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dig > Digestion and Absorption of Carbohydrate, Protein and Fat > Flashcards

Digestion and Absorption of Carbohydrate, Protein and Fat Flashcards

1
Q

What percentage of dietary carbs is starch?

A

45-60%

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2
Q

What is starch composed of?

A
  • Amylose
  • Amylopectin
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3
Q

Amylose structure

A

Straight-chain glucose polymer connected by α-1,4 linkages

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4
Q

Amylopectin structure

A

Branched glucose polymer with both α-1,4 + α-1,6 linkages

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5
Q

How is glycogen similar and different to amylopectin?

A
  • S = α-1,4 + α-1,6 linkages
  • D = more highly branched
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6
Q

What percentage of dietary carbs are disaccharides, and what are the 2?

A
  • 30-40%
  • Sucrose + lactose
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7
Q

What percentage of dietary carbs are monosaccharides, and what are the 2?

A
  • 5-10%
  • Fructose + glucose
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8
Q

What is the only type of carbohydrate the small intestine can absorb?

A

Monosaccharides

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9
Q

2 steps in the process of digestion of carbs

A
  • Intraluminal hydrolysis of starch to oligosaccharides
  • Membrane digestion of oligosaccharides to monosaccharides
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10
Q

Which enzymes are responsible for each step of the digestion of carbs?

A
  • Intraluminal hydrolysis = salivary + pancreatic amylases
  • Membrane digestion = brush-border disaccharidases
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11
Q

What is salivary amylase deactivated by?

A

Gastric acid

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12
Q

What is pancreatic amylase induced by?

A

CCK

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13
Q

How does amylase work, and what is produced?

A
  • Cleaves internal α-1,4 linkages of starch (not terminal, α-1,6 or α-1,4 next to α-1,6)
  • Maltose, maltotriose, α-limit dextrins
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14
Q

3 brush-border disaccharidases

A
  • Lactase
  • Maltase
  • Sucrose-isomaltase
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15
Q

What does lactase digest and what is produced?

A
  • Lactose
  • Glucose + galactose
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16
Q

What linkages do maltase, sucrase and isomaltase cleave?

A

Terminal α-1,4 linkages of maltose, maltotriose + α-limit dextrins

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17
Q

What dose sucrase digest and into what?

A
  • Sucrose
  • Glucose + fructose
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18
Q

What linkages can only isomaltase cleave?

A

Branching α-1,6 linkages of α-limit dextrins

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19
Q

Where is peak oligosaccharide distribution?

A

Proximal jejunum

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20
Q

How are glucose and galactose transported into epithelial cells?

A
  • Na+/K+ ATPase establishes Na+ electrochemical gradient
  • Sodium glucose linked transporter 1 (SGLT1) co-transports carbs in with Na+
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21
Q

How does fructose enter epithelial cells?

A

Through GLUT5 transporter

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22
Q

How are glucose, fructose and galactose effluxed out across the basolateral membrane?

A

Through GLUT2

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23
Q

Why does breath H2 increase in patients with a primary lactase deficiency ingesting lactose?

A
  • Non-absorbed lactose is metabolised by colonic bacteria to H2
  • This is absorbed into the blood and secreted by the lungs
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24
Q

Treatment of a lactase deficiency

A
  • Reducing/eliminating milk + milk products from diet
  • Use milk products with commercial lactase preparation
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25
Q

What percentage of protein comes from diet and endogenous sources?

A
  • D = 50%
  • E = 50%
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26
Q

What are gastric + pancreatic proteases secreted as?

A

Proenzymes

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27
Q

What do gastric chief cells secrete, what is it activated to and by what?

A
  • Pepsinogen
  • Pepsin
  • Low intragastric pH
28
Q

What type of enzymes is pepsin?

A

Endopeptidase

29
Q

5 pancreatic proteases

A
  • Trypsin
  • Chymotrypsin
  • Elastase
  • Carboxypeptidase A
  • Carboxypeptidase B
30
Q

2 types of pancreatic proteolytic enzyme

A
  • Exopeptidase
  • Endopeptidase
31
Q

What do endopeptidases have an affinity for, and what do they produce?

A
  • Peptide bonds adjacent to specific AAs
  • Oligopeptides with 2-6 AAs
32
Q

What do exopeptidases have an affinity for, and what do they produce?

A
  • Peptide bonds adjacent to c-terminus
  • Individual AAs
33
Q

How are large and small oligopeptides digested?

A
  • Large = brush-border peptidases
  • Small = cytoplasmic peptidases
34
Q

Where is most of the body’s fat depost?

A

Subcutaneous adipose tissue layers

35
Q

Where can fat also be found in obese/older people?

A
  • Muscle
  • Visceral deposits
36
Q

Fat-soluble vitamins

A

A, D, E, K

37
Q

What do fat-soluble vitamins depend on for intestinal absorption?

A

Solubilisation within bile salt micelles

38
Q

What does vitamin A deficiency cause?

A
  • Night blindness
  • Corneal drying
  • Corneal degeneration + blindness
  • Impaired immunity
  • Hypokeratosis
  • Keratosis pilaris
39
Q

What causes vitamin D deficiency?

