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Metabolism > Energy storage and lipid transport > Flashcards

Energy storage and lipid transport Flashcards

1
Q

what is the glycogen stored in the liver used for?

A

replacing blood glucose

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2
Q

Other than liver, where is glycogen stored?

A

muscle

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3
Q

Describe the structure of glycogen?

A

glucose linked by a-1-6 glycosidic bones and every 8-10 resides there is an a1-4 bond which creates branching
At the molecules core is a protein called glycogenin

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4
Q

From glucose uptake into a cell, how is it transfered into glycogen?

A
  • Hexokinase/ glucokinase + ATP converts it into glucose6- phosphate
  • phosphoglucomutate makes it into glucose1- phosphate
  • G1P uridyltransferase + UTP + H20 makes it into UDP glucose
  • Glycogen synthase and branching enzyme make 1-4 and 1-6 bonds to make glycogen
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5
Q

Which enzyme is regulated in glycogen synthesis? How is it regulated?

A
  • Glycogen synthase
  • When adrenaline and glucagon is released it is phosphylated, this inhibits it
  • When insulin released it is dephosphylated and so activated
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6
Q

How is glycogen converted in to glucose?

A
  • glycogen phosphylase and debranching enzyme + Pi convert it into G1P
  • Phosphoglucomutase converts it into G6P
  • In muscle and liver this used directly for glycolysis
  • In liver this can be converted into glucose by glucose-6- phosphatase
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7
Q

How is glycogen breakdown regulated?

A
  • Phosphylation of glycogen phosphorylase by glucagon and adrenalin increase its activity
  • Dephosphylation of glycogen phosphorylase by insulin inhibits it
  • Muscle cells have no glucagon receptors
    But AMP will act as an allosteric activator of it here but not in the liver form of the enzyme
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8
Q

What is the name for glycogen synthesis and breakdown?

A

synthesis- glycogensis

breakdown- glycogenolysis

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9
Q

Give two inherited diseases of glycogen metabolism

A

Von Dierkes disease- G6P phosphatase deficiency leads to liver enlargement as it cant release the glucose
McArdles disase- muscle glycogen phosphylase deficiency meaning they cant break down glycogen, leading to exersize intolerance and excess glycogen damages muscle tissues

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10
Q

What is gluconeogenesis? When and where does it occur?

A

Production of glucose from non carbohydrate substances
After more than 8hrs of fasting after liver glycogen stores have run out.
In liver and adrenal cortex

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11
Q

What are the 3 main precursors used in gluconeogenesis?

A

lactate
glycerol
glucogonic amino acids

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12
Q

Where do lactate, glycerol and amino acids enter the reverse glycolysis needed for gluconeogenesis?

A

Lactate converted to pyruvate by oxidation
Glucogonic amino acids are converted either into pyruvate or oxaloacetate
Glycerol enters higher up at glyceraldehyde

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13
Q

How are the irreversible steps of glycolysis overcome for gluconeogenesis?

A
  • Pyruvate–> phosphophenylpyruvate overcome by going from pyruvate to oxaloacetate and then to phosphophenylpyruvate by PEPCK
  • Fructose1-6, bisphosphate–> fructose 6 bisphosphate by fructose 1-6 bisphosphatase
  • Glucose 6phosphate–> glucose by glucose 6 phosphatase
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14
Q

How is gluconeogenesis regulated?

A
  • Fructose 1,6 bisphosphate and PEPCK regulated
  • Glucagon and cortisol stimulate them (PEPCK by amount and F16BP by amount and activity)
  • Insulin inhibits them in same ways
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15
Q

When are lipid stores used?

A

Prolonged exersize
pregnancy
stress
starvation

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16
Q

What enzyme in adipose tissue is activated by glucoagon and adrenaline and inhibted by insulin to break down TAG?

A

homone sensitive lipase

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17
Q

Where does lipogenesis occur?

A

liver- uses C from glucose

18
Q

Describe the process of lipogenesis

A
  • pyruvate from glycolysis converted into Acetyl co A and oxaloacetate (OAA)
  • OAA and acetyl coA condense to form citrate which leaves mitochondria
  • in cytoplasm OAA and acetyl coA reform
  • ACETYL CO A CARBOXYLASE converts acetyl coA to malonyl coA w/ ATP
  • OAA converted to malate- goes back into glycolysis, also makes NADPH
  • many Malonyl CoA + FATTY ACID SYNTHASE and NADPH make fatty acid chain + 1 CO2 per malonyl coA
  • glycerol from glycolysis + fatty acid = TAG which leaves liver in VLDL
19
Q

How is lipogenesis regulated?

A
  • acetyl coA carboxylase
  • Insulin (dephosphorylates) and citrate (allosteric) INCREASE activity
  • Glucagon/ adrenaline (phosphorylate) and AMP (allosteric) DECREASE activity
20
Q

How are lipids transported in blood?

