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Nutrition > Lipid metabolism > Flashcards

Lipid metabolism Flashcards

1
Q

Which lipids are used as fuel

A

Triacylglycerols

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2
Q

Which lipids are used in membranes

A

Glycerophospholipids

Cholesterol

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3
Q

Which lipids are used in lipid digestion

A

Bile salts (from cholesterol)

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4
Q

Which lipids are used in communication

A

Steroid hormones (from cholesterol)

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5
Q

Which lipids are used in vision, growth

A

Vitamins

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6
Q

Triacylglycerols composed of

A

Glycerol and three fatty acids

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7
Q

Triacylglycerols joined by

A

Ester bonds

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8
Q

Triacylglycerols efficient form to

A

Store energy
Body has almost unlimited ability to store these
Can be saturated or unsaturated

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9
Q

Fatty acids

A

Have variable length

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10
Q

Sources of lipids

A

Diet

Carbohydrates (in liver)

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11
Q

Major dietary lipid

A

Triacylglycerols

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12
Q

Digestion of dietary lipids: what emulsifies

A

Bile salts

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13
Q

Digestion of dietary lipids: what breaks down fatty acids from triacylglycerols

A

Lipases

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14
Q

Digestion of dietary lipids: fatty acids form

A

Micelles, absorbed by epithelial cells, packaged as chylomicrons

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15
Q

Chylomicrons

A

Comprised of layer of phospholipids (hydrophilic head, hydrophobic tails)
Apoproteins added in RER, packaged together in golgi and then become part of chylomicron

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16
Q

What happens to chylomicrons?

A

Triacylglycerols digested by lipoprotein lipase (LPL)
LPL produced by adipose, muscle and lactating mammary gland cells
Regulated by insulin
Fatty acids absorbed by cells; other remnants absorbed by liver

17
Q

HDL (high density lipoprotein)

A

Mature them into final chylomicrons by adding components

18
Q

Lipoprotein lipase sat on surface of cells

A 
Recognise apoproteins (e.g. C2)
Receptor and enzymes
Digesting fatty acids, remnants back into blood stream, apoproteins recognised by liver
19
Q

Endogenous lipids

A 
Fatty acids synthesised in liver
Glucose is source of carbons
Reactions occur in cytosol
Fatty acids can be stored as triacylglycerols, oxidised as fuel or used to make components of membranes
Packaged with proteins to form VLDL
20
Q

Endogenous lipids

A

Fatty acids synthesised in liver
Glucose is source of carbons
Reactions occur in cytosol
Fatty acids can be stored as triacylglycerols, oxidised as fuel or used to make components of membranes
Packaged with proteins to form VLDL (released to blood)

21
Q

Functions of TCA cycle except for to produce energy

A

To make fats

e.g. Citrate –> fatty acid synthase

22
Q

VLDL

A

Newly formed triaglycerides packaged into lipoproteins for secretion
Very low density lipoprotein
In this form they are transported to other tissues
Similar structure to chylomicron

23
Q

VLDL Fate

A

Triacylglycerols digested by lipoprotein lipase (LPL)
LPL produced by adipose, muscle and lactating mammary gland cells
Regulated by insulin
Fatty acids absorbed by cells
VLDL remnant remains

24
Q

Fatty acid oxidation

A

Fatty acids are important fuel source
During fasting, fatty acids become main energy source
Long chain fatty acids released from adipose tissue, stimulated by < insulin and > glucagon
Taken up by other tissues e.g. muscle
Several different pathways but main one is beta-oxidation

25
Q

Beta-oxidation

A

Fatty acids enter tissues by diffusion
Then activated to acetyl CoA, producing NADH and FAD2H
Repeated until all Cs have been converted to acetyl CiA (2C)
Acetyl CoA can enter TCA cycle
Fatty acids can be very long, containing many carbons, producing a lot of energy

26
Q

Beta-oxidation

A

Fatty acids enter tissues by diffusion
Then activated to fatty acyl CoA using ATP
Fatty acyl-CoA transported into mitochondria
Then activated to acetyl CoA, producing NADH and FAD2H
Repeated until all Cs have been converted to acetyl CiA (2C)
Acetyl CoA can enter TCA cycle
Fatty acids can be very long, containing many carbons, producing a lot of energy

27
Q

Fed vs fasting

A

Fed: triacylglycerols being taken up into tissues
Fasting: released to bloodstream

28
Q

Cholesterol

A 
Can be synthesised or obtained from diet
Major component of blood lipoproteins
Important as:
-component of cell membranes
-precursor of bile salts
-precursor of steroid hormones
-precursor of vitamin D
29
Q

Cholesterol absorption

A

Enters gut enterocytes predominantly by diffusion
Cholesterol cannot be fully metabolised - entry must be regulated
Enterocytes transport excess back into gut lumen
-cholesterol and bile salts excreted in faeces
Defects in proteins which transport cholesterol out of leads to chlolesterol accumulation and cardiovascular disease

30
Q

Cholesterol synthesis

A 
Occurs in cytosol (mainly liver)
4 stages:
1. Acetyl-CoA --HMG-CoA reductase --> mevalonate
2. Mevalonate --> isoprenes
3. Isoprenes (5C) --> Squalene (30C)
4. Squalene ---> Cholesterol
31
Q

Cholesterol fate

A

Secreted from liver as:

  • bile salts
  • ->stored in gallbladder
  • ->secreted into gut
  • ->aid digestion by emulsifying fat
  • biliary cholesterol
  • ->secreted into gut
  • ->can be reabsorbed
  • cholesterol ester
  • ->packaged in VLDL and transported to tissues
32
Q

Bile salts

A

Charged molecules, effective as detergents

Predominantly recycled to liver

33
Q

Cholesterol transport

A

Cholesterol and cholesterol esters transported in lipoproteins
Cholesterol helps to stabilise lipoprotein

34
Q

Cholesterol cell entry

A

When triglycerides removed from VLDL and absorbed, VLDL ‘remnant’ remains
Converted to IDL and then LDL
LDL contain a lot of cholesterol and cholesterol esters
This can be:
-returned to liver to make more VLDL
-taken up by other cells needing cholesterol
(membrane synthesis and steroid hormone synthesis)
Excess LDL can be endocytosed by macrophages
This can cause inflammation and contribute to atherosclerosis

35
Q

What happens to excess LDL?

A

Excess cholesterol taken up by macrophage –> foam cell
Creates turbulence/ narrowing
Damages blood vessel
Thrombus develops whilst trying to heal BV
Major cause of cardiovascular disease

36
Q

How is cholesterol taken up by cells

A

LDL particle containing apoprotein and cholesterol ester recognised by cell membrane –> receptor-mediated endocytosis
Useful stuff absorbed by endosome, digested by lysosome, used by cell
LDL receptor recycled out of cell and used again

37
Q

Statins

A

Used to combat high cholesterol levels in the blood
Competitively inhibit HMG Co-reductase, an enzyme required for cholesterol synthesis
Structural analogues of natural substrate, compete for binding - have higher affinity
-mimic part of substrate that fits into active site of enzyme to inhibit it

38
Q

What affects action of HMG-CoA reductase?

A

Cholesterol, glucagon and cholesterol lowering drugs inhibit it.
Insulin increases its action

Nutrition (13 decks)

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