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Integration Flashcards

1
Q

Insulin is synthesised as __________ in ___ cells of the pancreas
______________ → _______________ → Insulin + _____________ (marker of insulin secretion)

A

Preproinsulin → Proinsulin (A+B+C) → Insulin (A+B) + C-peptide

  • ß-cells of pancreas
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2
Q

How is insulin secretion measured?

A

Indirectly via measurement of C-peptide

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3
Q

Describe the signal transduction pathway of insulin.

A

→ bind to RTK → P IRS (insulin receptor substrate)

1) → Activate Protein phosphatase-1

a) Dephosphorylate glycogen synthase → active → ↑glycogenesis

b) Dephosphorylate glycogen phosphorylase → inactive → ↓glycogenolysis

2)

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4
Q

What are 3 metabolic effects of insulin?

A

Anabolic hormone:
1) ↑Glycogenesis
2) ↑FA synthesis and storage
3) ↑ Protein synthesis

4) ↑ Glucose uptake (via GLUT4)
- in skeletal muscle and adipocytes

5) ↑Cell proliferation and differentiation

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5
Q

What type of membrane receptor is activated by insulin?

A

Tyrosine Kinase Receptor

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6
Q

Glucagon is synthesised as a (active/inactive) precursor and secreted by ___ cells in the pancreas is inhibited by __________ and activated by _______________

A

Glucagon (inactive) ← α cells
+: Amino acids
-: Insulin

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7
Q

What are 2 biochemical effects of glucagon?

A

Liver:
1) ↑Glycogenolysis
2) ↑Gluconeogenesis

Adipose tissue:
3) ↑Lipolysis

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8
Q

What type of membrane receptor is activated by glucagon?

A

GPCR

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9
Q

Describe the cell signalling pathway for glucagon.

A

→ bind to GPCR → release α-subunit
→ activate adenylate cyclase → (ATP→cAMP)
→ activate Protein Kinase A

a) → P glycogen synthase (inactive)
→ ↓glycogenesis

b) → P phosphorylase kinase → P glycogen phosphorylase
→ ↑glycogenolysis

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10
Q

Adrenaline is a ___________ synthesised from __________ by the ________________. It is stimulated by ______________.

A

Catecholamine from Tyrosine by Adrenal glands.
+: Acute stress

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11
Q

What are 2 receptors and their organ locations that respond to adrenaline.

A

1) α-adrenergic receptor (eg. liver and pancreas)

2) ß-adrenergic receptor (eg. liver, skeletal muscle, adipose tissue)

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12
Q

What type of membrane receptors respond to adrenaline (RTK or GPCR)?

A

GPCR

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13
Q

What are 3 metabolic effects of adrenaline?

A

1) ↑Glycogenolysis in liver and muscles
2) ↑Lipolysis
3) ↑Gluconeogenesis

4) ↑Glucagon ↓Insulin by pancreas

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14
Q

Describe the cell signalling pathway in adrenaline via the α-receptor.

A

→ bind to α-adrenergic GPCR
→ Activate PLCß
→ PIP2 → IP3 + DAG

IP3 → IP3-gated Ca2+ channel on ER

Ca2+ + DAG → Protein kinase C

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15
Q

Adrenaline ________ insulin secretion and _________ glucagon secretion.

A

↓Insulin
↑Glucagon

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16
Q

What is the moa of cholera toxin from Vibrio cholera?

A

ß-subunit bind to intestinal cells → allow α-subunit entry

α-subunit → ARF → ribosylation of GPCR → active

α-subunit of GPCR → cAMP → PKA activation → Pi of CFTR → efflux of Cl- and water → diarrhoea

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17
Q

What are the biochemical pathways affected in a early refed state and how are they affected?

A

Early refed → ↑insulin ↓glucagon

Liver:
↑Gluconeogenesis → ↑Glycogenesis
- rate of gluconeogenesis declines as insulin ↑

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18
Q

How does blood glucose ↓ after a meal?