A
  • Inadequate intake
  • Inadequate sunlight exposure
40
Q

What does vitamin D deficiency cause?

A
  • Impaired bone mineralisation
  • Rickets (children)
  • Osteomalacia (adults)
  • Osteoporosis
  • Cancer
41
Q

Role of vitamin E

A

Antioxidant role in protection against cardiovascular disease + cancer

42
Q

What does vitamin E deficiency cause?

A

Neurological problems (poor nerve conduction)

43
Q

How is vitamin K obtained?

A
  • Diet
  • Produced by intestinal bacteria
44
Q

What is vitamin K involved in?

A
  • Carboxylation of specific glutamate residues in proteins
  • Forms Gla-residues
45
Q

Key roles of Gla-proteins

A
  • Blood coagulation
  • Bone metabolism
  • Vascular biology
46
Q

What are fatty acids important in?

A
  • Formation of healthy cell membranes
  • Development + functioning of brain + nervous system
  • Production of eicosanoids
  • Regulating BP, blood viscosity, vasoconstriction, immune + inflammatory response
47
Q

Percentages of types of dietary fats

A
  • Triglyceride = 90%
  • Phospholipids = 5%
  • <5% = cholesterol + lipovitamins
48
Q

What does emulsification take place by?

A
  • Food preparation (eg. blending)
  • Chewing + gastric churning
  • Squirting of gastric content into duodenum
  • Intestinal peristalsis
49
Q

What prevents lipid particles coalescing?

A
  • Emulsion droplets coated with membrane lipids, denatured protein, dietary polysaccharides, products of digestion, biliary phospholipids + cholesterol
  • Polar groups of phospholipids project into water
50
Q

What is the core of an emulsion particle composed of?

A
  • Triglyceride
  • Cholesteryl esters
  • Non-polar lipids
51
Q

What is lipid digestion in the mouth mediated by?

A

Lingual lipase

52
Q

What enzymes digest lipids in the stomach?

A
  • Lingual lipase
  • Gastric lipase
53
Q

How is gastric lipase secreted and where from?

A
  • Response to gastrin/ACh
  • Chief cells
54
Q

What do lingual and gastric lipases produce?

A
  • Single fatty acid
  • Diglyceride
55
Q

Why are long chain fatty acids released in the stomach not absorbed there, and where do they remain?

A
  • Insoluble at acidic pH
  • In the core of the triglyceride droplet
56
Q

Where are medium- and short-chain fatty acids absorbed, why, and where into?

A
  • In the stomach
  • Ionised at gastric pH
  • Into gastric mucosa –> portal blood
57
Q

How do patients with pancreatic insufficiency partly alleviate fat malabsorption?

A
  • Lingual + gastric lipase continues in duodenum
  • pH remains low as bile not neutralising
58
Q

What do fatty acids trigger the release of in the duodenum, and from where?

A
  • CCK
  • I-cells in duodenal mucosa
59
Q

What does CCK stimulate?

A
  • Flow of bile into duodenum by gallbladder contraction + relaxation of sphincter of Oddi
  • Secretion of pancreatic enzymes
60
Q

What does pancreatic co-lipase do?

A

Act as anchor for binding of lipase by forming co-lipase-pancreatic lipase complex

61
Q

Products of pancreatic lipase

A
  • Fatty acids
  • 2-monoacylglyceride
62
Q

Mechanics of lipid absorption

A
  • Surface triglycerides of emulsion droplet hydrolysed + replaced by more from core –> size decreasing
  • Leads to budding off of main droplet to form multi-lamellar vesicle
  • Addition of more bile slats to vesicles thins out lipid coating –> uni-lamellar vesicle
  • These converted into mixed micelles containing bile salts + mixed lipids
63
Q

Barriers for lipolytic products to overcome to enter enterocytes

A
  • Mucous gel layer
  • Unstirred water layer
  • Apical membrane
64
Q

Movement of short-/medium-chain vs long-chain fatty acids into enterocytes

A
  • S/M = readily soluble in water, diffuse easily through water layer into cell
  • L = solubility decreases, but partitioning into micelles increases –> fatty acids protonated by low pH generated by Na+/H+ exchange at cell –> leave micelle and enter cell
65
Q

What is the enterohepatic circulation?

A
  • Bile salts enter terminal ileum + colon after lipids absorbed
  • Redirected to liver in portal blood
66
Q

What happens to lipolytic products once in the enterocyte?

A
  • Triglycerides re-formed in SER
  • Fat droplets formed in SER from triglycerides
  • Apoproteins formed in RER + transferred to SER to be combined with fat droplets
  • Lipid droplets enter chylomicrons and travel in vesicles
  • Vesicles fuse with basolateral membrane –> chylomicron enters lymph
67
Q

What happens to exported chylomicrons?

A
  • Encounter lipoprotein lipase at cells –> triglycerides hydrolysed to FAs + glycerol
  • FA + glycerol –> muscle + adipose
  • Remnant chylomicrons –> liver

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