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MEH > (ignore) Energy Storage And Lipid Transport > Flashcards

(ignore) Energy Storage And Lipid Transport Flashcards

1
Q

Energy stores in 70kg man

A

Triglycerides (Triacylglycerol) = 15kg
Glycogen = 0.4kg
Muscle protein = 6kg

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2
Q

Difference in energy stores in healthy end obese people

A

Glycogen and music protein= same
Triacylglycerols = much higher

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3
Q

Gluconeogenesis used when

A

When glycogen stores and therefore glucose stores are depleted

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4
Q

Glycogen structure

A

Highly branched polymer of glucose
Glucose residues joined by a1-4 and a1-6 glycosidic bonds

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5
Q

Adv of glycogen being highly branched

A

MAny sites where glycogen can be degraded back to glucose or more glycogen can be formed
Branch very 10 units

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6
Q

Glycogen stored where?

A

Liver + skeletal muscles in granules

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7
Q

Glycogenesis

A

Formation of glycogen from glucose

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8
Q

Glycogenesis steps = 4

A

1.) Glucose + ATP —-> Glucose 6-P + ADP
Catalysed by hexokinase (GLucokinase in liver)
2.) Glucose 6-P ——> Glucose 1-P
Catalysed by phosphoglucomutase
3.) Glucose 1-P + UTP + H2O —->UDP-glucose + 2Pi
UTP = Uridine Triphosphate is similar to ATP
4.) ????

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9
Q

Glycogen metabolism regulation

A

Enzymes in irreversible reactions in the pathways regulated
Glycogen synthase (biosynthetic pathway)
Glycogen phosphorylase ( Degradative pathway)

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10
Q

How is the activity of Glycogen synthase changed?

A

Inhibited by phosphorylation
Activated by dephosphorylation

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11
Q

How is the activity of Glycogen phosphorylase changed?

A

Inhibited by dephospharylation
Activated by phosphorylation

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12
Q

Glucagon and Adrenalines affect on glycogen synthase and glycogen phosphorylase

A

It increases phosphorylation
Therefore:
Glycogen synthase Inhibited (so less glycogen made)
Glycogen phosphorylase Activated (more glycogen broken down)

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13
Q

Glycogen synthase function

A

Joins glucose residues by a1-4 glycosidic bonds

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14
Q

What is the role of Glycogen phosphorylase?

A

Breaks down the a1-4 glycosidic bonds by phosphorylysis so residues released as glucose-1-phosphate

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15
Q

Insulins affect on Glycogen Synthase and Glycogen Phosphorylase

A

Causes dephosphorylation
Therefore:
Glycogen Synthase activated (Increased Glycogen production)
Glycogen Phosphorylase deactivated (Less Glycogen Breakdown)

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16
Q

Glycogen storage diseases
(Deficiency/Dysfunction of Glycogen synthase or glycogen phosphorylase)

A

So Increased/Decreased amounts of Glycogen:
-Tissue damage (Excessive storage)
-Fassting Hypoglycaemia
-Poor exercise tolerance

Abornormal glycogen structure
Liver and muscles are affected (where its stored)

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17
Q

Gluconeogenesis substrates

A

-Pyruvate, lactate and glycerol all convert to glucose
-Amino acids whose metabolism involves pyruvate or Krebs cycle intermediates can all convert to glucose

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18
Q

Gluconeogenesis Key control enzymes:

A

Fructose 1,6- bisphosphatase converts Fructose 1,6- bis phosphate to Fructose 6-phosphate and Pi (Phosphate)

PEPCK - Converts Oxaloacetate to Phosphoenolpyruvate

Glucose-6-Phosphatase (Converts Glucose-6-Phosphate to Glucose

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19
Q

How is Gluconeogenesis regulated?

