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Nutrition and Metabolism > Integration Of Metabolism > Flashcards

Integration Of Metabolism Flashcards

1
Q

Definition of hypoglycaemic hormone

A

Hormones that lower blood glucose such as insulin

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2
Q

Definition of hyperglycaemic hormone

A

Hormones that raise blood glucose such as glucagon, adrenaline

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3
Q

Describe the supply and demand for fuel

A

Demand=constant
Supply=intermittent
Changes in circulating [hormones] allows body to
-store fuel when available
-mobilise in starvation, injury and stress

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4
Q

Ways to change metabolic patterns

A

Variation in amount of substrate available
Allosteric effects
Covalent modification
Enzyme synthesis changes

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5
Q

How does variation in the amount of substrate available change metabolic patterns
What happens when there isn’t enough glucose

A

FA used in starvation when there is not enough glucose

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6
Q

How do allosteric effects change metabolic patterns

What molecule stimulates glycolysis in skeletal muscle, what enzyme is stimulated

A

Increase in AMP activates phosphofructokinase in muscle for more ATP production in glycolysis

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7
Q

How does covalent modification change metabolic patterns

How is the enzyme glycogen phosphorylase modified so that it is active

A

Phosphorylation of glycogen, phosphorylase, synthesise

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8
Q

How does a change in enzyme synthesis affect metabolic patterns
How does the amount of dietary cholesterol alter the enzymes activity

A

Glucokinase and dietary CHO

If you eat more CHO, increase in glucokinase, increase in HMG CoA reductase, cholesterol synthesis

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9
Q

Hormones involved in intermediary metabolism control

What 3 hormones inhibit insulin

A

Insulin, hypoglycaemic hormone
Glucagon, hyperglycaemic hormone

Adrenaline (adrenal medulla)
Cortisol (adrenal cortex)
GH (anterior pituitary), all counter regulatory of insulin

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10
Q

Describe the structure of the Islets of Langerhans

What are the 3 main endocrine cells

A 
Endocrine pancreas (2%)
a cells (30-40%) secrete glucagon
b cells (60-70%) secrete insulin
d cells secrete somatostatin
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11
Q

When is insulin released and what happens when it is?

What inhibits insulin

A

Increase in [glucose], [AA] in the blood

Gut hormones
-secretin, GI hormones released after food intake before [glucose] increases

Glucagon
-released to fine tune [glucose]

Insulin inhibited by adrenaline

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12
Q

Describe the process that causes the beta cells to release insulin

A

Glucose enters via GLUT2, AA enter cell via channels into B cell
Glucokinase acts on glucose, respires it, ATP synthesised
AA transaminated, ATP synthesised

Increasing ATP conc causes K channels to close, changes polarity of membrane
This opens the Ca channels

Increasing [Ca] in the cell causes insulin release

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13
Q

Processing of pro insulin

A

Proinsulin has a square spiral shape with 3 disulphides bonds and a C peptide

Proteolysis separates insulin from C peptide
Function of C peptide unknown

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14
Q

What happens when glucagon is released

A

Released when [glucose] decreases, [AA] increases in blood to prevent hypoglycaemia after protein meal

Adrenaline released regardless of [glucose]

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15
Q

5 main metabolic effects of insulin on the body

A

Promotes fuel storage after a meal
Promotes growth
Stimulates glycogen synthesis and storage
Stimulates FA synthesis and storage from CHO when intake exceeds glycogen storing capacity
Stimulates AA uptake and protein synthesis

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16
Q

Describe the structure of the insulin receptors

A

Transmembrane
2 alpha subunits on extracellular side
2 transmembrane b subunits
Cytosidic part has 3 Pi attached to each subunit

First Pi, docking site for insulin receptor substrate
Second Pi, used in kinase activation, attached to tyrosine kinase
Third Pi, growth promoting activity

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17
Q

Describe the metabolic pathway of insulin after it has bound to the insulin receptor

A

Once insulin has bound to the receptor
Tyrosine kinase is activated (auto phosphorylation)
Secondary messenger signalling via a chain of phosphorylation reactions occur which activates Akt protein kinase

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18
Q

Describe the effects of insulin on glucose transport
What are the enzymes involved
How are they activated
How do we increase the amount of glycogen formed

A

Glycogen synthase kinase =(Akt/PKB)=> glycogen synthase kinasePi
Glycogen synthase kinasePi inactivated so cannot phosphorylate GS

glycogen synthase => activated

Active Akt/PKB => GLUT 4 containing vesicles fuse with membrane => more glucose can be converted to glycogen

In the liver, GLUT2 is used instead of GLUT4

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19
Q

Describe the effects of insulin on the inhibition of lipolysis in adipocytes
What enzymes are involved
What enzymes are inhibited as a result
Describe the effects of glucagon on hormone sensitive lipase

A

PDE =(Akt/PKB + Pi)=> PDE(Pi)

