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GDAN year 2 nutrition > lipid metabolism > Flashcards

lipid metabolism Flashcards

1
Q

types of lipids and functions

A

triglycerides (fuel)
glycerophospholipids (membranes)
cholestserols (steroid hormones for communication, bile salts for digestion)
vitamins

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2
Q

triglycerdies

A

glycerol
3 fatty acids
joined by ester bonds
unsaturated or saturated

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3
Q

sources of triglycerides

A

diet

carbohydrates (in liver)

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4
Q

how can we absorb dietary liqpids

A

need to be converted to a more absorbable form

1) Bile salts (from gull bladder) and molecules from the pancreas ( lipases, co-lipases, bicarbonate ions) emulsify into small droplets of the fat
2) These have larger SA
3) therefore can be broken down by lipases into fatty acids from triacylglycerols
4) form micelles (fatty acids and 2 monoaclglycerol), absorbed by epithelial cells lining the small intestine (via the action of bile salts)
5) fatty acids and 2 mono..) are put together with some other fats, cholesterol and apolypoproteins which then bind with nascent chylomicrons
6) leave the cell into the lymphatics, packaged as chylomicrons to move around the bloodstream

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5
Q

chylomicrons

A

fat bundled in micelles

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6
Q

how are chylomicrons formed

A
  • micelles enter via diffusion (fat soluble) through membrane
  • processed through small ER which reforms the triaglycerols from the fatty acids
  • apolypoprotiens are added from vesicles from RER
  • proteins added to the bundles of fat
  • golgi then processes further to modify them ect
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7
Q

chylomicron strucures

A 
phospholids on outside
inside
- non polar fats
- tryglycerols, cholesterol ext
apopprotin can sit or embed in phospholiuds
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8
Q

where are chylomicrons exocytosed to

A

into lymphatics

mature in blood stream

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9
Q

Chylomicron fate

A
  • Chylomicrons formed by cells of gut and enter lymphatics into blood stream
  • recognised by lipoproteins of target cells
  • lipoprotein lipase recognise due to the apoproteins in the surface (recognition signals)
  • allows fatty acids to enter the tissues
  • glycerol and other remnants go back to the liver
  • can then be repackage into chylomicrons or other
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10
Q

fate of fatty acids and tissues

A

muscle use for energy

repacked into triglycerol to store fat

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11
Q

what happens to chylokmiron remnants

A
  • recognised by receptors on liver
  • taken up in endocytic vesicles
  • components left over from the chylomicrons (cholesterol, cholesterol ester, amino acids- from the apoproteins, glycerol) can be used in the liver
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12
Q

chylomicrons entering fatty tissue

A
  • Triacylglycerols digested by lipoprotein lipase (LPL), sits on surface of cells that want to use fat
  • LPL produced by adipose (Fat storage), muscle (for burning energy) and lactating mammary gland cells (production of milk)
  • Regulated by insulin, can be released and absorbed
  • Fatty acids (from the triacylglycerols) absorbed by cells; other remnants (glycerol) are absorbed by liver
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13
Q

generating fat from carbs

A

e. if you eat too much food, stored as fat
- fatty acids and glycerol synthesized in the liver
- glucose is the source of carbons
- reactions occur in the cytosol/cytoplasm
fatty acids can be stored as triacylglycerols, oxidised as fuel or used to make components of membranes

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14
Q

wha are fatty acids packaged with once synthesised in liver

A

with proteins to form VLDL(lipoprotein)

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15
Q

what happens if fats are required for tissues outside the liver

A

need to be package

then can circulate rest of body

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16
Q

where are endogenous lipids formed and how

A

in liver
- Glycolysis pathway from glucose
- DHAP (dihydroxyacetone phosphate) precursor for glycerol 3 phosphate then into glycerol
- other components of the pathway can be used to make fatty acids(citrate to acetyl co a to malonyl co a to palmitate), this can combine with the glycerol 3 phosphate made to form triacylcerate
(glycolysis can use intermediates)
- once triglycerols made packaged with apoldprotein, phosphloids, cholesterol, cholesterol estesrs
- released as low density lipoprotein into the blood

17
Q

how are the endogenous lipids (triglycerides) packages to form lipoprotins

A 
with proteins from RER
processes through golgi
into exocytic vesicles
- into lipoproteins termed VLDL (very low density lipoproteins)
FROM ENDOGENOUS LIPIDS NOT DIETARY
18
Q

