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Y1 - 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
Insulins affect in Gluconeogenesis
Inhibits it
26
Triacylglycerols are efficient energy stores because:
-Stored in bulk in anhydrous form in adipose tissue -Highly calorific (store lots of fuel molecules, fattty acids and glycerol)
27
Lipid/Triacylglycerol/Triglyceride storage under hormonal control. Which hormones reduce its storage? Which hormone increases its storage?
Glucagon, cortisol, adrenaline, growth hormone and thyroxine reduces its storage. Ensures it remains mobilised Insulin Inncreases its storage
28
What is Lipogenesis?
Fatty acid synthesis
29
Where does lipogenesis occur?
Cytoplasm
30
What is the Basic idea of lipogenesis?
Acetyl CoA along with ATP and NADPH used to make fatty acids
31
Where does the NADPH come from that’s needed for lipogenesis
THE PENTOSE PHOSPHATE PATHWAY (A type of metabolic pathway that glucose-6-phosphate undergoes)
32
Where does the Acetyl CoA come from needed for lipogenesis?
The Mitochondria Citrate cleaved to oxaloacetate and acetyl CoA
33
What is the Fatty acid synthase complex ?
Multi enzyme complex that carries out most of the steps of lipogenesis
34
Acetyl CoA carboxylase
Enzyme that controls rate of fatty acid synthesis Is not part of fatty acid synthase complex
35
Acetyl CoA carboxylase regulation
Modification of protein structure Insulin activates. (Promotes its dephosphorylation) Glucagon and adrenaline inhibit (Promotes its phosphorylation)
36
Most excess carbs and proteins converted to Triacylglycerols in adispose tissue
Excess = Type 2 diabetes and atherosclerosis
37
Fatty acid synthesis and fatty acid oxidation (B Oxidation) Are not reverse reaction of each other
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
Fatty acid synthesis
Cycles that add 2 carbons every time Glucagon and adrenaline inhibit Insulin stimulates
39
Fatty acid oxidation
Cycle of reactions that remove 2 carbons each time Glucagon and adrenaline stimulate Insulin inhibits
40
Classes of lipids
Triacylglycerols Fatty acids Cholesterol esters Cholesterol Phospholipids
41
Lipids insoluble in water
Transported in blood plasma associated with proteins
42
Lipoprotein particles
The highly specialised non covalent assemblies that transport lipids in the blood
43
Small amount of fatty acids carried non covalently bound to Albumin
The fatty acids came from lypolysis from adipose tissue
44
Apoprotein
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
Lipoprotein structure
Spherical Surface coat/shell (Apoproteins, Phospholipids and cholesterol Hydrophobic core (Triacylglycerols and cholesterol esters)
46
Classes of lipoproteins(Differ in composition of types of lipids and apoprotein comp)
Chlyomicrons VLDL (Very Low Density Lipoproteins) IDL (Intermediates Density Lipoproteins) LDL (Low Density Lipoproteins) HDL (High Density Lipoproteins)
47
Chlyomicrons function
Transport dietary Triacylglycerol from intestine to tissues like adipose tissues
48
VLDL
Transport Triacylglycerols SYNTHESISED in liver to adipose tissue for STORAGE
49
IDL
Transports cholesterol SYNTHESISED in LIVER to tissues Precursor for LDL
50
LDL
Transport cholesterol SYNTHESISED in liver to tissues
51
HDL
Transports excess tissue CHOLESTEROL to liver for disposal as BILE SALTS
52
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?
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
LCAT (Lecithin:Cholesterol Acyltransferase)
Converts some surface lipids to core lipids to balance out the ratio of surface to core lipids to ensure lipoprotein stability
54
What occurs as a result of LCAT Deficiency?
Unstable lipoproteins of abnormal structure Lipid transport process fails
55
VLDL particles made in
Liver
56
LDLs (Low density Lipoproteins) clinical relevance
Susceptible to Oxidative Damage leads to formation of atherosclerotic plaques (build up of fats in/on artery walls)
57
Familial hypercholsterolaemia
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
HDL Clinical relevance
HDL particles remove cholesterol and return it to liver as bile salts This reduces likelihood of foam cells and atherosclerotic plaque formation
59
Dyslipoproteinaemias
Means any defect in metabolism of plasma lipoproteins Primary dyslipoproteinaemia (familial inborn error of lipoprotein metabolism) Secondary dyslipoproteinaemia (acquired through life)
60
Hyperlipoproteinaemias
Raised levels of plasma lipoproteins
61
Treating Hyperlipoproteinaemia
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
Normal Blood Glucose Levels
5mmol/L
63
What level of blood glucose in Hypoglycaemia causes confusion
2.8mmol/L
64
Why is muscle glycogen trapped in the muscle? How is glycogen used for energy?
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
Liver Glycogen roles
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
Glycogen storage disease examples
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
What is Glycogenin?
Protein dimer core of glycogen
68
What is the function of Pancreatic Lipase ?
Breaks down Triacylglycerides in smalle intestine into Fatty acids + GLycerol
69
Intestine epithelial cells remake TAG Which lipoprotein molecule then transports the TAG?
Chlyomicron
70
Malonyl CoA

Y1 - MEH (33 decks)

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