A

1) ↑ Liver uptake by GLUT 2

2) ↑insulin → ↑muscle and adipose tissue uptake by GLUT 4

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19
Q

What are the biochemical pathways affected in a well fed state and how are they affected?

A

Well fed → High insulin, low glucagon

Liver:
1) ↑Glycogenesis
2) ↑Glycolysis
3) ↑TG synthesis

Adipose tissue:
1) ↑TG synthesis (↑LDL + ↑GLUT4)

Muscles:
1) ↑Glycogenesis (↑GLUT4)

All tissues:
↑ Protein synthesis

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20
Q

What happens to lactate produced in RBC?

A

Handled by Cori cycle → Liver → NAD+ → Pyruvate

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21
Q

Why does the muscle use FAs and KBs instead of glucose in a early fasting state?

A

During fasting → ↓insulin → GLUT 4 is endocytosed to be stored in vesicles
→ ↓ glucose uptake

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22
Q

What are the biochemical pathways affected in a early fasting state and how are they affected?

A

Early fast: High glucagon, low insulin

Liver:
1) ↑Glycogenolysis
2) ↑Gluconeogenesis (esp from glucogenic amino acids)
3) Ketogenesis (if excess Acetyl CoA)

Adipose tissue:
1) ↑ß-oxidation
2) ↑Lipolysis (↑HSL)

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23
Q

Why do patients doing blood tests for annual checkups need to fast overnight?

A

Removes confounding factor of meal contents

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24
Q

Why are patients doing blood tests for annual checkups not tested for chylomicrons and VLDL?

A

Chylomicrons and VLDL removed by liver in prolonged fast → too low for meaningful measurement

