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MCD - NAGE - Laz > 9 Integration Of Metabolism > Flashcards

9 Integration Of Metabolism Flashcards

1
Q

Q: What are measures of metabolism? (3)

A

A: oxygen uptake, CO2 production, heat generation

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2
Q

Q: How and why does the body balance energy intake and output? Need to attempt to?

A

A: controlling carbohydrate stores and the carbohydrate release systems so that you can continuously supply fuel for activities

Need to attempt to coordinate sporadic food intake and different types of food substrate with the requirements for energy by different tissues

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3
Q

*Q: When does muscle tissue have high ATP demand? What does it do? (2) What does it normally undergo? using? (3)

A

A: can have periods of v high ATP demand during vigorous contraction where ATP consumption is more than supply via oxidative phosphorylation-> (skeletal) glycogen store in muscle is broken down and pyruvate is converted into lactate which leaves muscle and travels to liver

Skeletal muscle- light contractions use aerobic respiration (oxygen and glucose and fatty acids from blood used)

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4
Q

*Q: What are the general metabolic features of specialised nervous and brain tissue? (3)

A

A: continuous high ATP requirement

Brain cannot utilise fatty acids

requires continuous supply of glucose (ketone bodies can partially substitute for glucose) as Brain can only metabolise glucose and ketone bodies

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5
Q

Q: What does adipose tissue store? Short or long term?

A

A: long term storage site for fats

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6
Q

*Q: What does heart tissue rely on in terms of energy resource? (2)

A

A: oxidise fats and carbohydrates

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7
Q

*Q: What are the metabolic roles of the liver? (4)

A

A: body’s main (glycogen) carbohydrate store and source of blood glucose

Immediate recipients of nutrients absorbed at intestines and carries out many metabolic processes (glycogenolysis, gluconeogenesis, glucose storage)

Can interconvert nutrient types

Lipoprotein metabolism

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8
Q

*Q: Explain glucose interactions with lipid and amino acid synthesis and breakdown. Draw a diagram to summarise including glycolysis.

A

A: Carbohydrates -> glucose / simple sugars

Simple sugars –phosphorylated–> G6P

excess glucose = G6P -> glycogen = stored in situ OR glucose is stored as glycogen in liver
If the TCA cycle slows down (e.g. due to anaerobic respiration) -> build up of PYRUVATE -> LACTATE = alternative fuel store

Excess Acetyl CoA –converted–> Ketone Bodies = used by BRAIN during starvation (little glucose available)

Acetyl CoA –converted–> fatty acids + cholesterol (stored)

Pyruvate and other substrates of the TCA cycle can be converted to amino acids which can then be converted to nucleotides which act as building blocks for anabolic purposes

G6P can be converted to pentose phosphates which can also be converted to nucleotides.

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9
Q

Q: Describe gluconeogenesis and draw a diagram.

A

A: OXALOACETATE (from the TCA cycle) -> GLUCOSE / GLYCOGEN

DIAGRAM

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10
Q

Q: Describe protein metabolism with a diagram.

A

A: Protein is broken down into amino acids.

Amino acids can feed into the Glycolysis or the TCA cycle in the form of pyruvate, acetyl CoA and other substrates in the TCA cycle.

Aa are excreted as urea.

The acetyl CoA that is produced can be channelled to produce fatty acids and ketone bodies which can be stored/used

As it is able to generate pyruvate, the breakdown of protein can be used to START GLUCONEOGENESIS (needs conversion of pyruvate to oxaloacetate to take place)

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11
Q

Q: Summarise fat metabolism with a diagram. By product? use?

A

A: Triglycerides are broken down into fatty acids and glycerol which enter glycolysis and the TCA cycle in the form of ACETYL CoA.

As a by-product you also form ketone bodies which can be used by the heart and the brain

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12
Q

*Q: What does muscle rely on in terms of energy resource?

A

A: carbohydrate and fat oxidation

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13
Q

*Q: How does insulin affect muscle glycolysis?

A

A: increase so more ATP can be produced

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14
Q

*Q: How does insulin affect (liver cell) gluconeogenesis? Why is this beneficial?

A

A: increases, before the ATP demand had increased and the needs were not met by the glucose in the bloodstream alone

Liver cells produce more glucose which moves into blood stream to tissues

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15
Q

*Q: How does adrenaline affect the release of fatty acids and why is this beneficial?

A

A: increases so more is available for ATP generation

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16
Q

*Q: Which hormone regulates the movement of transporters to the plasma membrane of muscle cells?

A

A: insulin

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17
Q

Q: What controls glucose metabolism? (3)

A

A: hormones

External signalling molecules relaying info from other pathways

Product of the reaction or pathways (p could be activator of inhibitor of E)

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18
Q

Q: What 3 factors has our metabolic system been designed to deal with?

