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Year 1 POM > Integration of metabolism > Flashcards

Integration of metabolism Flashcards

1
Q

What is the process in gluconeogensis?

A

-Non-carbohydrate precursors enter the pathway namely e.g.
1. lactate
2 amino acids
3. glycerol

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2
Q

What are the enzymes used in bypass reactions of gluconeogensis?

A
  1. The first reaction is catalysed by pyruvate carboxylase occurs in the mitochondria
  2. Whereas the remaining reactions are cytosolic
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3
Q

What can fatty acids be converted into?

A

Fatty acids can be converted into ketone bodies and used by tissues such as muscle and brain

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4
Q

What happens in anerobic conditions?

A
  1. Glycogen within the muscle is therefore broken down to meet these demands
  2. To replenish NAD+ levels and maintain glycolysis pyruvate is taken up by the liver and converted into lactate by lactate dehydrogenase
  3. Pyruvate can then be used by the liver to generate glucose by gluconeogensis
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5
Q

What is the control of metabolic pathways?

A
  • reactions that are irreversible steps
  • At these points, increases the rate of enzyme activity greatly increases the rate of the downstream steps and for the greatest levels of control it is desirable that these control steps are reasonably early in the pathway
  • Control can be at several levels including:
    1. Product inhibition
    2. Under the influence of signalling molecule such as hormones
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6
Q

Describe the control of blood glucose levels

A
  1. Insulin is secreted when glucose levels rise: it stimulates uptake and use of glucose and storage as glycogen and fat
  2. Glucagon is secreted when glucose levels fall: it stimulates production of glucose by gluconeogensis and breakdown of glycogen and fat (both are secreted by islets of the pancreas)
  3. Adrenaline (or epinephrine): strong and fast metabolic effects to mobilise glucose for “flight or fight”
  4. Glucocorticoids: steroid hormones which increase synthesis of metabolic enzymes concerned with glucose availability
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7
Q

What happens when you eat a meal?

A

On having a meal blood glucose levels initially rise which is controlled by increased secretion of insulin (and reduced glucagon) from islets and this has several effects including:

  1. Increased glucose uptake by liver: used for glycogen synthesis and glycolysis (acetyl-CoA produced is sued for fatty acid synthesis)
  2. Increased glucose uptake and glycogen synthesis in muscle
  3. Increased triglyceride synthesis in adipose tissue
  4. Increased usage of metabolic intermediates throughout the body due to a general stimulatory effect on synthesis and growth
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8
Q

What happens after you eat a meal?

A

After a meal blood glucose levels start to fall and are controlled by:

  1. Increased glucagon secretion (and reduced insulin) from islets
  2. Glucose production in liver resulting from glycogen breakdown and glucoenogensis
  3. Utilisation of fatty acid breakdown as alternative substrate for ATP production (important for preserving glucose for brain)
    - Adrenilin has similar effects on liver, but also stimulates skeletal muscle towards glycogen breakdown and glycolysis, and adipose tissue towards fat lipolysis to provide other tissues with alternative substrate to glucose
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9
Q

What happens in prolonged fasting?

A
  1. Glucagon/insulin ratio increases further
  2. Adipose tissue begins to hydrolyse triglyceride to provide fatty acids for metabolism
  3. TCA cycle intermediates are reduced in amount to provide substrate for gluconeogensis
  4. Protein breakdown provides amino acid substrates for gluconeogensis
  5. Ketone bodies are produced from fatty acids and amino acids in liver to substitute partially the brains requirement for glucose
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10
Q

Describe Diabetes Mellitus

A

Diabetes Mellitus: is a disorder of insults release and signalling, resulting in an impaired ability to regulate blood glucose concentration:
Two types
1. Type 1 diabetes which individuals fail to secrete enough insulin (beta cell dystfunction)
2. Type 2 diabetes in which individuals fail to respond appropriately to insulin levels (insulin resistance)
The overall effect is that metabolism is controlled as if the person is undergoing starvation, regardless of dietary glucose uptake

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11
Q

What are the complication of diabetes?

A
  1. . Hyperglycaemia with progressive tissue damage (e.g. retina, kidney, peripheral nerves
  2. Increase in plasma fatty acids and lipoprotein levels with possible cardiovascular complication
  3. Increase in ketone bodies with risk of acidosis
  4. Hypoglycaemia with consequent coma if insulin dosage is imperfectly controlled
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12
Q

What specialised tissues are there which need metabolic function?

A
  • Muscle
  • Brain and nervous tissue
  • Adipose tissue
  • Heart
  • Liver
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13
Q

Where does muscle get ATP from?

A
  1. Relies on carbohydrate and fatty acid oxidation

2. Can have periods of every high ATP requirement during vigorous contraction

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14
Q

Where does brain and nervous tissue get ATP from? What can it not utilise as a fuel source?

