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
What percentage of protein comes from diet and endogenous sources?
- D = 50% - E = 50%
26
What are gastric + pancreatic proteases secreted as?
Proenzymes
27
What do gastric chief cells secrete, what is it activated to and by what?
- Pepsinogen - Pepsin - Low intragastric pH
28
What type of enzymes is pepsin?
Endopeptidase
29
5 pancreatic proteases
- Trypsin - Chymotrypsin - Elastase - Carboxypeptidase A - Carboxypeptidase B
30
2 types of pancreatic proteolytic enzyme
- Exopeptidase - Endopeptidase
31
What do endopeptidases have an affinity for, and what do they produce?
- Peptide bonds adjacent to specific AAs - Oligopeptides with 2-6 AAs
32
What do exopeptidases have an affinity for, and what do they produce?
- Peptide bonds adjacent to c-terminus - Individual AAs
33
How are large and small oligopeptides digested?
- Large = brush-border peptidases - Small = cytoplasmic peptidases
34
Where is most of the body's fat depost?
Subcutaneous adipose tissue layers
35
Where can fat also be found in obese/older people?
- Muscle - Visceral deposits
36
Fat-soluble vitamins
A, D, E, K
37
What do fat-soluble vitamins depend on for intestinal absorption?
Solubilisation within bile salt micelles
38
What does vitamin A deficiency cause?
- Night blindness - Corneal drying - Corneal degeneration + blindness - Impaired immunity - Hypokeratosis - Keratosis pilaris
39
What causes vitamin D deficiency?
- Inadequate intake - Inadequate sunlight exposure
40
What does vitamin D deficiency cause?
- Impaired bone mineralisation - Rickets (children) - Osteomalacia (adults) - Osteoporosis - Cancer
41
Role of vitamin E
Antioxidant role in protection against cardiovascular disease + cancer
42
What does vitamin E deficiency cause?
Neurological problems (poor nerve conduction)
43
How is vitamin K obtained?
- Diet - Produced by intestinal bacteria
44
What is vitamin K involved in?
- Carboxylation of specific glutamate residues in proteins - Forms Gla-residues
45
Key roles of Gla-proteins
- Blood coagulation - Bone metabolism - Vascular biology
46
What are fatty acids important in?
- Formation of healthy cell membranes - Development + functioning of brain + nervous system - Production of eicosanoids - Regulating BP, blood viscosity, vasoconstriction, immune + inflammatory response
47
Percentages of types of dietary fats
- Triglyceride = 90% - Phospholipids = 5% - <5% = cholesterol + lipovitamins
48
What does emulsification take place by?
- Food preparation (eg. blending) - Chewing + gastric churning - Squirting of gastric content into duodenum - Intestinal peristalsis
49
What prevents lipid particles coalescing?
- Emulsion droplets coated with membrane lipids, denatured protein, dietary polysaccharides, products of digestion, biliary phospholipids + cholesterol - Polar groups of phospholipids project into water
50
What is the core of an emulsion particle composed of?
- Triglyceride - Cholesteryl esters - Non-polar lipids
51
What is lipid digestion in the mouth mediated by?
Lingual lipase
52
What enzymes digest lipids in the stomach?
- Lingual lipase - Gastric lipase
53
How is gastric lipase secreted and where from?
- Response to gastrin/ACh - Chief cells
54
What do lingual and gastric lipases produce?
- Single fatty acid - Diglyceride
55
Why are long chain fatty acids released in the stomach not absorbed there, and where do they remain?
- Insoluble at acidic pH - In the core of the triglyceride droplet
56
Where are medium- and short-chain fatty acids absorbed, why, and where into?
- In the stomach - Ionised at gastric pH - Into gastric mucosa --> portal blood
57
How do patients with pancreatic insufficiency partly alleviate fat malabsorption?
- Lingual + gastric lipase continues in duodenum - pH remains low as bile not neutralising
58
What do fatty acids trigger the release of in the duodenum, and from where?
- CCK - I-cells in duodenal mucosa
59
What does CCK stimulate?
- Flow of bile into duodenum by gallbladder contraction + relaxation of sphincter of Oddi - Secretion of pancreatic enzymes
60
What does pancreatic co-lipase do?
Act as anchor for binding of lipase by forming co-lipase-pancreatic lipase complex
61
Products of pancreatic lipase
- Fatty acids - 2-monoacylglyceride
62
Mechanics of lipid absorption
- 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
Barriers for lipolytic products to overcome to enter enterocytes
- Mucous gel layer - Unstirred water layer - Apical membrane
64
Movement of short-/medium-chain vs long-chain fatty acids into enterocytes
- 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
What is the enterohepatic circulation?
- Bile salts enter terminal ileum + colon after lipids absorbed - Redirected to liver in portal blood
66
What happens to lipolytic products once in the enterocyte?
- 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
What happens to exported chylomicrons?
- Encounter lipoprotein lipase at cells --> triglycerides hydrolysed to FAs + glycerol - FA + glycerol --> muscle + adipose - Remnant chylomicrons --> liver