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POM > MBC - Integration of Metabolism > Flashcards

MBC - Integration of Metabolism Flashcards

(58 cards)

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1
Q

What can’t the brain metabolise?

A

Fatty acids

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2
Q

What is the condition name for too little glucose?

A

Hypoglycaemia

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3
Q

What is the condition name for too much glucose?

A

Hyperglycaemia

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4
Q

What can hypoglycaemia cause?

A

Faintness & Coma

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5
Q

What can hyperglycaemia cause?

A

Irreversible damage to tissues rich in nerve (eg retina)

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6
Q

What happens when O2 becomes a limiting factor?

A

Glycogen breakdown

Lactate form

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7
Q

Where does lactate go after being formed?

A

Leave muscle into liver via blood

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8
Q

What can be used as fuel for OxPhos?

A

Oxygen, glucose, fatty acid

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9
Q

What attribute to heart working constantly?

A

Utilises TCA cycle substrates (free fatty acid, ketone bodies)

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10
Q

Why is loss of O2 supply to heart devastating?

A

Heart is designed completely for aerobic respiration

Rich in mitochondria

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11
Q

What happens when there is no oxygen supply to the heart?

A

Cell death, myocardial infarction (Energy demand > supply)

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12
Q

What is the role of the liver?

A

WIDE REPERTOIRE of METABOLIC PROCESSES:

  • Intermediate recipient of nutrient from intestines
  • Maintain blood glucose lv.
  • Glucose storage (as glycogen)
  • Lipoprotein metabolism (transport of triglycerides & cholesterol)
  • Produces ketone bodies
  • Produces bile for emulsification
  • Glycolysis
  • Transamination
  • Gluconeogenesis
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13
Q

What is adipose tissue?

A

Fat - storage tissue for fatty acid in form of triglycerides

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14
Q

What is the aim of gluconeogenesis?

A

Generate glucose from pyruvate

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15
Q

When is gluconeogenesis needed?

A

During fasting or starvation (decrease in blood glucose lv.)

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16
Q

What does the body do to avoid hypoglycaemia coma?

A

Breakdown liver glycogen (used by brain)

Release free fatty acid from adipose tissue (muscle)

Convert Acetyl CoA into ketone bodies via liver (muscle)

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17
Q

When and where is lactate generated?

A

When rate of glycolysis > rate of TCA & ETC

In the skeletal muscle

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18
Q

Where are amino acids derived from?

A

Breakdown of skeletal muscle

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19
Q

What is used to generate DHAP?

A

Glycerol backbone from triglyceride hydrolysis

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20
Q

How many reactions need to be bypassed in gluconeogenesis?

A

4, with 4 enzymes needed to turn energetically favourable

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21
Q

Why do we need to bypass the reaction?

A

Because there are 3 irreversible reactions catalysed by hexokinase, phosphofructokinase, pyruvate kinase

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22
Q

Where does excess glucose-6-phosphate go?

A

Stored as glycogen in liver or muscle

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23
Q

What does Acetyl CoA do during fasting?

A

Turn into ketone bodies

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24
Q

Where does excess Acetyl CoA go?

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A

Turn into fatty acid, cholesterol etc. and stored as triglycerides in adipose tissue