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25
Describe the changes in liver glycogenolysis and gluconeogenesis from early to prolonged fasting.
Early: Liver glycogenolysis peak @8-10hrs → ↓rate Glucogenic phase: - glycogen stores depletes by day 1.5-2 - rising and peak gluconeogenesis
26
What is the glucogenic phase (3 features)?
Phase where early and prolonged fasting overlap: 1) Brain uses glucose 2) Glucose mainly from gluconeogenesis 3) High rate of proteolysis
27
What is the protein conservation phase (2 features)?
Prolonged fasting: 1) Brain progressively use > ketone bodies 2) ↓Proteolysis as rate of gluconeogenesis ↓ (still occurring but lower rate)
28
What are the hormones produced in prolonged fast?
Glucagon and cortisol
29
What are the biochemical pathways affected in a prolonged fasting state and how are they affected?
Prolonged fast → high glucagon and cortisol Liver: - gluconeogenesis Adipose tissue: - Lipolysis Skeletal muscle: - Proteolysis
30
What is the effect of elevated cortisol in a prolonged fast?
1) Lipolysis → glycerol → gluconeogenesis 2) Proteolysis → Glucogenic amino acids → gluconeogenesis
31
Describe the process of cortisol secretion during starvation.
Starvation → hypoglycemia Hypothalamic regulation center → ACTH from pituitary → Cortisol from adrenal gland
32
How does the main fuel of the liver and brain differ in (i) well fed, (ii) overnight fasting, (iii) prolonged fasting?
Liver: i) Glucose ii) FA iii) FA Brain: i) Glucose ii) Glucose iii) KB/Glucose
33
What is the range for moderate BMI in singapore?
23 - 27.4
34
Why is waist circumference measured?
For abdominal obesity: - most practical anthropometric measurement - must be used in conjuction with BMI
35
What is the cutoff for waist circumference for abdominal obesity?
M: <90cm F: <80cm
36
What are the 2 types of adipose tissue?
1) Subcutaneous 2) Visceral
37
What is the difference between subcutaneous and visceral obesity?
Subcutaneous: - can expand through hyperplasia - safe and normal Visceral: - stores excess fat from SAT - enlargement of VAT (hypertrophy) → pathology (M2 → M1/proinflammatory macrophage)
38
What are 2 functions of adipocytes?
1) Storage of fats 2) Production and secretion of adipokines and cytokines
39
How does visceral obesity lead to insulin resistance?
Accumulation of visceral fat → M2 → M1 → ↑pro-inflammatory cytokines → ↑FFA release FFA → inhibit insulin signalling pathway → insulin resistance → ↓uptake by GLUT 4 + ↑gluconeogenesis
40
What is the criteria for metabolic syndrome?
≥ 3 of: 1) ↑Waist circumference (>80/90) 2) ↑HDL (<1.3/1mmol/L) 3) ↑Fasting blood glucose (6.1mmol/L) 4) ↑BP (>130/85mmHg)
41
What is the significance of having metabolic syndrome?
- 2x more likely to have heart disease - 5x more likely to have DM - even 1 risk factor → heart disease
42
With a low carbohydrate diet, what happens after feeding?
Low carbohydrate → no ↑blood glucose → low insulin, high glucagon → Liver remains in gluconeogenic and ketogenic mode
43
Why is there a loss in lean body mass/muscle in a low-carbohydrate diet? How is it prevented?
Low carb diet → Liver maintain gluconeogenesis (must come from glucogenic amino acids) → proteins undergo proteolysis to provide glucogenic amino acids - Ensure sufficient protein in diet
44
What happens hormonally after a low carb, high protein meal?
1) Significant ↑↑glucagon → ↑gluconeogenesis → ↑lipolysis → ↑ketogenesis 2) Small ↑insulin → protein synthesis
45
Why is a high protein diet not suitable for px with renal dysfunction?
↑↑Urea need to be excreted
46
What are 2 anti-obesity medications approved in singapore and what are their moas?
1) Orlistat - lipase inhibitor → ↓TG digestion and absorption 2) Phentermine - stimulate NE release → ↑satiety → ↓appetite - may trigger NE/E from adrenal glands → fuel mobilisation
47
What is the moa of GLP-1 receptor agonists (eg. semaglutide)?
Mimic endogenous incretins (eg. GLP-1) → Stimulate GLP-1 receptor: 1) Stimulate insulin secretion 2) ↓appetite and hunger
48
What is high fructose corn syrup?
Corn syrup subjected to enzymatic rxn to convert glucose and fructose → sweeter
49
Why does the consumption of high fructose corn syrup lead to increased lipogenesis?
Fructose metabolised in liver a) Dihydroxyacetone-P→ G3P → Lipogenesis b) Dihydroxyacetone-P or Glyceraldehyde-3-P → Glycolysis → Acetyl-CoA → Lipogensis
