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POM > MBC - Integration of Metabolism > Flashcards

MBC - Integration of Metabolism Flashcards

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?

A

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

25
Q

What does glucogenic do as a fuel source?

A

Store in skeleton turn into glucose in gluconeogenesis

26
Q

What does ketogenic do as a fuel source?

A

Synthesises fatty acid + ketone bodies

No gluconeogenesis

27
Q

What does triglyceride do as a fuel source?

A

Breakdown into fatty acid & glycerol

  • Fatty acid produces ketone bodies (used by muscle & brain)
  • Glycerol backbone used to generate DHAP
28
Q

How to we access the greatest level of control with metabolic pathways?

A

“Irreversible step” catalysed by enzyme needs to be early in the pathway

29
Q

How do we compare the activities of the different enzymes at different concentrations of substrate?

A

Michaelis constant (K_M)

  • The concentration of substrate at which enzyme function at half-maximal rate (V_MAX)
30
Q

What isoform of hexokinase are at muscle and liver?

A

Hexokinase I (muscle)

Hexokinase IV (liver)

31
Q

Is muscle Hk high or low glucose affinity?

A

High

32
Q

Is liver Hk high or low glucose affinity?

A

Low

33
Q

What does it mean if muscle Hk I is high glucose affinity (K_M of 0.1mM) ?

A

It is active at low glucose conc. - therefore active at MAX velocity at all times

34
Q

What happens to muscle Hk I under anaerobic conditions?

A

Due to TCA rate dropping and glycolysis slowing, Hk I is inhibited by the increase level of glucose-6-phosphate

35
Q

Where is glucose-6-phosphatase found & what does it do?

A

Liver only - it can catalyse reverse reaction to hexokinase

generate glucose from glucose-6-phosphate

36
Q

Under aerobic conditions, how are energy demands met?

A

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
Q

In the case of adrenaline under aerobic conditions, what would happen?

A

Increase rate of glycolysis in muscle
Increase rate of gluconeogenesis in liver
Increase release of fatty acid from adipose

38
Q

Under anaerobic conditions, how can energy demands be met?

A

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
Q

What are the 4 hormones that control blood glucose level?

A

Insulin, Glucagon, Adrenaline (epinephrine), Glucocorticoids

40
Q

Where are insulin and glucagon produced?

A

Islet of Langerhans in the pancreas

41
Q

What does insulin do?

A

Stimulate uptake of glucose, store as glycogen & fat

42
Q

What does glucagon do?

A

Stimulate production of glucose (Gluconeogenesis), breakdown of glycogen & fat

43
Q

What does Adrenaline do?

A

Mobilise glucose for “Fight or flight”

44
Q

What does glucocorticoids do?

A

Increase synthesis of metabolic enzymes (glucose availability)

45
Q

What happens when glucagon lv. increases and insulin lv. reduces?

A

Gluconeogenesis

Fatty acid breakdown as alternative for ATP production (In order to preserve glucose for brain)

46
Q

What happen in prolonged fasting? (No glycogen reserves)

A

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
Q

What are the two types of diabetes mellitus?

A

Type I - Beta cell dysfunction (don’t secrete enough insulin)

Type II - Insulin resistance (don’t respond to insulin)

48
Q

What happens to metabolism if you have diabetes?

A

Goes into starvation mode (prolonged fasting)

49
Q

What are the complications with diabetes?

A
  • 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
Q

How does glucagon protect against hypoglycaemia?

A
  • Liver glucagon stimulate gluconeogenesis & glycogenolysis
  • Insulin deficiency and excess glucagon –> increased hepatic output of glucose (hyperglycaemia)
51
Q

In fasting state, what are the main metabolic fuel for Heart and Brain?

A

Heart - fatty acid

Brain - Glucose if available (ketone body)

52
Q

Why is there an increase of glucose transporters on adipocytes when BGL increases?

A

To increase uptake to make triglycerides

53
Q

Where are ketone bodies produced?

A

Liver

54
Q

What increases oxaloacetate production?

A

Breakdown of amino acids

55
Q

What molecules does glucagon increases the synthesis of glucose from?

A

Glycogen, glycerol, amino acids

56
Q

What increases the synthesis of protein in a fed state?

A

Insulin

57
Q

At what plasma glucose level induces unconsciousness?

A

=< 2mmoL

58
Q

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?

A

The KM for Hexokinase IV is approximately 4mM

POM (22 decks)

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