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Dentistry Biological Science > Integration of Metabolism 1 > Flashcards

Integration of Metabolism 1 Flashcards

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1
Q

What do changes in the circulating hormones allow the body to do? 2 things

A
  • store metabolic fuel

- metabolise this fuel when it is in starvation

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2
Q

What are changes in metabolic pattern achieved by and examples?

A
  1. Variation in the amount of substrate e.g. FA used in starvation
  2. Allosteric effects on enzymes e.g. AMP and PFK in muscle
  3. Covalent modification of enzymes e.g. phosphorylation of glycogen phosphorylase and synthetase
  4. Changes in enzyme synthesis e.g. Glucokinase and dietary CHO
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3
Q

What does AMP presence suggest? What occurs?

A

Energy is low and this activates PFK and this increases glycolysis rate.

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4
Q

Glucagon activates —– to increase blood glucose levels.
Km of glucokinase is —– than hexokinase which means that glucose will only be taken up by the liver to turn to glycogen if blood glucose levels are ——

A

Glycogen phosphorylase

Lower

High

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5
Q

What does the enzyme HMG CoA reductase regulate?

A

Cholesterol production

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6
Q

What type of hormone is insulin?

How about glycogen?

A

Hypoglycaemic

Hyperglycaemic

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7
Q

Other than insulin and glucagon, what other hormones regulate blood glucose levels and where do they come from?

A

Adrenaline (adrenal medulla) - reduces insulin production so blood glucose levels increase
Cortisol (adrenal cortex)
Growth hormone (anterior pituitary)

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8
Q

What does the FED state mean and what occurs?

Do liver transporters have a high or low affinity to glucose?

A

The increase in blood glucose after eating.
In a beta cell, glucose is metabolised and then insulin in released.

Low

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9
Q

What organ secretes insulin and glucagon?

A

Pancreas

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10
Q

Give some details on the islets of Langerhans

A
  • endocrine part of the pancreas
  • 2% of the total pancreatic mass
  • adult pancreas contains 1 million islets
  • beta cells (60-70%) secrete insulin
  • alpha cells (30-40%) secrete glucagon
  • deta cells secrete somatostanin (growth hormone that regulates the endocrine system, affecting neurotransmission and cell proliferation)
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11
Q

What is insulin secretion stimulated by? (long)

What inhibits it?

A
  • a rise in blood glucose
  • a rise in amino acid
    concentration in blood
  • gut hormones (secretions and other GI hormones release after food intake before blood glucose is elevated
  • glucagon to provide the fine tuning of blood glucose homeostasis

Inhibited by adrenaline

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12
Q

What is the process which leads to insulin secretion?

A
  1. Glucose comes in and is metabolised
  2. This closes potassium channels so the cell depolarises (K+ cannot leave)
  3. Calcium channels open to cause more depolarisation
  4. This causes secretion of insulin from vesicles in the beta cell
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13
Q

What happens to the insulin once it leaves the beta cell?

A

Insulin comes out the vesicles and comes in contact with the protease enzyme. This creates 2 chains (one alpha and one beta). C-peptide comes off of this (clinical use to tell if someone is producing insulin)

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14
Q

What is the secretion of glucagon stimulated by?

A
  • low blood glucose
  • high concentration of amino acids in blood (prevents hypoglycaemia)
  • adrenaline (glucagon secreted stimulated in periods of stress regardless of blood glucose)
  • can be stimulated by insulin production to stop a sudden fall in blood glucose
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15
Q

What are the metabolic effects of insulin? (5 things)

A
  1. Promotes fuel storage after a meal
  2. Promotes growth
  3. Stimulates glycogen synthesis and storage
  4. Stimulates fatty acid synthesis (once enough glycogen in liver) and storage from CHO when the intake exceeds glycogen storing capacity
  5. Stimulates amino acid uptake and protein synthesis
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16
Q

What type of receptor is the insulin receptor?

A

Tyrosine Kinase receptor

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17
Q

Explain the activation of Akt protein kinase when insulin binds

A

Insulin binds to the receptor (catalytic receptor). This receptor is a tyrosine kinase (involved in growth). This causes the receptor to phosphorylate itself.
The activated receptor is called P13. This leads to a cascade of phophorylysing all these enzymes which gives us a active protein kinase B

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18
Q

What is the effect of insulin on glucose transport?

A

More glucose is taken up into the cell and converted to glycogen by activating glycogen synthase (dephosphorylating it) to cause glucagon production.

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19
Q

Explain what GLUT 4 is and what it does

A

It is a transporter on a membrane.
When glucose levels are low, GLUT 4 is inside the cell and it is taken to the cell surface when insulin is present. It works to get more glucose into the cell.

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20
Q

How is fat breakdown stopped?

