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MEH > Energy Storage > Flashcards

Energy Storage Flashcards

1
Q

What is the normal plasma glucose level

A

5 mmol/l

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2
Q

What tissues / cells have an absolute requirement for glucose as an energy source

A
  • Red blood cells
    (no mitochondria to rely on for glycolysis)
  • Neutrophils
    Needed for Respiratory Bursts
  • Innermost cells of kidney medulla
    Low O2 area thus relys on glycolysis
  • Lens of the eye
    Low O2 area thus relys on glycolysis
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3
Q

What lowers plasma glucose levels

A

Insulin lowers glucose levels to maintain Homeostasis

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4
Q

What is Glycogen

A

To enable blood glucose to be kept at required levels, a store of glucose is required…GLYCOGEN

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5
Q
  • What is Hypoglycaemia
  • What are the different levels and their consequences
A

Hypoglycaemia is then there is low Glucose levels

2.8mmol/L - Confusion
1.7mmol/L - Weakness, Nausea
1.1mmol/L - Muscle Cramps
0.6mmol/L - Brain Damage, Death

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6
Q

What is Hyperglycaemia

A

This is when glucose levels get too high

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7
Q

What happens when Glucose levels surpass 8mmol/L
- when can It occur

A

If glucose levels goes too high, Past 8mmol/L it surpasses the renal threshold, and glucose begins to show up in the urine
This occurs in diabetes 1

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8
Q

What is a respiratory burst

A

Respiratory burst predominately occurs in neutrophils and causes the release of reactive oxygen species to kill pathogens.

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9
Q

How is glycogen stored, what are its two main stores

A

Glycogen is stored as granules

Its two main stores are,
1. Muscle Glycogen
2. Liver Glycogen

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10
Q

Can glycogen stores be used anywhere else

A

In muscle glycogen can only be used by muscles

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11
Q

Glycogen Structure

A
  • Glycogen is a polymer consisting of chains of glucose residues
  • Chains are organized like the branches of a tree originating from a dimer of the protein glycogenin (acts as a primer at core of glycogen structure).
  • Glucose residues linked by α-1-4 glycosidic bonds with α-1-6 glycosidic bonds forming branch points every 8-10 residues
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12
Q

What is the benefit of branching in glycogen

A

More sites for enzymes to act upon, so they can release glucose monomers from the polymer

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13
Q

What is Glycogenesis

A

Glycogen Synthesis from Sugar (Glucose)

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14
Q

Steps of Glycogenesis

A
  1. Glucose + ATP —> Glucose - 6 - Phosphate + ADP
    (Uses Hexokinase, or (Glucokinase enzyme in liver))
  2. Glucose - 6 - Phosphate —> Glucose 1- Phosphate
    (uses Phosphoglucomutase Enzyme )
  3. Glucose - 1 - Phosphate + UTP + H2O —>
    UDP-Glucose + Pi
    (UTP = glucose-1-phosphate uridylyltransferase enzyme)
  4. Glycogen(n residues) + UDP-glucose —>
    Glycogen(n +1 residues) + UDP
    ( Glycogen synthase –> α-1-4 Glycosidic bonds, Joins chain)
    ( Branching Enzyme –> α-1-6 Glycosidic bonds, Joins Branch point)
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15
Q

What is Glycogenolysis

A

(Glycogen Degradation)

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16
Q

Steps of Glycogenolysis

A
  1. Glycogen(n residues) + Pi —> Glucose 1–phosphate + Glycogen(n -1 residues)

(Glycogen Phosphorylase Enzyme - Main chain)
(De-branching Enzyme - Branch points)

  1. Glucose 1–phosphate —> Glucose 6–phosphate
    ( Phosphoglucomutase Enzyme)
  2. Glucose - 6 - Phosphate
    - Goes to liver - broken down by Glucose - 6 - Phosphatase to glucose.
    Buffer for plasma glucose levels
    - Goes to muscles - broken down by glycolysis to form lactate, CO2 and ATP
    Used by muscles for energy production
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17
Q

How does the glucose - 6 - phosphate know which pathway to go under in Glycogenolysis

A

Different enzymes allow for simultaneous inhibition of one pathway and stimulation of another

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18
Q

How much glycogen is in the liver and the muscles

A

100g of glycogen in the liver
300g of glycogen in the muscles

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19
Q

What is the difference between what happens to Glucose - 6 - Phosphate in the liver and in the muscles.

A

LIVER - G6P converted to glucose by Glucose - 6 - Phosphatase and exported to blood. Liver glycogen is a buffer of blood glucose levels.