VLDL fate

A

Triacylglycerols digested by lipoprotein lipase (LPL) (just as chlymicrons

  • LPL is produced by adipose, muscle and lactating mammary gland cells
  • Regulated by insulin
  • Fatty acids absorbed by cells, by the cells that need access to this fat
  • VLDL remnant remains
19
Q

what happens to the VLDL remnants

A
  • Glycerol recycled to the liver, can then be packaged with fatty acids (produced from citric acid cycle) packaged together to form CLDL
  • recognised by lipoprotein lipase on target cells
  • fatty acids taken up by cell
  • glycerol released, remnant components remain
20
Q

what is an energy source during fasting

A

fatty acids

21
Q

fatty acid oxidation

A
  • long chain fatty acids released from adipose tissue, stimulated by reduced insulin and increased glucagon (when we need to release fuel for the tissues)
  • taken up by other tissues and used as a fuel eg muscle, either come from the chylomicrons, VLDL or from acids released from adipose tissue (3 different sources)
  • several different pathways but main one is Beta oxidation
22
Q

Beta oxidation steps

A

Fatty acids enter tissues by diffusion
activated to fatty acyl CoA (via fatty acyl AMP) using ATP
- fatty acyl-CoA transported into mitochondria
- converted to acetyl CoA, producing NADH, FADH2
repeated until all carbons have been converted to acetyl CoA (2C)
- acetyl CoA enters TCA cycle (to produce electron carriers to donate e-) to produce ATP
Fatty acids can be very long i.e. contain lots of carbon, this produces lots of energy

Acetyl Co A only 2 carbons

  • 1 ATP used in the TCA cycle, but can still produce much more ATP overall as many carbons are found in the fatty acid tails (net gain)
  • Fatty acyl Co A processed to produce acetyl co A to enter TCA cycle
  • process repeats again due to the long chain
23
Q

what can fatty acyl Co A be used for

A
  • remake triacylglycerols for energy storage
  • used to make membrane lipids (eg phospholipids)
  • used to make energy
24
Q

types of cholesterol

A

bile salts

steroid hormones

25
Q

use for cholesterol

A
  • component of cell membranes
  • precursor of bile salts
  • precursors of steroid hormones
  • precursor of Vit D
    Major components of blood lipoproteins eg VLDL
  • important in transportation of fats around the body (chylomicron or VLDL carriers)
26
Q

cholesterol absorption

A

1) Enters gut enterocytes (epithelial cells) predominantly by diffusion
2) cholesterol cannot be fully metabolised - amount absorbed must be regulated
3) enterocytes transport excess back into gut lumen
- cholesterol and bile salts excreted in faeces

27
Q

where does cholesterol synthesis occur

A

cytosol (mainly liver)

28
Q

what is the precursor for cholesterol

A

Acetyl - CoA

29
Q

stages of cholesterol synthesis

A

1) Acetyl Co A is converted into mevalonate
- HMG-CoA reductase
- cholesterol lowering drugs
This enzyme is
- increased via inulin
- inhibited by glucagon and cholesterol
- cholesterol works as a negative feedback system
2) Mevalonate to isoprene
3) isoprene (5C) to squalene (30c)
4) squalene to cholesterol
- aromatises it

30
Q

statin use and how

A

used against high cholesterol levels in blood

- competitively inhibit HMG Co- reductase, an enzyme required for cholesterol synthesis

31
Q

cholesterol is secreted from the liver as

A

bile salt
biliary cholesterol
cholesterol esters

32
Q

what happens to bile salts

A
  • stored in gallbladder
  • secreted into gut
  • aid digestion by emulsifying fat, help form micelles that are absorbed
33
Q

what happens to cholesterol esters

A

packaged in VLDL and transported to tissues

34
Q

what happens to biliary cholesterol

A

secreted into gut

can be rebasorebd

35
Q

what can cholesterol do to bile salts

A

dehydroxylate and deconjugte bile salts

36
Q

how is cholesterol transported

A

in lipoproteins

-helps stalibilse the protiens

37
Q

how does cholesterol enter the cell

A

When triglycerides are removed from VLDL and absorbed, a VLDL remnant remains
Remnant mainly cholesterol and cholesterol esters
- when triglycerides are removed from VLDL and absorbed a VLDL remnant remains
- these are then converted to IDL (intermediate density) then LDL
- LDL contain a lot of cholesterol and cholesterol esters

LDL are endocytosed by LDL receptors
- these recognise the apo proteins on the lipoprotein surface

38
Q

what can happen to LDLs (from cholesterol)

A
  • returned to liver to make more VLDL
  • taken up by other cells needing cholesterol
  • membrane synthesis
  • steroid hormone synthesis
39
Q

excess LDL and consequences

A

endocytosed by macrophages (excess LDL from excess cholesterol)

  • this can cause inflammation and contribute to atherosclerosis (in blood vessels)
  • clots form, contribute to a thrombus leading to CVD ect
  • foam cells

GDAN year 2 nutrition (14 decks)

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