Lecture 12 - Digestion and Absorption of Fat Flashcards

1
Q

What is fatty acid beta-oxidation?

A

The process where fatty acids are broken down to produce energy. The transfer of electrons in the form of hydrogen from fatty acids to specific molecules, can then be used to generate ATP.

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2
Q

Wha are the stages of beta-oxidation?

A

1 - Fatty acid chain initially is converted to fatty acyl-CoA. It utilises energy here, it consumes energy.
2 - Fatty acyl-CoA enters a cycle of reactions. Firstly, an oxidation step that liberates energy in the form of FAD –> FADH2 via acyl-CoA dehydrogenase
3 - Hydration step
4 - Oxidation step, liberating energy in form of NAD+ –> NADH via L-hydroxyacyl-CoA dehydrogenase
5 - Cleavage step, cleavage of acetyl-CoA from fatty acyl-CoA.
6 - Depending on how long the remnant fatty acyl-CoA is, it can then go back into this cyclical process and liberate more energy and acetyl-CoA

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3
Q

What are the symptoms of vitamin A deficiency?

A
  • Night blindness
  • Corneal dying
  • Corneal degeneration
  • Blindness
  • Impaired immunity
  • Hypokeratosis
  • Keratosis pilaris
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4
Q

What are the symptoms of vitamin A overdosing?

A
  • Hair loss
  • Nausea
  • Jaundice
  • Irritability
  • Vomiting
  • Blurry vision
  • Headaches
  • Muscle and abdominal pain
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5
Q

What are the symptoms of vitamin D deficiency?

A
  • Impaired bone mineralisation
  • Bone softening diseases
  • Rickets in children
  • Osteomalacia in adults
  • Possibly contributes to osteoporosis
  • May also be linked to cancer
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6
Q

What is the main symptom of vitamin E deficiency?

A

Neurological problems due to poor nerve conduction

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7
Q

What are the symptoms of essential fatty acid deficiency?

A
  • hemorrhagic dermatitis
  • Skin atrophy
  • Scaly dermatitis
  • Dry skin
  • Weakness
  • Impaired vision
  • Tingling sensations
  • Mood swings
  • Edema
  • High blood pressure
  • High triglycerides
  • hemorrhagic foliculitis
  • Immune and Mental deficiencies
  • Impaired growth
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8
Q

What are the stages of emulsification?

A
  1. Food preparation
  2. Chewing and gastric churning which allows mixing lingual and gastric juices
  3. Squirting gastric contents into the duodenum
  4. Interstitial peristalsis mixes luminal contents with pancreatic and biliary secretions
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9
Q

What prevents these lipid particles from coalescing?

A
  • Coating the emulsion droplets with membrane lipids, denatured protein, dietary polysaccharides, production of digestion and biliary phospholipids and cholesterol.
  • The polar groups of the phospholipids project into the water; and thus prevent coalescence of the emulsion particles
  • The core of the emulsion particle is composed of triglycerides, which also contains cholesterol esters and other non-polar lipids
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10
Q

What does lingual and gastric lipase initiate?

A

Lipid digestion

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11
Q

What does CCK stimulate?

A
  1. flow of bile into the duodenum by gall bladder contraction and relaxation of odd.
  2. The secretion of pancreatic enzymes, including lipase and esterase’s.
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12
Q

How is CCK released?

A

Once the fatty acids generated in the stomach reach the duodenum, they trigger the release of CCK from I cells in the duodenal mucosa.

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13
Q

What does full lipolytic activity of pancreatic lipase require?

A

Colipase, alkaline pH, bile salts, fatty acids.

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14
Q

What is the function of co-lipase?

A
  • acting as an anchor for the binding of lipase

- first forms a collapse-pancreatic-lipase complex that can then bind to the lipase interface.

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15
Q

What barriers need to be overcome for lipolytic products to get into enterocytes?

A
  1. Mucous gel layer that lines the intestinal epithelial surface.
  2. Unstirred water membrane.
  3. Apical membrane.
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16
Q

How do short/medium chain fatty acids get into enterocytes?

A

Diffusion through the unstirred water layer and into the enterocyte is efficient.
As chain length increases, solubility in water decreases, whereas its partitioning into micelles increases.

17
Q

What happens when fatty acid/bile salt mixed micelles reach the enterocyte surface?

A

They encounter a low-pH generated by Na-H exchange at the brush-border membrane. The fatty acids are protonated and leave the mixed micelle to enter the enterocyte by either non-ionic diffusion, collision and incorporation into cell membrane, active carrier mediated processes.

18
Q

What happens to the remaining bile salts after entry into the enterocyte?

A

Absorbed at the terminal ileum and colon, where they are redirected to the liver in the portal blood. This is known as the enterohepatic circulation.

19
Q

Describe re-esterification?

A
  1. Long chain fatty acids bind to fatty acid-binding proteins.
  2. The re-esterification to form triglycerides occurs within the SER, using either absorbed 2-MG or glycerol-3-phosphate as a substrate.
20
Q

What happens to exported chylomicrons?

A

Find their way to the endothelial surface, where they encounter lipoprotein lipase, which hydrolyses triglycerides in the chylomicrons to fatty acids and glycerol-muscle and adipose tissue.

21
Q

What is the main symptom of fat malabsorption?

A

Steatorrhea - bulky stool

22
Q

What are some reasons for fat malabsorption?

A
  • Impaired bile acid production.
  • Lipase activity.
  • Compromised small bowel.
  • Impaired chylomicron formation.