A

Under Hormonal Control:
Regulatory enzymes that are affected are
-PEPCK
-Fructose 1-6 bisphosphatase

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20
Q

Insulin affect on Fructose 1-6 bisphosphatase (Key in Gluconeogensis)

A

Decrease amount of the enzyme Fructose 1-6 bisphosphatase

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21
Q

Insulin affect on enzyme PEPCK

A

Decreases amount and activity

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22
Q

Insulin affect on both Fructose 1-6 Bisphosphatase and PEPCK

A

Decreases amount of enzymes
Decreases activity of PEPCK

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23
Q

Glucagon and Cortisol affects on PEPCK and Fructose 1-6 bisphosphatase

A

Increased amounts and increase activity of PEPCK

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24
Q

Glucagon and Cortisol affect on Gluconeogenesis

A

Stimulates it

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25
Q

Insulins affect in Gluconeogenesis

A

Inhibits it

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26
Q

Triacylglycerols are efficient energy stores because:

A

-Stored in bulk in anhydrous form in adipose tissue
-Highly calorific (store lots of fuel molecules, fattty acids and glycerol)

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27
Q

Lipid/Triacylglycerol/Triglyceride storage under hormonal control.
Which hormones reduce its storage?
Which hormone increases its storage?

A

Glucagon, cortisol, adrenaline, growth hormone and thyroxine reduces its storage. Ensures it remains mobilised

Insulin Inncreases its storage

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28
Q

What is Lipogenesis?

A

Fatty acid synthesis

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29
Q

Where does lipogenesis occur?

A

Cytoplasm

30
Q

What is the Basic idea of lipogenesis?

A

Acetyl CoA along with ATP and NADPH used to make fatty acids

31
Q

Where does the NADPH come from that’s needed for lipogenesis

A

THE PENTOSE PHOSPHATE PATHWAY
(A type of metabolic pathway that glucose-6-phosphate undergoes)

32
Q

Where does the Acetyl CoA come from needed for lipogenesis?

A

The Mitochondria
Citrate cleaved to oxaloacetate and acetyl CoA

33
Q

What is the Fatty acid synthase complex ?

A

Multi enzyme complex that carries out most of the steps of lipogenesis

34
Q

Acetyl CoA carboxylase

A

Enzyme that controls rate of fatty acid synthesis
Is not part of fatty acid synthase complex

35
Q

Acetyl CoA carboxylase regulation

A

Modification of protein structure
Insulin activates. (Promotes its dephosphorylation)
Glucagon and adrenaline inhibit (Promotes its phosphorylation)

36
Q

Most excess carbs and proteins converted to Triacylglycerols in adispose tissue

A

Excess = Type 2 diabetes and atherosclerosis

37
Q

Fatty acid synthesis and fatty acid oxidation (B Oxidation) Are not reverse reaction of each other

A

Adv of catabolic and anabolic pathways occur in different routes:
-Greater flexibility (different substrates and intermediates)
-Better control
-Thermodynamically 8irreversible step can be by passed

38
Q

Fatty acid synthesis

A

Cycles that add 2 carbons every time
Glucagon and adrenaline inhibit
Insulin stimulates

39
Q

Fatty acid oxidation

A

Cycle of reactions that remove 2 carbons each time
Glucagon and adrenaline stimulate
Insulin inhibits

40
Q

Classes of lipids

A

Triacylglycerols
Fatty acids
Cholesterol esters
Cholesterol
Phospholipids

41
Q

Lipids insoluble in water

A

Transported in blood plasma associated with proteins

42
Q

Lipoprotein particles

A

The highly specialised non covalent assemblies that transport lipids in the blood

43
Q

Small amount of fatty acids carried non covalently bound to Albumin

A

The fatty acids came from lypolysis from adipose tissue

44
Q

Apoprotein

A

The protein component of Lipoprotein Molecules
Package the non soluble lipid into a water lobule form
Hydrophobic region of apo protein interacts with lipid
Hydrophilic region of apoprotein interacts with water

45
Q

Lipoprotein structure

A

Spherical
Surface coat/shell (Apoproteins, Phospholipids and cholesterol
Hydrophobic core (Triacylglycerols and cholesterol esters)

46
Q

Classes of lipoproteins(Differ in composition of types of lipids and apoprotein comp)

A

Chlyomicrons
VLDL (Very Low Density Lipoproteins)
IDL (Intermediates Density Lipoproteins)
LDL (Low Density Lipoproteins)
HDL (High Density Lipoproteins)