A
  1. Requires continuous high ATP requirement

2. CANNOT utilise fatty acids as a fuel source

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15
Q

What is adipose tissue?

A

Long term storage site for fatty acids in form of triglycerides

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16
Q

What can the heart oxidise?

A

Can oxidise fatty adds and carbohydrates

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17
Q

What is the liver?

A
  • Main carbohydrate store (glycogen) and source of blood glucose
  • Undertakes a wide repertoire of metabolic processes (e.g. glycolysis, gluconeogensis, transamination)
  • Highly metabolically active (only 2.5% of body mass, but contributes >20% of metabolic rate
  • Plays a key role in lipoprotein metabolism (transport of triglycerides and cholesterol
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18
Q

Is the metabolic function of skeletal muscle flexible ?

A

Skeletal Muscle is capable of large and rapid increases in ATP demands during exercise

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19
Q

What happens during light contraction for skeletal muscle?

A

ATP consumption is met by:

-oxidative phosphorylation (O2 and blood borne glucose and fatty acids are used as fuel)

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20
Q

What happens during vigorous contraction for skeletal muscle?

A
  • ATP consumption is faster than the ATP supply by oxidative phosphorylation (O2 and blood-borne substrate diffusion is limiting)
  • Muscle stores of glycogen are subsequently broken down to produce ATP
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21
Q

What happens under anaerobic conditions in skeletal muscle?

A

-pyruvate is converted to lactate, which can leave muscle and reach the liver via the blood

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22
Q

What can then brain not metabolise?

A

Fatty acids

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23
Q

What can partially substitute for glucose in the brain?

A

Ketone bodies (e.g. beta-hydroxy-butyrate) can partially substitute for glucose

24
Q

What happens when there is too little glucose for the brain?

A

Too little glucose (hypoglycaemia) causes faintness and coma

25
Q

What happens when there is too much glucose for the brain?

A

Too much glucose (hyperglycaemia) can cause irreversible damage

26
Q

What is the heart designed for?

A

The heart must beat constantly, it is designed for completely aerobic metabolism, and is rich in mitochondria

27
Q

What substrates does the heart use?

A

The heart utilises TCA cycle substrates, e.g. free fatty acids, ketone bodies

28
Q

What happens when there is a loss of O2 for the heart?

A

Loss of O2 supply to the heart is devastating, elating to cell death and myocardial infraction (energy demand&raquo_space;> energy supply)

29
Q

Outline respiration

A
  1. Carbohydrate broken down into simple sugars and enter glycolytic pathway leading to production of pyruvate
  2. Decarboxylation and reduction of pyruvate process acetyl CoA which can enter the TCA cycle and this produces reduced co-factors which are deoxidised by the electron transport chain which in turn in coupled to ATP production (Oxidative phosphorylation)
30
Q

What happens to excess glucose-6-phosphate?

A

Excess glucose-6-phosphate can be used to generate glycogen in liver and muscle (red arrow)

31
Q

What happens to excess acetyl CoA?

A

Excess acetyl coA can be used to generate fatty acids which are stored as triglycerides in adipose tissue (red arrow)

32
Q

What happens during extreme exercise?

A

During extreme exercise, ATP demands of the muscle outstrip oxygen supple needed for aerobic respiration and lactate is produced (blue arrow)

33
Q

What happens during fasting?

A

During fasting, rather than enter the TC, much of the acetyl CoA produced results in ketone body production (purple arrow)

34
Q

What can pyruvate and other TCA cycle intermediates be used for?

A

Pyruvate and other TCA cycle intermediates can also be a spruce of amino cids, and the backbone of these molecules can be used to make nucleotides

35
Q

What can glucose 6 phosphate also be used for?

A

Glucose-6-phosphate via the pentose phosphate pathway can also be used as a source for nucleotide production in a pathway that generate the blue of NADPH needed for anabolic pathway (e..g. cholesterol synthesis\

36
Q

What happens if plasma glucose concentration falls?

A

-Brain largely depended upon glucose as a metabolic fuel and during fasting is plasma glucose concentration fall below 3mM then the body will exert a hypoglycaemic coma and in the short term to avoid hypoglycaemia

37
Q

What happens in gluconeogenesis?

A
  1. Breakdown liver glycogen stores occurs to maintain plasma glucose levels
  2. Releases free fatty acids from adipose tissue
  3. Convert Acetyl CoA into ketone bodies via the liver
38
Q

What can the fatty acids and ketone bodies be used for in gluconeogenesis?

A
  • Both fatty acids and ketone bodies can be used by muscle making more of the plasma glucose available for the brains, however within 12-18 hours all glycogen stores are typically exhausted, hence need for another pathway to generate glucose (gluconeogensis)
  • Aim of pathway is to generate glucose form pyruvate\
39
Q

How is lactate generated?