PDE inhibits PKA
cAMP =(PDE)=> AMP

Hormone sensitive lipase is inhibited so TAGs cannot be hydrolysed to glycerol and FA

Glucagon activates hormone sensitive lipase

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20
Q

Describe the effect of insulin on gene expression through Ras and MAPK

A

SHC is phosphorylated and phosphorylates Ras
Ras GTP =>Ras GDP, activates Raf
Raf causes the phosphorylation of Mek
Phosphorylated Mek phosphorylates Erk

Erk (MAPK) acts on the transcription factors and alters gene expression

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21
Q

1 main function of insulin
Effects of insulin, long term and short term
What happens to the sensitivity of the insulin receptors when insulin is high

A

Promotes appearance of GLUT4 in muscle and adipose
Brain, liver, RBCs, pancreas have GLUT2, not insulin dependent

Increase in [insulin], down regulation of its receptors

Short term action, glucose transport and enzyme activation
Long term action, enzyme synthesis

22
Q

Functions of glucagon

What 5 processes does it activate

A

Mobilises fuel
Maintains blood glucose during fasting

Activates
Glycogenolysis
Gluconeogenesis
Uptake of AA by liver for gluconeogenesis
FA release from adipose
FA oxidation and ketone body formation in the liver

23
Q

3 main functions of adrenaline

A

Mobilises fuel during stress
Increases glycogenolysis in muscle and liver
Increases FA release from adipose tissue

24
Q

3 main functions of cortisol

A

Long term requirements
Increases AA mobilisation for muscle,
increased gluconeogenesis
increase FA release from adipose

25
Q

Describe the fed state

A

2-4 hours after a meal
Increase in [glucose], AA, TAGs as chylomicrons
Synthesis/storage of glycogen, TAG and proteins
Liver receives nutrients before other tissues via hepatic portal vein
Excess glucose in liver => acetyl CoA => VLDL

26
Q

Describe the liver when it metabolises carbohydrate
What are the main processes active in
-the fed state
-the fasting state

How is the Km different in the liver compared to the brain

A

Fasting
-Gluconeogenesis

Fed

  • Glycolysis activated through PFK and pyruvate kinase
  • Glycogen synthase (active when dephosphorylated)
  • Gluconeogenesis inhibited

High Km, no competition with brain when [glucose] is low

27
Q

Describe the metabolism of fat in the liver

How are TAGS made from excess glucose

A

Dihydroxyacetone-3-phosphate => glycerol phosphate

Acetyl CoA + Oxaloacetate =(citrate synthase)=> citrate
Citrate =(citrate ATP lyase)=> oxaloacetate + acetyl CoA
Acetyl CoA + CO2 =(Acetyl CoA carboxylase)=> Malonyl CoA

Malonyl CoA inhibits carnitine transferase

Glycerol phosphate + 3 FA => TAGS

28
Q

Describe metabolism in the brain and RBCs
What substrates does it use and why
What GLUT channels are used?

A

Both rely on glucose, FA cannot cross blood brain barrier, RBC has no mitochondria
Glucose transport independent of insulin GLUT1
Allows use of glucose at high and low conics

29
Q

Muscle and metabolism here in the fed state
What GLUT transporters are used
What process is dominant here and what enzyme is key
What else happens in the muscle

A

Glucose transport into muscle increases
GLUT4 transporters increase in no
Glycogen synthase activated, phosphorylase inhibited
AA uptake and protein synthesis increases

30
Q

Adipose tissue in the fed state
What enzyme is activated by insulin
Why is this enzyme important in storage
What GLUT transporter is found here and why is it important
What enzyme is inhibited by insulin and why

A

Lipoprotein lipase activated by insulin
Allows FA entry for esterification, TAG storage

Glucose transport increases via GLUT4
Glucose needed for glycerol phosphate production, TAG esterification

Hormone sensitive lipase in adipocytes inhibited, TAG not degraded

31
Q

What is the fasting state

A

[glucose] peak an hour after eating
Return to normal by 2 hours after a meal
Blood glucose removed for oxidation/storage
[insulin] decreases and [glucagon] increases

32
Q

Describe the early events of the fasting state in the liver, adipose tissue
What is the main energy source
What enzyme is activated by which 2 hormones
How are the FA transported to the liver

A

Liver maintains [glucose] at 4mM
Adipose tissue provides greatest energy source (TAG)
Hormone sensitive lipase activated by glucagon, adrenaline
FA transported => liver, bound to albumin

33
Q

Describe glucose production by the liver during the fasting state
What is the main source of energy
What is the other process that occurs and what 3 substrates are broken down
After 24hrs, what is the dominant process

A

1st supplier = liver glycogen
Gluconeogenesis follows from lactate (RBC and muscles), glycerol (adipose), AA (muscle)

After 24hours, glucose comes only from gluconeogenesis

34
Q

FA and gluconeogenesis precursors
What reaction is inhibited by glucagon and stimulated by insulin
What is the key enzyme here