MUSCLES - Muscle lacks the enzyme Glucose-6-phosphatase. G6P enters glycolysis for energy production

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20
Q

What is the rate limiting enzyme for Glycogen Synthesis and Glycogen Degradation

A

Glycogen synthesis - Glycogen synthase

Glycogen degradation - Glycogen phosphorylase

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21
Q

How does the hormone Glucagon, Adrenaline effect Glycogen metabolism
What does it do

A
  • Glycogen synthase - Phosphorylation - Decreases Glycogen synthase enzymes activity. - reducing Glycogen synthesis
  • Glycogen phosphorylase - Phosphorylation - Increases Glycogen phosphorylase enzymes activity - Increasing Glycogen degradation
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22
Q

How does the hormone insulin effect Glycogen metabolism
What does it do

A
  • Glycogen Synthase - De-Phosphorylates - Increases Glycogen synthase enzymes activity - increasing glycogen synthesis
  • Glycogen phosphorylase - De-Phosphorylation - decreases Glycogen phosphorylase enzymes activity - decreasing Glycogen degradation
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23
Q

What is the difference between glycogen metabolism in muscles and liver

A
  • Muscle glycogen stores differ in that Glucagon has no effect.
  • Also AMP is an allosteric activator of muscle glycogen phosphorylase but not of the liver form of enzyme
24
Q

How does Glycogen Storage Diseases occur
How many types are there
How rare is it

A

W* Inborn errors of metabolism (inherited diseases)
* Arise from deficiency or dysfunction of enzymes of glycogen metabolism
* 12 distinct types.
Incidence varies ~1 in 20,000 – ~1 in 100,000. Severity depends on enzyme/tissue affected

