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Nutrition and Metabolism > Integration Of Metabolism > Flashcards

Integration Of Metabolism Flashcards

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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

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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

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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

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A

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

24
Q

3 main functions of cortisol

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A

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

25
Describe the fed state
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
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
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
Describe the metabolism of fat in the liver | How are TAGS made from excess glucose
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
Describe metabolism in the brain and RBCs What substrates does it use and why What GLUT channels are used?
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
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
Glucose transport into muscle increases GLUT4 transporters increase in no Glycogen synthase activated, phosphorylase inhibited AA uptake and protein synthesis increases
30
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
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
What is the fasting state
[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
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
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
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
1st supplier = liver glycogen Gluconeogenesis follows from lactate (RBC and muscles), glycerol (adipose), AA (muscle) After 24hours, glucose comes only from gluconeogenesis
34
FA and gluconeogenesis precursors What reaction is inhibited by glucagon and stimulated by insulin What is the key enzyme here
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
Describe the pathway for glucose in the liver during the fed state
``` Glucose Pyruvate (Pyruvate dehydrogenase) Acetyl CoA (Acetyl CoA carboxylase) FA ```
36
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
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
How are ketone bodies formed What molecules are they formed from Name the 3 ketone bodies What tissues can metabolise KB?
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
Why are ketone bodies metabolised
Conserves protein and glucose
39
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
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
4 main functions of ketone bodies
Acts on pancreas, stimulate insulin release Limits muscle proteolysis Limits adipose tissue lipolysis Muscle tissue conserved, less urea lost
41
How will you die in starvation | What macronutrient determines your survival
Amount of adipose tissue=important determinant of survival | Death, from fuel exhaustion, loss of function from protein loss, immune system impairment, infection
42
Describe the glucose tolerance curves of normal and diabetic subjects
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
What is the renal threshold
The max conc that the kidney can process and reabsorb
44
Types of diabetes mellitus
T1, insulin dependent | T2, non insulin dependent
45
What is T1D What are the associated symptoms What 2 conditions are they at risk for How is it treated
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
What is T2D What are they at risk for How is it managed
Usually late onset, insulin resistant Lifestyle associated, major increase in incidence Hyperglycaemia, normally no ketoacidosis Responds to diet and hypoglycemic agents
47
Metabolic patterns in uncontrolled diabetes mellitus
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
4 main chronic complications of diabetes mellitus
Microangiopathy Retinopathy Nephropathy Neuropathy
49
Treatment for T1
Exogenous insulin injection | Balance dosage with amounts in food
50
Treatment for T2D | 2 drugs that help manage T2D
Weight reduction, dietary modification Biguianides increase GLUT4 number Sulphonyureas act on b cells, increase insulin secretion
51
Criteria for a metabolic syndrome
High fasting glucose/insulin resistance/diabetes T2 ``` 2 of Hypertension Dyslipidaemia (increased TAG, decreased HDL) Central obesity Microalbuminuria ```
52
The mechanism by which glucagon functions
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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