25
What does glucogenic do as a fuel source?
Store in skeleton turn into glucose in gluconeogenesis
26
What does ketogenic do as a fuel source?
Synthesises fatty acid + ketone bodies | No gluconeogenesis
27
What does triglyceride do as a fuel source?
Breakdown into fatty acid & glycerol - Fatty acid produces ketone bodies (used by muscle & brain) - Glycerol backbone used to generate DHAP
28
How to we access the greatest level of control with metabolic pathways?
"Irreversible step" catalysed by enzyme needs to be early in the pathway
29
How do we compare the activities of the different enzymes at different concentrations of substrate?
Michaelis constant (K_M) - The concentration of substrate at which enzyme function at half-maximal rate (V_MAX)
30
What isoform of hexokinase are at muscle and liver?
Hexokinase I (muscle) Hexokinase IV (liver)
31
Is muscle Hk high or low glucose affinity?
High
32
Is liver Hk high or low glucose affinity?
Low
33
What does it mean if muscle Hk I is high glucose affinity (K_M of 0.1mM) ?
It is active at low glucose conc. - therefore active at MAX velocity at all times
34
What happens to muscle Hk I under anaerobic conditions?
Due to TCA rate dropping and glycolysis slowing, Hk I is inhibited by the increase level of glucose-6-phosphate
35
Where is glucose-6-phosphatase found & what does it do?
Liver only - it can catalyse reverse reaction to hexokinase | generate glucose from glucose-6-phosphate
36
Under aerobic conditions, how are energy demands met?
OxPhos --> ATP eg muscle contract more, require actomyosin ATPase & cation balance (Ca2+/Na+k+ATPase) - increase in glucose transporters on membranes of muscle cell
37
In the case of adrenaline under aerobic conditions, what would happen?
Increase rate of glycolysis in muscle Increase rate of gluconeogenesis in liver Increase release of fatty acid from adipose
38
Under anaerobic conditions, how can energy demands be met?
Glycogen within muscle breakdown Pyruvate taken up by liver, replenish NAD+ & maintain glycolysis Pyruvate --> lactate (lactate dehydrogenase) Lactate is used by liver to generate glucose (Gluconeogenesis)
39
What are the 4 hormones that control blood glucose level?
Insulin, Glucagon, Adrenaline (epinephrine), Glucocorticoids
40
Where are insulin and glucagon produced?
Islet of Langerhans in the pancreas
41
What does insulin do?
Stimulate uptake of glucose, store as glycogen & fat
42
What does glucagon do?
Stimulate production of glucose (Gluconeogenesis), breakdown of glycogen & fat
43
What does Adrenaline do?
Mobilise glucose for "Fight or flight"
44
What does glucocorticoids do?
Increase synthesis of metabolic enzymes (glucose availability)
45
What happens when glucagon lv. increases and insulin lv. reduces?
Gluconeogenesis Fatty acid breakdown as alternative for ATP production (In order to preserve glucose for brain)
46
What happen in prolonged fasting? (No glycogen reserves)
Further increase in glucagon and decrease in insulin - Adipose hydrolyse triglyceride to form fatty acid - Reduce TCA intermediates & Protein breakdown to amino acid (substrate for gluconeogenesis) - Fatty acid --> ketone bodies & amino acid in liver (substitute glucose for brain)
47
What are the two types of diabetes mellitus?
Type I - Beta cell dysfunction (don't secrete enough insulin) Type II - Insulin resistance (don't respond to insulin)
48
What happens to metabolism if you have diabetes?
Goes into starvation mode (prolonged fasting)
49
What are the complications with diabetes?
- Hyperglycaemia & progressive tissue damage - Increase plasma fatty acid + lipoprotein lv. (possible cardiovascular complications) - Increase ketone bodies from liver (Risk of Acidosis) - Hypoglycaemia (if insulin dosage no properly controlled --> coma)
50
How does glucagon protect against hypoglycaemia?
- Liver glucagon stimulate gluconeogenesis & glycogenolysis - Insulin deficiency and excess glucagon --> increased hepatic output of glucose (hyperglycaemia)
51
In fasting state, what are the main metabolic fuel for Heart and Brain?
Heart - fatty acid | Brain - Glucose if available (ketone body)
52
Why is there an increase of glucose transporters on adipocytes when BGL increases?
To increase uptake to make triglycerides
53
Where are ketone bodies produced?
Liver
54
What increases oxaloacetate production?
Breakdown of amino acids
55
What molecules does glucagon increases the synthesis of glucose from?
Glycogen, glycerol, amino acids
56
What increases the synthesis of protein in a fed state?
Insulin
57
At what plasma glucose level induces unconsciousness?
=< 2mmoL
58
After a meal, the blood glucose concentration in the hepatic portal vein is high. What properties of Hexokinase IV allow a marked increase in production of hepatic of glucose 6-phosphate (G-6-P) in response to the increased portal glucose concentration?
The KM for Hexokinase IV is approximately 4mM

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