A
  • Lactate is generate by skeletal muscle during strenuous exercise when rate of glycolysis exceeds rate of the TCA cycle and the ETC.
  • Lactate can be taken up by the liver and utilised to regenerate pyruvate by lactate dehydrogenase (LDH) also known as Cori cycle
40
Q

When are amino acids derived?

A

Amino acids can be derived from the diet of during times of starvation e.g. from the breakdown of skeletal muscle

41
Q

What yields amino acids?

A

Triglyceride hydrolysis yields fatty acids and glycerol, the glycerol backbone being used to generate dihydroxyacetone phosphate (DHAP)

42
Q

What are the enzymes that catalyse the three irreversible reactions in glycolysis?

A
  1. kinases hexokinase
  2. phosphofructokinase
  3. pyruvate kinase
43
Q

What does the deamination of the 20 amino acids give rise to?

A
  1. pyruvate
  2. acetyl CoA
  3. acetoacetyl CoA
  4. alpha-ketoglutarate
  5. succinyl CoA
  6. fumerate
  7. oxaloacetete
44
Q

What is lost as a waste product?

A

Urea

45
Q

What do ketogenic amino acids give rise to?

A

-Ketogenic amino acids give rise to skeletons which cannot enter gluconeogenesis but can be used to synthesis fatty acids and ketone bodies

46
Q

How are triglycerides broken down?

A

Triglycerides are broken down into fatty acids and glycerol and glycerol can be converted to DHAP and enter the gluconeogenic pathway upstream

47
Q

Can fatty acids be converted into glucose?

A

-Fatty acids CANNOT be converted into glucose by gluconeogenesis

48
Q

Why can there be no net synthesis of oxaloacetate or pyruvate from acetyl CoA?

A

2C atoms enter the TCA cycle as acetyl CoA by combining with oxaloacetate to form citrate and as the cycle progresses, two carbon atoms are sequentially loser as CO2 before oxaloacteeta is eventually regenerated, hence no net synthesis of oxacloaceteta or pyruvate is possible from acetyl CoA

49
Q

What happens during moderate levels of excerise?

A

-During moderate levels of exercise where oxygen supply is adequate, the ATP demands of muscle can be met by oxidative phosphorylation using glucose and other substrates as fuels

50
Q

How does the body know more glucose is needed?

A
  1. As a muscle contracts the demand for ATP increase e.g. requirements of muscle actomyosin ATPase and cation balance.
  2. Increased demand for glucose is set by an increase in the number of glucose transporters on the membranes of muscle cells
51
Q

How does adrenalin help the body meet the demand for ATP?

A
  1. increasing rate of glycolysis in muscle
  2. increasing the rate of gluconeogensis by the liver
  3. increasing the release of fatty acids from adipocytes
52
Q

Why is the body in trouble in anaerobic conditions?

A

-Adrenalin plays key role in meeting demand for ATP by increasing rate of glycolysis in msucle, increasing the rate of gluconeogensis by the liver, and increasing the release of fatty acids from adipocytes

53
Q

Do enzymes act differently in different parts of the body?

A
  • Muscle and liver contain suitably different forms (isoforms) of hexokinase and both isodorms catalyse the same reaction
  • However they are maximally active at different concentrations of glucose
  • The KM of hexokinase 1 found in muscle 0.1mM so its active at low concentrations of glucose and is essentially operating at maximal velocity at all times
  • Hexokinase IV found in liver behaves a little differently, having
  • Much higher KM of around 4mM and therefore is much less sensitive to blood glucose conventions and it is also less sensitive to the inhibitory effects of G-6-P (glucose 6 phosphate)
  • Glucose 6 phosphatase ( found in liver but not in muscle) can catalyse the reverse reaction to hexokinase, generating glucose from glucose-6-phosphate
54
Q

What are blood glucose levels usually?

A

maintained at a round 4mM

55
Q

How can you compare different activities of enzymes?

A

can compare relative activities of enzymes using KM (conc of substation functions at half maximal rate Vmax)

56
Q

What is Hexokinase 1 sensitive to?

A
  1. highly sensitive to inhibition by the product glucose-6-phosohate
  2. Therefore under anaerobic conditions when the rate of the TCA cycle drops and glycolysis therefore slows, Hexokinase 1 is inhibited by accumulating levels of glucose 6-phosphate
57
Q

How is Glucagon important in protection against hypoglycaemia?

A
  1. Major site of action is liver where glucagon stimulates gluconeogenesis and glycogenolysis
  2. Insulin deficiency and relative excess of of glucagon leads to increased hepatic output of glucose and thus hyperglycaemia

Year 1 POM (39 decks)

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