A

a small % on albumin- mainly just fatty acids

most carried in lipoproteins

21
Q

What is cholesterol and how are they transported around the body?

A

they are important in membranes, steroid hormone synthesis and bile acid synthesis
They’re transported around body as cholesterol esters

22
Q

What do lipoproteins transport?

A

TAG, cholesterol esters, Vitamins A,D,E,K

23
Q

Describe the structure of a lipoprotein?

A

A micelle, with cholesterol and apolipoproteins in the membrane (integral) or on the membrane (peripheral)

24
Q

What is the difference between Chylomicrons, LVLD, IDL, LDL and HDL ?

A
  • chylomicrons take cholesterol and TAG from intestine to tissues and liver
  • VLDL take TAG from liver to adipose
  • IDL is after VLDL has lost some TAG so mostly cholesterol
  • LDL formed when more TAG lost so mostly takes cholesterol from liver to tissues
  • HDL take excess cholesterol from cells to liver or to cells needing more cholesterol
25
Q

What happens to chylomicrons upon their creation?

A
  • ApoB48 added before entering lymphatic system in s. intestine
  • apoE and C added when entering blood at left subclavian thoracic duct
  • ApoC binds to lipoprotein lipases in capillary walls in muscle and adipose tissue and fatty acids are released
  • When 80% contents lost ApoC dissociates and it becomes chylomicron remnant
  • apoE on remnant binds to LDL receptor in liver and it is endocytosed and contents used
26
Q

What apolipoproteins are on VLDLs?

A

ApoB100
ApoC
ApoE

27
Q

What can happen to an IDL?

A

Taken up by liver or keep being depleted of TAG and become LDL

28
Q

How does an VLDL become an IDL?

A

ApoC binds to lipoprotein lipases and they become depleted of their contents by 70%

29
Q

When does and IDL become and LDL

A

when its been depleted to 10% of original content

it looses apoC and apoE so cant loose more or be taken back up by liver as efficiently

30
Q

How do empty HDLs form?

A

they can be produced by liver and intestine
they can bud off of VLDLs and chylomicrons
or apo A-1 can aquire cholestrol from other lipoproteins and cell membranes to form nascent like HDL

31
Q

How do HDL fill with cholesterol?

A

ABCA1 protein facilitates removal of cholesterol from cholesterol laden cells and into HDL, LCAT converts this into cholesterol ester for transport
No enzyme activity needed for this

32
Q

How do HDLs empty?

A

Cells requiring cholesterol take up HDLs by scavenger receptors (SR-B1)
HDL can exchange cholesterol ester for TAG with VDLS by the CETP (cholesterol ester transfer protein)
HDLs can be taken up into liver by specific receptors

33
Q

Describe the process by which LDLs enter cells needing more cholesterol

A
  • receptor mediated endocytosis
  • they present the LDL receptor when cholesterol needed
  • ApoB100 on LDL binds to LDL receptor
  • Receptor/ LDL complex taken up by endocyotosis into endosomes
  • endosomes fuse with lysosomes for digestion to release cholesterol and fatty acid
34
Q

What is a hyperlipoproteinaemia and what is its cause?

A

Any condition in which, after a 12 hour fast, the
plasma cholesterol and/or plasma triglyceride is
raised. This can be due to enzyme, receptor or apolipoprotein defects.

35
Q

What is type1 hyperlipoproteinaemia?

A

lipoprotein lipase deficiency meaning more chylomicrons in blood plasma. LDLs normal so no increased risk of CVD

36
Q

What is type2a hyperlipoproteinaemia?

A

LDL receptor deficiency, more LDLs in blood so increased CVD risk

37
Q

What is type 3 hyperlipoproteinaemia?

A

ApoE defect, raised IDL and chylomicron remnants as they cant be removed by liver, so more LDL- associated with increased CVD risk

38
Q

What is a hypercholesterolaemia?

A
  • high blood cholesterol levels
39
Q

What are common signs of hypercholesterolaemia?

A
  • Xantheasma: yellow patches on eye lids
  • Tendon xanthoma: nodules in tendons- particularly in hand
  • Corneal arcus: white circles around eye, common in elderly but sign in young person
  • early CVD
40
Q

What are treatments for hypercholesterolaemia?

A
  • reduce cholesterol and lipids in diet, increase fibre
  • increase exercise decrease smoking
  • statins (inhibit HMG coA reductase) eg atrovastatin
  • Bile salt sequestrants: binds bile salts together in GI tract so liver thinks there is less bile than there is so it produces more using up more cholesterol
41
Q

What level in blood should total cholesterol, LDL cholesterol, HDL cholesterol and triglyceride be?

A 
total= <5mmol/L
HDL= > 1mmmol/L
LDL= <3mmol/L
TAG= <2mmol/L (fasting)
42
Q

how does hyperlipidaemia present?

A

abdominal pain after eating fatty meals

Metabolism (8 decks)

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