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BMED2405 > Fat disposal > Flashcards

Fat disposal Flashcards

1
Q

Properties of Fat

A
  • hydrophobic
  • fats need to be carried around bloodstream within capsules (lipoproteins)
  • need to emulisfy for digestion
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2
Q

Formation of Emulsions

A

using molecules that have both hydrophobic/philic properties
e.g. phospholipids

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3
Q

purpose of amphiphilic molecules

A
  • acts as a detergent
  • emulsify fat into tiny particles
  • micelles
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4
Q

Where are bile salts made and what from

A
  • liver and from cholesterol
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5
Q

where are bile salts secreted?

A
  • in small intestines

- stored in gall bladder

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6
Q

after digestion what happens to bile salts

A

reabsorbed and taken back into the liver via hepatic portal vein.

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7
Q

purpose of bile salts

A

to surround fat and emulsify

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8
Q

pancreatic lipase

A

hydrolyses fat into FA and glycerol

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9
Q

what happens if bile duct is blocked

A

no bile secreted –> less fat digestion –> lower calorie intake

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10
Q

Orlistat

A

side effects:

  • oily spotting in stool
  • gas with oil discharge
  • need to go to bathroom often
  • fat in faecal species

This indirectly causes people to stop eating fatty foods as if they do they will suffer the consequences

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11
Q

why do we need Lipoproteins

A
  • fats need to be packaged for transport
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12
Q

structure of lipoprotein

A

inside a phospholipid shell - a lipoprotein (shell around the fat which is a monolayer)

coat studded with proteins (apoproteins - enzyme and docking)

different types of lipoproteins (size, internal composition and apoproteins)

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13
Q

Lipoproteins from gut

A
  • lipoproteins made by -intestinal cells
  • chylomicrons (contains fat and dietary cholesterol)
  • they do not enter bloodstream instead go through lymphatics
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14
Q

packaging cholesterol

A
  • esterify

- just to make it completely hydrophobic

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15
Q

chylomicrons

A

interact lipoprotein lipase

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16
Q

what stimulates LPL (lipoprotein lipase)

A

insulin

17
Q

remnants of chylomicron

A
  • remove of fat from chylomicrons (still contains fat)
  • endocytose by liver
  • any fats in the remnants will be in the liver and engulfed by hepatocytes and enter liver
18
Q

What does VLDL stand for

A

Very low density lipoproteins

  • they assemble from fat
  • excreted into bloodstream
19
Q

LDL

A

low density lipoproteins –> strip fat

20
Q

how is cholesterol delivered

A

tissues take LDL through LDL receptor
- cell will indicate through expressing LDL receptors if they want cholesterol. If cells have enough cholesterol they stop expressing LDL receptors

21
Q

What regulates cholesterol

A
  • insulin, cholesterol levels
  • gene expression, enzyme degradation
  • can be inhibited by statins
22
Q

LDL is bad

A
  • LDL become oxidised with time
  • macrophages take up LDL without control (become foam cells)
  • creates inflammatory env –> formation of plagues
23
Q

Reverse Cholesterol transport - HDL

A
  • High density lipoprotein
  • produced by liver ( thins disc of phospholipids)
  • goes back to liver with rest –> bile salts
  • get rid of cholesterol
24
Q

CETP

A

cholesterol ester transfer protein

- catalyses exchange of cholesterol ester for triglyceride

25
Q

consequence of CETP

A

HDL takes back more fat and less cholesterol
Cholesterol remains in circulation
- VLDVL enriched with cholesterol

26
Q

ways to reduce blood cholesterol

A
  • reduce consumption of cholesterol
  • inhibit absorption of choelsterol from gut via competitive inhibitors
  • decrease reabsorption of bile salts using resins that bind bile salts (liver has to make more bile salts from cholesterol)
27
Q

ways to reduce blood cholesterol

A
  • reduce consumption of cholesterol
  • inhibit absorption of choelsterol from gut via competitive inhibitors
  • decrease reabsorption of bile salts using resins that bind bile salts (liver has to make more bile salts from cholesterol)
28
Q

importance of cholersterol

A
  • steroid hormone synthesis

- regulating membrane fluidity

29
Q

Membrane with saturated FA

A
  • no double bonds

- membrane is crystalline

30
Q

Membrane with Unsaturated FA - structure

A
  • unsaturated FA –> kinks

- membrane is less crystalline, more fluid and permeable

31
Q

Trans fats

A
  • catalytic hydrogenation of polyunsaturated fatty acids ( add hydrogen to naturally occuring fat acids, incomplete and random formation of new TRANS double bonds)

BMED2405 (9 decks)

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