energy storage- glycogen and fat Flashcards

1
Q

where is glucose a required substrate and why

A

in RBC- no mitochondria, in neutrophils- mitochondria specialised for respiratory burst, middle kidney medulla cells- deep in centre, poor blood supply, lens of the eye- not many blood vessels so we can see. all these cells rely on anaerobic glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is hypoglycaemia

A

+8.0mmol. common in diabetics, no insulin/ don’t respond to it. affects the microvasculculture so when ulcers develop on foot they don’t notice, becomes infected and they need it amputated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is hyperglycaemia

A

2.8-0.6 mol. leads to confusion and even brain damage and death as brain requires glucose and can only make 50% use of ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do glycogen stores look like under microscope, where is it stored

A

they are black granules found in muscle and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the glycogen structure

A

has branched structure due to the 1,6 glycosidic bonds ever 25 monomers. in the centre there is a dimer protein called glycogenin which the glycogen polymers are attached to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the advantages of glycogen being branched

A

multiple points where enzymes can release glucose form and it doesnt have an osmotic effect on cell being stored in one structure like it would if they were monomers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

explain the process of glycogenesis (build up)

A

build up of glycogen. adding phosphate group to glucose using ATP and enzyme hexokinase to make G6P. converted to G1P via phosphoglutamase. then G1P added to UTP and water to make UDP glucose and PPi. Add UDP glucose to glycogen to extent it by 1 glucose molecule. UDP given off. keep doing this to extend by 1 monomer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

name the enzymes used to add UDP glucose to glycogen in glycogenesis

A

glycogen synthesis adds a monomer with a 1,4 bond and branching enzyme adds a glucose with a 1,6 monomer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

explain glycogenolysis (degradation)

A

add a phosphate to glycogen to form G1P and glycogen with on less glucose. catalysed by glycogen phosphorylase or de-branching enzyme. G1P is then converted to G6P by phosphoglutamase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what happens to G6P when it enters the muscle

A

enters glycolysis. no way of G6P being converted back to glucose so can’t leave the muscle. this is because it lacks the glucose 6 phophotase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what happens to G6P when it enters the liver

A

converted to glucose and enters plasma via a GLUT transporter. conversion catalysed by the enzymes glucose 6 phosphatase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which transporters are used to get glucose in and out of the muscle and the liver from the blood

A

GLUT 4 transports glucose into the muscle and GLUT 2 transports glucose in and out of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how are enzymes in the process of glycogenolysis and glycogeneisis regulated

A

glucagon/ adrenaline stimulate glycogen phosphorylase and inhibit glycogen synthase. insulin inhibits glycogen phosphorylase and stimulate glycogen synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which enzyme is activated by AMP and why

A

glycogen phosphorylase because when ATP low means need more glucose for production of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why does glucagon have no effect on muscle - can’t get glucose to be released into the blood

A

because muscles do not have glucagon receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is von gierkes

A

G6Phosphatase deficiency where can’t relate gycogen from liver. leads to hepatomegaly

17
Q

what is mcardle disease

A

muscle glycogen phosphorylase deficiency where get very tiered when exercising because no energy for muscle contraction

18
Q

when does gluconeogenesis take place

A

8 hours into starving this process happens when glycogen stores are used up

19
Q

what are the precursors of gluconeogeneis

A

lactate (from anaerobic respiration), glycerol (from adipose break down) and amino acids

20
Q

why is lactate an important precursor for the muscle

A

because lactate enters the cori cycle where it is taken to the liver and broken down to glucose and then travels back to the muscles where it can be used again

21
Q

draw out the entry points of the precursors in gluconeogensis and add in the relevant enzymes

A

enzymes include PEPCK, fructose 16 bisphosphate and glucose 6 phosphate

22
Q

how are fructose 1,6 bisphophate and PEPCK regulated

A

glucagon and cortisol stimulate these enzymes because need new glucose whereas insulin inhibits these enzymes because already got enough glucose

23
Q

time course of the utilisation of these process’

A

glucose can be used for 2 hours, then glycogen stores last up to 10 hours after this and then over this glujconeogeneis is used

24
Q

how is lipid stored

A

lipid droplet with TAG/cholesterol in it. organelles found at edge of cytoplasm. more fat = more fats cells = easier to regain weight because fat cells have already divided

25
Q

how fat is metabolised

A

broken down in small intestine by pancreatic lipase into fatty acids and glycerol. absorbed by epthithelal cell and then carried into the lymph via a chylomicron. enters blood stream at left subclavian vein and is then either stored in adipose tissue or is utilised in the tissue to produce energy

26
Q

how is adipose tissue metabolised

A

its release is stimulated by glucagon and adrenaline and it is carried to tissue by albumin to be converted to energy

27
Q

explain lipogenesis (lipid synthesis)

A

occurs in liver. glucose is converted to pyruvate by glycolysis and then converted to citrate and acetyl co A in the mitochondria. citrate is then converted to acetyl co A in the cytoplasm and this is converted to mayor coA (3C). in a fatty acid complex manoyl co A and NADPH from the pentose phosphate pathway and synthesis of maleate is used to add 2 carbons to the fatty acid tail attached to the glycerol. co2 is given off from manoyl co A (DRAW)

28
Q

how is TAG transferred outside the cell once it is synthesised

A

transferred by very low density lipoprotein

29
Q

explain lipolysis

A

TAG is related from adipose by hormone sensitive lipase. it enters the blood as glycerol and fatty acids . goes to the liver for glycogenesis and with an albumin to the muscle where it undergoes beta oxidation and is used as energy

30
Q

how is the release of TAG from adipose regulated

A

glucagon/ adrenaline activate HSL (hormone sensitive lipase) to break down TAG and insulin inhibits its break down.

31
Q

where are fats lipids stored in the body

A

as liver glycogen, muscle glycogen, muscle protein and as TAG. most of it is stored as TAG and is the only store that will increase when you gain weight.

32
Q

differences between fatty acid synthesis and beta oxidation (fatty acid metabolism)

A

beta oxidation; occurs in mitochondria, is oxidative (produces NADH) and is inhibited by insulin.
Fatty acid synthesis; occurs in cytoplasm, is reductive (requires NADH) and is stimulated by insulin

33
Q

clinical consequences of glycogen storage diseases

A

liver/muscle damage, excess glycogen storage leads to tissue damage, hypoglycaemia and poor exercise tolerance

34
Q

why is TAG an efficient energy storage molecule in adipose tissue

A

hydrophobic (stored in anhydrous form n adipose tissue)

efficient energy storage molecule

prolonged exercise, stress, starvation, during pregnancy

storage/mobilisation under hormonal control