A

Inhibition by insulin through activation of Akt/PKB, and inhibition of hormone sensitive lipase.
This is processed by cAMP. Protein kinase A activates hormone sensitive lipase to breakdown triglycerides into glycerol and fatty acids.
Remove cAMP to stop the breakdown of the fatty acids due to no activation of protein kinase A

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21
Q

Explain how insulin links to RAS and MAPK

A

This is how insulin affects gene expression.
RAS binds to GDP which causes a phosphorylating cascade producing MAPK.
This forms transcription factors which can then affect protein transcription and translation.

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22
Q

Give 4 points on the hormone insulin

A
  • promotes the appearance of GLUT4 (glucose transporter) in muscle and adipose tissue
  • brains, liver, erythrocytes and pancreaus have GLUT which are not insulin dependant
  • high concentrations of insulin dependant
  • high concentrations of insulin lead to down regulation of its receptors
  • insulin effects vary in time, GLC transport and enzyme activation are very rapid, synthesis of enzymes is slow
23
Q

Give some info on glucagon

A
  • mobolises fuel
  • maintains blood glucose during fasting
  • activates glycogenolysis
  • activates gluconeogenesis
  • activates uptake of amino acids by the liver for gluconeogeneiss
  • activates FA release rom adipose tissue
  • activates FA oxidation and ketone body formation in the liver
24
Q

Give info on adrenaline and cortisol

A

Adrenaline

  • mobolises fuel during stress
  • stimulates glycogenolysis
  • stimulated fatty acid synthesis from adipose tissue

Cortisol

  • provides for long term requirements
  • stimulates amino acid mobilisation from muscle
  • stimulates gluconeogenesis
  • stimulates FA release from adipose tissue
25
Q

Explain metabolism in the FED state

A

High insulin, low glucagon
Excess of glucose is converted to fat as an LDL in adipose tissue
The transporters only appear when insulin is present
Glycogen is produced in the liver, liver takes up glucose.

Synthesis of glycogen, TAG and protein.
increase in blood glucose, amino acids and TAG and chylomicrons

26
Q

Explain metabolism in the fasting state

A

Glycogen is converted to glucose due to glucagon secretion.
The glucose can then go to the brain for the TCA cycle, to a erythrocyte to be converted to lactate.

Fatty acids (from adipose tissue) will be converted to acetyl CoA and transported to the muscle for the TCA cycle.

Amino acids need to go to the liver to make glucose (gluconeogenesis).
Liver produces ketone bodies (useful for long term energy deprivation). Liver does not have enzymes to use ketone bodies so had to go into the blood to be used by other tissues.

27
Q

When is the liver not undergoing glycogenesis?

A

In the FED state

28
Q

Explain carbohydrate and fat metabolism in the liver

A

Carbohydrate: glycogen synthesis is activated.(activates glycogen synthase and inhibits phosphorylase).
Glycolysis is activated through PFK and pyruvate kinase.
Gluconeogenesis is inhibited.

Fat: fatty acid and TAG synthesis are activated, acetyl Co A carboxylase is activated (rate limiting step). Malonyl CoA inhibits carnitine transferase. This means newly synthesised FA do not enter the mitochondria for oxidation but instead esterify to TAG.

29
Q

What happens to glucose in the brain and erythrocyte?

A

They both rely on glucose, FA cannot cross the blood-brain barrier and erythrocytes have no mitochondria.
Glucose is transported into brain and erythrocytes is independant of insulin, allowing glucose at high and low concentrations.

30
Q

What happens to glucose in adipose tissue?

A

Lipoprotein lipase is activated by insulin, allowing entry for FA for esterification and storage of TAG.
Glucose transport is increased through GLUT4 as this is needed for production of glycerol phosphate and esterification of TAG. Hormone sensitive lipase in the adipocyte is inhibited so TAG is not degraded.

31
Q

What happens to glucose in the muscle?

A

Glucose transport into muscle is increased. GLUT4 transporters increase in numbers. Glycogen synthetase is activated and phosphorylase is inhibited in the liver.
Amino acid uptake is activated and protein synthesis is increased.

32
Q

Give some details on the fasting (post-absorptive) state

A

Blood glucose concentrations peak after each and return to normal within 2 hours.
Blood glucose is removed for oxidation or storage. Concentration of insulin drops and glucagon rises.

33
Q

Where is the largest glycogen reserve?
TAG?
Protein?

A

muscle

adipose tissue
muscle

34
Q

How does glucose production in the liver occur?

A

The first supplier of blood glucose is liver glycogen.
Gluconeogenesis follows from lactate (erythrocytes and muscle), glycerol (from adipose tissue) and amino acids (from muscle).
After 24 hours, fatting all blood glucose comes from gluconeogeneis.

35
Q

What are the early events of liver and adipose tissue?

A
  • the liver maintains blood glucose concentrations at about 4mM
  • adipose tissue provides the greatest source of energy as TAGs
  • hormone sensitive lipase activated by glucagon and adrenaline
  • FA transported to the liver bound to albumin
36
Q

Explain what is meant by FA is not a gluconeogenic precursor?