A

A: food intake being sporadic, different food types, tissues having different requirements

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19
Q

*Q: Use a MUSLCE | BLOOD | LIVER diagram to explain the effect of exercise on aerobic respiration.

A

A: 1. Contractions increase ATP demand due to E and proteins needed to control contractile activity

  1. Therefore increase glucose transport into muscle cells via glucose transporters (demand involves more transport proteins moving to membrane)
  2. Muscle glycolysis increases (adrenaline) (and the TCA cycle = ATP production)
  3. Gluconeogenesis increases (adrenaline)
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20
Q

*Q: Use a MUSLCE | BLOOD | LIVER diagram to explain the effect of exercise on anaerobic respiration.

A

A: 1. (TCA cycle and ETC slow down/halt) ATP demand can’t be matched by oxygen delivery

  1. Transport can’t keep up with glucose demand
  2. Muscle glycogen breakdown increases = more glucose to enter glycolytic pathways and TCA cycle
  3. Lactate increases due to increased glycolysis which causes increased pyruvate
  4. Lactate transported from muscle to liver -> feeds into gluconeogenic pathway (make glucose) via conversion to pyruvate (recovery)
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21
Q

Q: What is the benefit of removing excess lactate from the blood? (2)

A

A: prevent acidosis and allows lactate to be used as alternative fuel substrate to generate more ATP

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22
Q

*Q: What does hexokinase do and how does it differ in liver cells compared to muscle cells? Use graphs to compare rate.

A

A: converts glucose to G6P (glucose 6 phosphate)

Muscle- HkI, high glucose affinity, rate is 1/2 maximal at 0.1mM, highly sensitive to g6p inhibition, r curve
Liver- Hk IV, low glucose affinity, rate is 1/2 maximal at 4mM, less sensitive to g6p inhibition, s curve

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23
Q

Q: When is insulin excreted and what does it do?

A

A: secreted when glucose levels rise from beta cells in islets of Langerhans, stimulates glucose uptake and use of glucose and storage of glycogen and fat

24
Q

Q: When is glucagon excreted and what does it do?

A

A: secreted when glucose levels fall, stimulates gluconeogenesis and breakdown of glycogen and fats

25
Q

Q: What does adrenaline do overall in terms of metabolism?

A

A: strong and fast metabolic effect to mobilise glucose for flight or fight

26
Q

Q: What are glucocorticoids and what do they do in terms of metabolism?

A

A: steroid hormones

Increase synthesis of metabolic E concerned with glucose availability

27
Q

*Q: How is diabetes a metabolic disorder?

A

A: disorder of insulin release and signalling which means your body doesn’t recognise that it has fuel and controls metabolism as if you were starving

28
Q

*Q: Compare T1 and T2 diabetes.

A

A: 1 can’t make insulin, 2 means reduced responsiveness to insulin

29
Q

*Q: What are the consequences of diabetes?

A

A: hyperglycaemia (high blood glucose) causing progressive tissue damage

Increase fatty acid and lipoproteins = possible cardiovascular complications

Hypoglycaemia (low) possible coma if insulin dosage is not correctly controlled

30
Q

*Q: Describe the effect of diabetes on metabolism with the aid of a diagram.

A

A: glucose is present in the blood but is not noticed as insulin is not released and therefore it’s signalling pathway not activated -> glucose is not taken up by muscle or liver cells

Regulation become one for starvation

Muscles breakdown glycogen stores and protein to produce aa as alternative substrate for gluconeogenesis in liver

Gluconeogensis leads to glucose production which is again not detected by tissue and aggravates hyperglycaemia (exacerbates)

Triglycerides in adipose tissue is broken down releasing glycerol and fatty acids

Glycerol is used in gluconeogenesis = exacerbates condition
Free fatty acids undergo beta oxidation = produce ketones

31
Q

*Q: What does excessive ketone body production lead to (diabetes)?

A

A: diabetic ketoacidosis

32
Q

Q: What do the islets of langerhans produce?

A

A: insulin (beta), glucagon (alpha), somatostatin, pancreatic polypeptide

33
Q

Q: Explain the regulation of hormone secretion in pancreatic beta cells. (4)

A

A: 1. Glucose is transported into beta cells

  1. Glucose metabolised-> ATP =signalling molecule in cell (binds to K ATP channel at cell surface and regulates its function)
  2. Upon binding and closing K channels = cell= depolarised -> opening of Ca2+ ion channels
  3. Increase of Ca conc in cells = exocytosis of insulin filled vesicles (+zinc)-> blood stream
34
Q

*Q: Which drug is used to treat T2 diabetes? How does it work?