A

Reaction catalysed by pyruvate dehydrogenase = irreversible
Pyruvate + CoA + NAD =(pyruvate dehydrogenase)=> acetyl CoA + NADH + H+

PDH is insulin activated, glucagon inhibited
Ensures that in fasting, gluconeogenic substrates are channeled => glucose production not acetyl CoA formation

35
Q

Describe the pathway for glucose in the liver during the fed state

A 
Glucose
Pyruvate
(Pyruvate dehydrogenase)
Acetyl CoA
(Acetyl CoA carboxylase)
FA
36
Q

Describe metabolism during the fasting state in the liver
How are FA used as a fuel source in fasting
What cells can use FA
How does acetyl CoA inhibit the Link reaction

A

FA can be used as a fuel by liver, adipocytes and muscle

FA => Acetyl CoA => ketone bodies
Acetyl CoA inhibits PDH so lactate, AA, pyruvate => glucose

37
Q

How are ketone bodies formed
What molecules are they formed from
Name the 3 ketone bodies

What tissues can metabolise KB?

A

FA =(B oxidation)=> acetyl CoA
Acetyl CoA => KB

  • Acetoacetate
  • b hydroxybutyrate
  • Acetone released into the blood

Most tissues can oxidise FA, KB
RBC only uses glucose,
Brain uses glucose and KB

38
Q

Why are ketone bodies metabolised

A

Conserves protein and glucose

39
Q

What happens during prolonged starvation
How much protein can be lost without adverse affects

What is the main fuel source for muscle
What is the main fuel source for the brain
What processes are less active

A

If the early pattern continues in prolonged starvation, protein=severely depleted
1/3 of protein can be lost without severe consequences

More KB recovered from kidney
Muscle uses FA
[FA] plateaus, [KB] increases
Brain uses more KB

Need for gluconeogenesis decreases
muscle protein breakdown, urea production decreases

40
Q

4 main functions of ketone bodies

A

Acts on pancreas, stimulate insulin release
Limits muscle proteolysis
Limits adipose tissue lipolysis
Muscle tissue conserved, less urea lost

41
Q

How will you die in starvation

What macronutrient determines your survival

A

Amount of adipose tissue=important determinant of survival

Death, from fuel exhaustion, loss of function from protein loss, immune system impairment, infection

42
Q

Describe the glucose tolerance curves of normal and diabetic subjects

A

Normal,
Starts below renal threshold, increases and decreases slightly. Never exceeds the threshold

T2D
Starts below renal threshold, increases gradually, exceeds threshold but decreases over a long period of time

T1D
Starts on or above the renal threshold.
Plasma glucose conc increases and does not come down

43
Q

What is the renal threshold

A

The max conc that the kidney can process and reabsorb

44
Q

Types of diabetes mellitus

A

T1, insulin dependent

T2, non insulin dependent

45
Q

What is T1D
What are the associated symptoms
What 2 conditions are they at risk for
How is it treated

A

Autoimmune destruction of B cells
Early onset

Polyuria, polydipsia, polyphagia, fatigue, weight loss, muscle wasting, weakness

Hyperglycaemia, keto acidosis (increase in ketones, increased H+, can’t be removed)

Needs insulin

46
Q

What is T2D

What are they at risk for

How is it managed

A

Usually late onset, insulin resistant
Lifestyle associated, major increase in incidence

Hyperglycaemia, normally no ketoacidosis

Responds to diet and hypoglycemic agents

47
Q

Metabolic patterns in uncontrolled diabetes mellitus

A

In starvation, decrease in insulin, absent in T1D
Glucagon acts unopposed

The following only occurs in starvation, not in T1, T2
KB, produced in starvation, stimulate insulin release
Limits muscle protein breakdown, release of FA from adipocytes

In T1D, sometimes in T2D

  • KB => ketoacidosis and v high glucose (no insulin, glucose can’t be taken up)
  • Protein breakdown and FA release not inhibited => weight loss
48
Q

4 main chronic complications of diabetes mellitus

A

Microangiopathy
Retinopathy
Nephropathy
Neuropathy

49
Q

Treatment for T1

A

Exogenous insulin injection

Balance dosage with amounts in food

50
Q

Treatment for T2D

2 drugs that help manage T2D

A

Weight reduction, dietary modification

Biguianides increase GLUT4 number
Sulphonyureas act on b cells, increase insulin secretion

51
Q

Criteria for a metabolic syndrome

A

High fasting glucose/insulin resistance/diabetes T2

2 of
Hypertension
Dyslipidaemia (increased TAG, decreased HDL)
Central obesity
Microalbuminuria
52
Q

The mechanism by which glucagon functions

A

GPCR Gs and some Gq
Increased levels of cAMP, activates PKA
PKA can phosphorylate glycogen phosphorylase b => a

More glucose can be released

Nutrition and Metabolism (14 decks)

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