A

Reaction catalysed by pyruvate dehydrogenase is pyruvate to acetyl CoA.
This reaction is irreversible.

Pyruvate dehydrogenase is activated by insulin and inhibited by glucagon. This ensures that in fasting gluconeogenic substrates are channelled into glucose production, not acetyl CoA formation. This is because we get a lot of acetyl CoA from fat.

37
Q

What are the 3 transfers of molecules that occurs in the liver in the FED state?

A

Glucose to pyruvate to acetyl CoA to FA.
Glycolytic enzymes are activated, pyruvate dehydrogenase is activated and excess acetyl CoA is channelled into FA synthesis by acetyl CoA carboxylase.

38
Q

What are the transfers the occur in the liver in the fasting state?

A

Gluconeogenic substrates into acetyl CoA is inhibited and conversion to glucose is favoured.

lactate and amino acids so pyruvate.
pyruvate to glucose or to acetyl CoA to be converted to ketone bodies.

39
Q

Give some information on ketone body formation

A

FA oxidation in the hepatocyte leads to high concentrations of acetyl CoA.
It exceeds to capacity of the TCA cycle and instead to ketone body formation.
Acetoacetate and beta hydroxybutyrate are released into the blood stream.
Most tissues oxidise a mixture of FA and KB.
Erythrocytes use glucose and the brain used glucose and kb.

40
Q

What fraction of body protein can we lose without consequences?

A

1/3

41
Q

What is the effect that fasting does on urea production?

A

Initially a lot of protein is broken down and this decreases after a few weeks due to ketone body production.

42
Q

What happens to the fuel source concentration in prolonged fasting?

A

Glucose decreased, fatty acid and ketone bodies increases.

Ketone bodies increase the most (being used the most)

43
Q

What happens to the metabolism in starvation?

A

Protein in the muscle is converted to glucose.
Liver forms ketone bodies to be used in the brain.
TAG in adipose tissue - glycerol comes off and goes to glucose in the liver.
Fatty acids are broken down and used by the liver in the TCA cycle.
Lactate produced by the erythrocytes is converted back to pyruvate.

44
Q

What happens as starvation continues?

A

More ketone bodies are recovered from the kidney.
Muscles uses FA rather than KB.
FA concentrations plateau and KB rise.
The brain can use more KB and less glucose.
The need for gluconeogenesis is reduced and muscle protein breakdown decreases.
Urea production decreases

45
Q

Explain the rate of ketone bodies with high blood glucose

A
  • act on the pancreas to stimulate insulin release
  • this limits muscle proteolysis
  • limits adipose tissue lipolysis
  • muscle tissue is conserved
46
Q

What eventually happens to during starvation?

A

The amount of adipose tissue is an important determinant of survival.
Death comes from fuel exhaustion, loss of function from loss of protein and from impairment of the immune system.
Death from starvation is very often due to infection.
About 40 days until death will occur.

47
Q

Explain the plasma glucose curves of normal and diabetic subjects

A

Type 1 and 2 diabetes will have a higher level of blood glucose.
Type 2 returns to normal blood glucose levels slower than the normal subject as some insulin is produced but the affect of it is less.
Type 1 produce no insulin so their blood glucose levels remains high.

48
Q

What are other names for type 1 and type 2 diabetes?

A

Type 1 = insulin dependant

Type 2 = non-insulin dependant diabetes

49
Q

Give some information on type 1 diabetes

A

Autoimmune destruction of beta cells.
It is an early onset and can lead to fatigue, weight loss, muscle wasting and weakness.
Leads to hyperglycemia and needs insulin treatment

50
Q

Give some information on type 2 diabetes

A

Usually late onset.
Insulin resistance (target tissues non responsive).
Association with diet and lifestyle.
Major increase in incidence.
Hyperglycaemia but usually no ketoacidosis.

51
Q

Explain how the metabolic pattern in uncontrolled diabetes resembles that or starvation

A

starvation = low insulin, diabetes = none or low insulin levels
Glucagon acts unopposed
KB produced in starvation stimulate insulin release.
This limits muscle protein breakdown, release of FA from adipocytes and the uncontrolled production of KB.

52
Q

Explain the metabolism in diabetes

A

Similar to starvation pattern.
Ketone bodies and glucose levels rise.
No insulin, high glucagon.

53
Q

What are the treatments for type 1 and type 2 diabetes?

A

Type 1: exogenous insulin by injection, important to balance dosage with amount if food to avoid hypoglycaemic incidents

Type 2 = weight reduction, dietary modification, oral hypoglycaemic agents, biguanides to increased the number of GLUT4, sulphonylureas act on the beta cells to improve insulin secretion

Dentistry Biological Science (88 decks)

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