
* Phospholipids

84
Q

What happens to dietary fat to be absorbed

A

Dietary fat is digested and absorbed in the small intestine, initially bile salts are required to emulsify the ingested triglyceride esters making them water soluble before digestion occurs through pancreatic lipases and phospholipases which hydrolyse dietary triglycerides to monoglycerides (glycerol) and fatty acids for absorption. Dietary cholesterol is cleaved by cholesterol esterases to fatty acids, and phospholipase A cleaves fatty acids from phospholipids. These factors are re-combined within enterocytes to triglycerides, cholesterol and phospholipids and transported to the blood stream in chylomicrons with the addition of apoliproteins through lymph via the thoracic duct to the R and L subclavians.

85
Q

How is cholesterol digested and absorbed

A

Dietary fat is digested and absorbed in the small intestine, initially bile salts are required to emulsify the ingested triglyceride esters making them water soluble before digestion occurs through pancreatic lipases and phospholipases which hydrolyse dietary triglycerides to monoglycerides (glycerol) and fatty acids for absorption. Dietary cholesterol is cleaved by cholesterol esterases to fatty acids, and phospholipase A cleaves fatty acids from phospholipids. These factors are re-combined within enterocytes to triglycerides, cholesterol and phospholipids and transported to the blood stream in chylomicrons with the addition of apoliproteins through lymph via the thoracic duct to the R and L subclavians.

86
Q

How are TG absorbed

A

Dietary fat is digested and absorbed in the small intestine, initially bile salts are required to emulsify the ingested triglyceride esters making them water soluble before digestion occurs through pancreatic lipases and phospholipases which hydrolyse dietary triglycerides to monoglycerides (glycerol) and fatty acids for absorption. Dietary cholesterol is cleaved by cholesterol esterases to fatty acids, and phospholipase A cleaves fatty acids from phospholipids. These factors are re-combined within enterocytes to triglycerides, cholesterol and phospholipids and transported to the blood stream in chylomicrons with the addition of apoliproteins through lymph via the thoracic duct to the R and L subclavians.

87
Q

What happens to dietary fat before it reaches the intestine

A
  • Lingual lipase contributes minor role to fat processing
  • Gastric lipase from chief cells minor role
88
Q

What happens to fats in the duodenum?

A

◦ Fat and carbohydrates in duodenum –> CCK release –> gallbladder contraction
◦ Bile salts emulsify fat
‣ ingested TG esters water soluble - dispersed more easily through water layer at surface of enterocyctes optimising diffusion of smaller particles
‣ Emulsification prevent re-coalescence of micelledfat reducing droplet size increasing surface area, while also pushing other substances from droplet surface optimising the action of enzymatic breakdown
* digestion occurs through pancreatic lipases and phospholipases (esp phospholipase A) which hydrolyse dietary triglycerides to monoglycerides (glycerol) and fatty acids for absorption.
‣ Dietary cholesterol is cleaved by cholesterol esterases to fatty acids
◦ Absorption in proximal small bowel via protein mediated transport and passive diffusion of FFA and monoacylglycerol
* These factors are re-combined within enterocytes to triglycerides, cholesterol and phospholipids and transported to the blood stream in chylomicrons with the addition of apoliproteins through lymph via the thoracic duct to the R and L subclavians.

89
Q

What does fat in the duodenum trigger in response

A

CCK release

90
Q

What breaks down fat in the duodenum

A
  • digestion occurs through pancreatic lipases and phospholipases (esp phospholipase A) which hydrolyse dietary triglycerides to monoglycerides (glycerol) and fatty acids for absorption.
    ‣ Dietary cholesterol is cleaved by cholesterol esterases to fatty acids
91
Q

Why is emulsification important?

A

‣ ingested TG esters water soluble - dispersed more easily through water layer at surface of enterocyctes optimising diffusion of smaller particles
‣ Emulsification prevent re-coalescence of micelledfat reducing droplet size increasing surface area, while also pushing other substances from droplet surface optimising the action of enzymatic breakdown

92
Q

What is the fate of dietary cholesterol

A

Cleaved to fatty acids by cholesterol esterases

93
Q

How are fatty acids absorbed

A

Small bowel by protein mediated transport and passive diffusion

94
Q
A

Gastro nutrition (7 decks)

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