47
Q

Chlyomicrons function

A

Transport dietary Triacylglycerol from intestine to tissues like adipose tissues

48
Q

VLDL

A

Transport Triacylglycerols SYNTHESISED in liver to adipose tissue for STORAGE

49
Q

IDL

A

Transports cholesterol SYNTHESISED in LIVER to tissues
Precursor for LDL

50
Q

LDL

A

Transport cholesterol SYNTHESISED in liver to tissues

51
Q

HDL

A

Transports excess tissue CHOLESTEROL to liver for disposal as BILE SALTS

52
Q

What is the function of Lipoprotein Lipase?
Where is it found?
What increases the amount of lipoprotein lipase?
What happens to the fatty acids and glycerols produced?

A

Removes core Triacylglycerols from Chlyomicrons and VLDLs
On inner surface of capillaries in adipose tissue and muscle
Hydrolyses Triacylglycerols. To fatty acids and glycerol. Fatty acids accepted by tissues glycerol taken to liver
Insulin increase synthesis of Lipoprotein Lipase

53
Q

LCAT (Lecithin:Cholesterol Acyltransferase)

A

Converts some surface lipids to core lipids to balance out the ratio of surface to core lipids to ensure lipoprotein stability

54
Q

What occurs as a result of LCAT Deficiency?

A

Unstable lipoproteins of abnormal structure
Lipid transport process fails

55
Q

VLDL particles made in

A

Liver

56
Q

LDLs (Low density Lipoproteins) clinical relevance

A

Susceptible to Oxidative Damage leads to formation of atherosclerotic plaques (build up of fats in/on artery walls)

57
Q

Familial hypercholsterolaemia

A

Abscence/deficiency of function LDL receptors
Homozygotes have abscence so get atherosclerosis early in life
Heterozygous have deficiency so get atherosclerosis later in life

58
Q

HDL Clinical relevance

A

HDL particles remove cholesterol and return it to liver as bile salts
This reduces likelihood of foam cells and atherosclerotic plaque formation

59
Q

Dyslipoproteinaemias

A

Means any defect in metabolism of plasma lipoproteins
Primary dyslipoproteinaemia (familial inborn error of lipoprotein metabolism)
Secondary dyslipoproteinaemia (acquired through life)

60
Q

Hyperlipoproteinaemias

A

Raised levels of plasma lipoproteins

61
Q

Treating Hyperlipoproteinaemia

A

Diet and lifestyle modification (reduce eliminate cholesterol, reduce Triacylglycerol intake)
Statins (lowers plasma cholesterol. Reduces synthesis of cholesterol in liver by inhibiting HMG-CoA REDUCTASE )
Statins also increase expression of LIpoprotien lipase

62
Q

Normal Blood Glucose Levels

A

5mmol/L

63
Q

What level of blood glucose in Hypoglycaemia causes confusion

A

2.8mmol/L

64
Q

Why is muscle glycogen trapped in the muscle?
How is glycogen used for energy?

A

Muscle has no Glucose - 6 - Phosphatase enzyme so it can’t be fully broken down into glucose so it is trapped in muscle
G6P enters glycolysis for energy production producing lactate

65
Q

Liver Glycogen roles

A

Broken down in liver then released into the blood
Glycogen -> GLucose-1-phosphate ->Glucose

Glucose 6 Phosphate to glucose catalysed by Glucose-6-phosphatase

66
Q

Glycogen storage disease examples

A

Von Gierkes disease (glucose-6-phosphatase deficiency) Liver can’t convert G6P to glucose so glucose trapped

McArdle disease - muscle glycogen phosphorylase deficiency (Glycogens 1-4 glycosidic bonds can’t be broken)

67
Q

What is Glycogenin?

A

Protein dimer core of glycogen

68
Q

What is the function of Pancreatic Lipase ?

A

Breaks down Triacylglycerides in smalle intestine into
Fatty acids + GLycerol

69
Q

Intestine epithelial cells remake TAG
Which lipoprotein molecule then transports the TAG?

A

Chlyomicron

70
Q

Malonyl CoA

A

MEH (33 decks)

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