25
How Glycogen Storage Diseases causes damage
* Liver and /or muscle can be affected * Excess glycogen storage can lead to tissue damage * Diminished glycogen stores can lead to hypoglycaemia & poor exercise tolerance
26
What is an example of glycogen storage diseases
- Von Gierke's Disease - Glucose 6 Phosphate deficiency - McArdle Disease - Muscle glycogen phosphorylase deficiency
27
What is Gluconeogenesis
Gluconeogenesis is the production of new glucose
28
When is Gluconeogenesis required
Beyond ~ 8 hours of fasting, liver glycogen stores start to deplete and an alternative source of glucose is required: Gluconeogenesis
29
Where does Gluconeogenesis occur
Occurs in the liver and lesser extend occurs in the Kidney Cortex
30
What are the three major precursors that can be used for Gluconeogenesis
- Lactate From anaerobic glycolysis in exercising muscle and red blood cells (Cori cycle) - Glycerol Released from adipose tissue breakdown of triglycerides. - Amino acids Mainly alanine.
31
What is the cori cycle
- In muscles glucose is converted into lactate - lactate is transported onto the liver - Via Gluconeogenesis lactate is converted to Glucose - Glucose is transported into the muscle
32
Can Acetyl-Coa synthesise Glucose
Acetyl-CoA cannot be converted into pyruvate (pyruvate dehydrogenase reaction is irreversible) so there is no net synthesis of glucose from acetyl-CoA
33
- What are the key enzymes In GLUCONEGENESIS - What are the 2 major controls to the pathway
- Key Enzymes = irreversible reaction enzymes 1. Glucose - 6- Phosphatase, Turns Glucose 6 phosphate into glucose (Major Control) 2. Fructose 1,6-bisphosphatase, turns Fructose 1,6-bis phosphate to Fructose 6- phosphate (Major Control) 3. PEPTAK, (Pyruvate can't turn directly back in to Phosphoenolpyruvate thus turns to Oxaloacetate, which then using PEPTAK turns to Phosphoenolpyruvate
34
Which enzymes are involved in regulation of gluconeogenesis
- Fructose 1,6-bisphosphatase - Phosphoenolpyruvate carboxykinase (PEPCK)
35
What is glyconeogenesis stimulated
* Starvation/fasting * Prolonged exercise * Stress
36
Hormones involved in glyconeogenesis regulation
Glucagon, Cortisol Insulin
37
What does Glucagon, Cortisol hormone do in gluconeogenesis
Enzyme - PEPCK, increases amount of PEPCK, Stimulating Gluconeogenesis Enzyme - Fructose 1,6 bisphosphatase, Increases amount and activity of enzyme, Stimulating Gluconeogenesis
38
What does the hormone insulin do in gluconeogenesis
Enzyme - PEPCK, decreases amount of PEPCK, inhibiting Gluconeogenesis Enzyme - Fructose 1,6 bisphosphatase, decreases amount and activity of enzyme, inhibiting Gluconeogenesis
39
What is the Time Course of Glucose Utilisation
Glucose from food ~2 Hours after food Glycogenolysis Up to 8-10 hours Gluconeogenesis 8-10 hours onwards
40
How much of the brains energy can come from ketone bodies How long would this take
BRAIN can only get 50% of energy from ketone bodies It takes time for pathway to kick in (almost two weeks)
41
How are lipids stored
Triacylglycerol (triglyceride)
42
What is the structure of Triacylglycerol (triglyceride)
Glycerol + 3 Fatty acid =Triacylglycerol (In an esterification reaction) The Triacylglycerol breaks in to glycerol and 3 fatty acids in an lipolysis reaction
43
What is Triacyglycerol's function When do they form How are they stored Why are they effective what controls their mobilisation
* Energy intake in excess of requirements is converted to Triacylglycerol (TAG) for storage * TAGs are hydrophobic and therefore stored in an anhydrous form in specialised tissue – adipose tissue * Highly efficient energy store. Energy content per gram twice that of carbohydrate or protein * Utilised in prolonged exercise, stress, starvation, during pregnancy * The storage & mobilisation of TAGs is under hormonal control
44
What are adipocytes What is its structure
Adipocytes, also known as lipocytes and fat cells, are the cells that primarily compose adipose tissue, specialized in storing energy as fat. Large lipid droplet (mainly TAG and cholesterol ester) Cytoplasm and organelles pushed to edge
45
What is the size of a typical adipocyte How many does an average adult have How much weight can they gain before they divide
* Typical adipocyte ~0.1mm in diameter. Cells expand as more fat added * Average adult ~30 billion fat cells weighing ~15 kg. * Can increase in size about fourfold on weight gain before dividing and increasing total number of fat cells
46
What happens to the number of adipocytes when you loose weight
Body produces more Adipocytes when you become Obese The number of adipocytes doesn't reduce when you loose weight, only the amount of fat with in them
47
What is the Overview of dietary triacylglycerol metabolism
In the Small intestines, Fat (TAG) is converted to Fatty acids + Glycerol using Pancreatic Lipase Enzyme. Fatty Acids and Glycerol are absorbed into the intestinal epithelial cell where It they are remain in to TAGS They are packaged into Chylomicrons where they are transported into the lymph. Then they are transported into the blood where they are then wither utilised in tissues or taken for storage in adipose tissue When TAG is stored as adipose tissue, it is hormone sensitive When Glucagon & Adrenaline increase it is broken down When Insulin increases in builds up When Glucagon & Adrenaline increase adipose is broken down and transported via FA- Albumin (carriers) to tissues At tissues there is fatty acid oxidation turning them into energy
48
what is a Chylomicron
Chylomicrons, also known as ultra low-density lipoproteins, are lipoprotein particles that consist of triglycerides, phospholipids, cholesterol, and proteins. They transport dietary lipids from the intestines to other locations in the body.
49
Where does Fatty acid oxidation into energy not occur
Not cells lacking mitochondria (e.g.RBC) or in Brain since FA’s do not easily pass blood-brain barrier
50
What Is Lipogenesis
Fatty Acid Synthesis
51
Steps of lipogenesis
* Mainly in liver. Dietary glucose as major source of carbon. * Excess Glucose turns pyruvate in cytoplasm (glycolysis). * Pyruvate enters mitochondria and forms acetyl-CoA & OAA (Oxaloacetic acid) which then condense to form citrate * Citrate --> cytoplasm and cleaved back to Acetyl-CoA & OAA. * Acetyl-CoA carboxylase (key regulator) produces malonyl-CoA from Acetyl-CoA. (malonyl-CoA, looses a CO2 When it binds thus is classified as a 2 carbon unit) * Fatty acid synthase complex builds fatty acids by sequential addition of 2 carbon units provided by malonyl- CoA. (Process requires both ATP and NADPH)
52
Steps in liver lipogenesis
look at lecture slide page 20
53
What effects Acetyl-CoA carboxylase What is it
Acetyl-CoA carboxylase = Key regulatory enzyme Insulin (covalent de-phosphorylation), & citrate (allosteric) increase activity Glucagon / adrenaline (covalent phosphorylation) & AMP (allosteric) decrease activity
54
- Fatty Acid Oxidation What is it What does it produce Where does it occur What type of reaction is it Does it require energy What regulates it What simulates and inhibits it
Cycle of reactions that remove C2 C2 atoms removed as acetyl~CoA Produces acetyl~CoA Occurs in mitochondria Separate enzymes (mitochondrial matrix) Oxidative - produces NADH and FAD2H Requires small amount of ATP to activate the fatty acid Intermediates are linked to CoA Regulated indirectly by availability of fatty acids in mitochondria. Glucagon and adrenaline stimulate Insulin inhibits
55
- Fatty Acid Synthesis What is it What does it produce Where does it occur What type of reaction is it Does it require energy What regulates it What simulates and inhibits it
Cycle of reactions that add C2 C2 atoms added as malonyl CoA Consumes acetyl~CoA Occurs in cytoplasm Multi-enzyme complex (cytoplasm) Reductive - requires NADPH Requires large amount of ATP to drive the process Intermediates are linked to fatty acid synthase by carrier protein Regulated directly by activity of acetyl~CoA carboxylase. Glucagon and adrenaline inhibit Insulin stimulates
56
What does Glucagon & Adrenaline do in fat mobilisation What does Insulin do in Fat Mobilisation
Glucagon & Adrenaline leads to phosphorylation and ACTIVATION of HSL (hormone sensitive lipase) Insulin leads to de- phosphorylation and INHIBITION of HSL (hormone sensitive lipase) Triacylglycerol is broken down by Hormone sensitive lipase which turns to glycerol and fatty acid Glycerol Travels to liver and utilised as carbon source for gluconeogenesis Fatty acids Travels complexed with albumin to muscle and other tissues (b- oxidation)

MEH (13 decks)

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