50
Which reducing equivalent is produced in ethanol metabolism?
NADH
51
What are 2 ways ethanol is metabolised?
1) Alcohol dehydrogenase (ADH) in cytoplasm 2) Microsomal ethanol oxidising system (MEOS, CYP2E1) in ER → Acetaldehyde (very reactive) → Acetaldehyde dehydrogenase → Acetate (non-toxic) in mitochondria
52
Acetate produced from the detoxification of acetaldehyde produces ____________ when metabolised.
Acetyl CoA and AMP
53
What is alcohol flushing syndrome?
Flushing after drinking alcohol due to high levels of acetaldehyde by: 1) Deficient ALDH2 (↓conversion to acetate) 2) Super-active ADH (↑production of acetaldehyde) 3) Alcohol itself → vasodilation under skin → flushing
54
How does ethanol consumption affect (i) glucose, (ii) lactate and (iii) blood pH?
Ethanol metabolism → ↑NADH → ↓gluconeogenesis → ↓glucose, ↑lactic acidosis
55
Why do alcoholics have increased risk of fatty liver?
↑Ethanol metabolism → ↑NADH → ↑ß-oxidation → ↑FA → ↑TG by: 1) ↑catalysis by ethanol (via acyltransferases) 2) ↓secretion of VLDL due to liver dmg 3) ↑NADH → ↑glycerol-3-P from dihydroxyacetone phosphate When rate TG synthesis >> VLDL packaging → Fatty liver
56
What are 3 reasons why acetaldehyde is toxic?
1) Forms covalent bonds with functional groups in proteins, nucleotides and phospholipid 2) Binds to glutathione → ↓antioxidant capacity 3) Inhibit tubulin polymerisation/damage microtubules → ↓secretion of VLDL secretion
57
Why are px with gout advised against consuming excessive alcohol?
↑Alcohol → ↑Acetate (+ AMP) AMP→...→Uric acid (beer also contains purines → uric acid)
58
What is the order of fuel consumption during anaerobic exercise?
1) Muscle ATP (1.2s) 2) Creatine phosphate (9s) 3) Muscle glycogen (anaerobic glycolysis)
59
What are 3 ways glycogenolysis is stimulated specifically during exercise?
1) Muscle contraction - AMP → P-ed Glycogen phosphorylase (active) → ↑glycogenolysis 2) Nerve impulse → Ca2+ → Calmodulin → P-ed Phosphorylase kinase → P-ed Glycogen phosphorylase (active) → ↑glycogenolysis 3) Epinephrine → cAMP → Protein Kinase A → P-ed Glycogen phosphorylase (active) → ↑glycogenolysis
60
What are the fuel(s) consumed during anaerobic exercise?
1) Glucose 2) Fatty acid 3) Amino acids
61
What 2 main hormonal control of metabolic events?
1) ↓Glucose → ↑Glucagon: - lipolysis → FA - Glycogenolysis + Gluconeogenesis → glucose 2) Epinephrine: - lipolysis → FA - glycogenolysis and gluconeogenesis in liver → glucose - glycogenolysis in skeletal muscle → G1P → G6P
62
What is the preferred fuel during aerobic exercise. Why?
Fatty acid. ß-oxidation → >ATP per C than glycolysis
63
What are 2 roles of AMP during exercise?
1) Allosteric activator of glycogen phosphorylase (glycogenolysis) and PFK-1 (glycolysis) 2) Activate AMPK Skeletal muscle: → ↑glucose uptake → ↑ß-oxidation Liver: → inhibit gluconeogenesis → inhibit TG and cholesterol synthesis → ß-oxidation
64
How does muscle contraction increase the muscle's sensitivity to insulin?
AMP activates AMPK: → exocytosis of GLUT4 vesicles
65
What are 3 situations during exercise where lactate/anaerobic metabolism occurs?
1) Short, intense exercise and only fast twitch 2) Initial period of exercise (>1 min lag time for sympathetic ↑ in blood flow) 3) Prolonged exercise (ATP Dd>Ss by oxphos)
66
What are 3 types of muscle fibres and how are they different?
Type 1 (slow twitch) - prolonged aerobic exercise - low glycogen stores - high myoglobin and capillaries - high aerobic capacity Type 2b (fast twitch) - sprinting and resistance - high glycogen stores - low myoglobin and mitochondria - mainly anaerobic → easily fatigued
67
What are the metabolic effects of training?
General: ↑glycogen stores ↑no. and size of mitochondria → > efficient oxidation of fuels Resistance training: ↑strength, power, endurance Hypertrophy of muscle via ↑protein synthesis and ↓proteolysis
68
What fuels are used by cardiac muscles in descending order?
1) fatty acids 2) glucose
69
Glucose transport in the heart is 90% via _____________, but also expresses ____________, despite having ___________ stores.
90% GLUT4 express GLUT 1 has glycogen stores
70
How does fuel metabolism in cardiac muscles differ in normal and ischemic conditions?
Normal: Aerobic (FA > glucose) Ischemic: Anaerobic → ↑lactate

Metabolism and Biochem (8 decks)

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