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
Beta-oxidation
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
Beta-oxidation
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
Fed vs fasting
Fed: triacylglycerols being taken up into tissues Fasting: released to bloodstream
28
Cholesterol
``` 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
Cholesterol absorption
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
Cholesterol synthesis
``` 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
Cholesterol fate
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
Bile salts
Charged molecules, effective as detergents | Predominantly recycled to liver
33
Cholesterol transport
Cholesterol and cholesterol esters transported in lipoproteins Cholesterol helps to stabilise lipoprotein
34
Cholesterol cell entry
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
What happens to excess LDL?
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
How is cholesterol taken up by cells
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
Statins
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
What affects action of HMG-CoA reductase?
Cholesterol, glucagon and cholesterol lowering drugs inhibit it. Insulin increases its action