A

A: GLP-1

Works in conjunction with glucose- if there is an increase in glucose then it can make beta cells more active so they release more insulin into bloodstream

35
Q

Q: What occurs to blood glucose after you eat and what does it cause?

A

A: initially rises and results in stimulation of synthetic (anabolic) pathways

36
Q

Q: Which enzymes does insulin affect and how?

A

A: increases activity of Hk IV and decreases activity of glucose 6 phosphatase

37
Q

*Q: What is the role of glucagon in T2 diabetes?

A

A: important protection against hypoglycaemia

Stimulates gluconeogenesis and glycogenolysis

38
Q

Q: How is glucagon release regulated?

A

A: glucose metabolism regulates it

Glucose is transported into alpha cells etc more ATP which signals to lots of ion channels which leads to inhibition of glucagon release

Insulin inhibits it’s release
So does GLP-1

39
Q

Q: What occurs in the islets of langerhans as blood glucose levels fall?

A

A: increase glucagon secretion and decrease insulin secretion

40
Q

Q: Why is it important to reserve some glucose and use alternative stores in organs?

A

A: needed for the brain

41
Q

*Q: What occurs in the liver as blood glucose levels fall?

A

A: increase glucose production by glycogen breakdown and gluconeogenesis

42
Q

Q: What occurs in terms of adrenaline as blood glucose levels fall?

A

A: Adrenaline stimulates glycogen breakdown and glycolysis in skeletal muscle and fat lipolysis in adipose tissue

43
Q

Q: What is used as an alternative substrate for ATP production during levels of low blood glucose?

A

A: Fatty acids are broken down

44
Q

*Q: What occurs in the islets of langerhans when blood glucose rises after eating?

A

A: increase secretions of insulin and reduce glucagon secretion

45
Q

*Q: What occurs in the liver when blood glucose rises after eating?

A

A: (hepatocytes) increase glucose uptake for glucagon synthesis and glycolysis

46
Q

*Q: What occurs in muscle cells when blood glucose rises after eating?

A

A: increases glucose uptake and glycogen synthesis

47
Q

*Q: What occurs in adipose tissue when blood glucose rises after eating?

A

A: increase triglyceride synthesis

48
Q

*Q: What occurs to the insulin/glucagon ratio during prolonged fasting? circumstance?

A

A: increases further (if Longer than can be covered by glycogen reserves)

49
Q

*Q: What occurs in adipose tissue after prolonged fasting when blood glucose levels fall? circumstance?

A

A: hydrolyses triglycerides to provide fatty acids for metabolism (if Longer than can be covered by glycogen reserves)

50
Q

*Q: What occurs to TCA cycle intermediates after prolonged fasting when blood glucose levels fall? circumstance?

A

A: reduced in amount to provide substrates for gluconeogenesis (if Longer than can be covered by glycogen reserves)

51
Q

*Q: What occurs in the liver after prolonged fasting when blood glucose levels fall? circumstance?

A

A: produces ketone bodies from fatty acids and aa to partially substitute the brains requirement for glucose (if Longer than can be covered by glycogen reserves)

52
Q

Q: How is gluconeogenesis different from glycolysis? (3) Include the difference in net ATP loss/yield.

A

A: Requires the conversion of pyruvate to oxaloacetate.

You need enough oxaloacetate to produce phosphoenolpyruvate.

Phosphoenolpyruvate is the intermediate which allows you to convert back to glucose.

GLYCOLYSIS: +2ATP

GLUCONEOGENESIS: -6ATP

53
Q

Q: What are 4 complications of diabetes?

A

A: -hyperglycaemia with progressive tissue damage

  • increase in plasma fatty acids and lipoproteins with possible cardiovascular complications
  • increase in ketone bodies with possible acidosis
  • hypoglycaemia with consequent coma if insulin dosage is imperfectly controlled
54
Q

Q: What occurs during the metabolism of non nutrient chemicals (xenobiotics) including plant metabolites, drugs etc? (2)

A

A: if water soluble- can be excreted in urine and bile

-if lipophilic, metabolised to make more water soluble

55
Q

Q: Where does gluconeogenesis take place? Energy? Relation to Glycolysis?

A

A: Essentially only done in the Liver
Energy Consuming Process - requires ATP hydrolysis

NOT exactly the reverse of glycolysis - different enzymes bypass some irreversible glycolysis steps.

It skips a couple of the glycolysis steps - gluconeogenesis DOES NOT PRODUCE ACETYL CoA or PYRUVATE.

56
Q

Q: What does fat metabolism not produce? therefore? (2)

A

A: pyruvate is not produced when fats are used in respiration -> hence no conversion of pyruvate to oxaloacetate, the lack of accumulation of oxaloacetate means that you CANNOT GENERATE GLUCOSE VIA GLUCONEOGENESIS.

MCD - NAGE - Laz (8 decks)

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