Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Metabolism and Biochem > Integration > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is insulin secretion measured?

A

Indirectly via measurement of C-peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of membrane receptor is activated by insulin?

A

Tyrosine Kinase Receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are 2 biochemical effects of glucagon?

A

Liver:
1) ↑Glycogenolysis
2) ↑Gluconeogenesis

Adipose tissue:
3) ↑Lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What type of membrane receptor is activated by glucagon?

A

GPCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Catecholamine from Tyrosine by Adrenal glands.
+: Acute stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

GPCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adrenaline ________ insulin secretion and _________ glucagon secretion.

A

↓Insulin
↑Glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 ↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to lactate produced in RBC?

A

Handled by Cori cycle → Liver → NAD+ → Pyruvate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Removes confounding factor of meal contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the changes in liver glycogenolysis and gluconeogenesis from early to prolonged fasting.

A

Early:
Liver glycogenolysis peak @8-10hrs → ↓rate

Glucogenic phase:
- glycogen stores depletes by day 1.5-2
- rising and peak gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the glucogenic phase (3 features)?

A

Phase where early and prolonged fasting overlap:
1) Brain uses glucose
2) Glucose mainly from gluconeogenesis
3) High rate of proteolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the protein conservation phase (2 features)?

A

Prolonged fasting:
1) Brain progressively use > ketone bodies

2) ↓Proteolysis as rate of gluconeogenesis ↓ (still occurring but lower rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the hormones produced in prolonged fast?

A

Glucagon and cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

Prolonged fast → high glucagon and cortisol

Liver:
- gluconeogenesis

Adipose tissue:
- Lipolysis

Skeletal muscle:
- Proteolysis

30
Q

What is the effect of elevated cortisol in a prolonged fast?

A

1) Lipolysis → glycerol → gluconeogenesis

2) Proteolysis → Glucogenic amino acids → gluconeogenesis

31
Q

Describe the process of cortisol secretion during starvation.

A

Starvation → hypoglycemia

Hypothalamic regulation center
→ ACTH from pituitary
→ Cortisol from adrenal gland

32
Q

How does the main fuel of the liver and brain differ in (i) well fed, (ii) overnight fasting, (iii) prolonged fasting?

A

Liver:
i) Glucose
ii) FA
iii) FA

Brain:
i) Glucose
ii) Glucose
iii) KB/Glucose

33
Q

What is the range for moderate BMI in singapore?

A

23 - 27.4

34
Q

Why is waist circumference measured?

A

For abdominal obesity:
- most practical anthropometric measurement

  • must be used in conjuction with BMI
35
Q

What is the cutoff for waist circumference for abdominal obesity?

A

M: <90cm
F: <80cm

36
Q

What are the 2 types of adipose tissue?

A

1) Subcutaneous
2) Visceral

37
Q

What is the difference between subcutaneous and visceral obesity?

A

Subcutaneous:
- can expand through hyperplasia
- safe and normal

Visceral:
- stores excess fat from SAT
- enlargement of VAT (hypertrophy) → pathology (M2 → M1/proinflammatory macrophage)

38
Q

What are 2 functions of adipocytes?

A

1) Storage of fats
2) Production and secretion of adipokines and cytokines

39
Q

How does visceral obesity lead to insulin resistance?

A

Accumulation of visceral fat
→ M2 → M1
→ ↑pro-inflammatory cytokines → ↑FFA release

FFA → inhibit insulin signalling pathway → insulin resistance → ↓uptake by GLUT 4 + ↑gluconeogenesis

40
Q

What is the criteria for metabolic syndrome?

A

≥ 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
Q

What is the significance of having metabolic syndrome?

A
  • 2x more likely to have heart disease
  • 5x more likely to have DM
  • even 1 risk factor → heart disease
42
Q

With a low carbohydrate diet, what happens after feeding?

A

Low carbohydrate → no ↑blood glucose
→ low insulin, high glucagon
→ Liver remains in gluconeogenic and ketogenic mode

43
Q

Why is there a loss in lean body mass/muscle in a low-carbohydrate diet? How is it prevented?

A

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
Q

What happens hormonally after a low carb, high protein meal?

A

1) Significant ↑↑glucagon
→ ↑gluconeogenesis
→ ↑lipolysis → ↑ketogenesis

2) Small ↑insulin
→ protein synthesis

45
Q

Why is a high protein diet not suitable for px with renal dysfunction?

A

↑↑Urea need to be excreted

46
Q

What are 2 anti-obesity medications approved in singapore and what are their moas?

A

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
Q

What is the moa of GLP-1 receptor agonists (eg. semaglutide)?

A

Mimic endogenous incretins (eg. GLP-1) → Stimulate GLP-1 receptor:
1) Stimulate insulin secretion
2) ↓appetite and hunger

48
Q

What is high fructose corn syrup?

A

Corn syrup subjected to enzymatic rxn to convert glucose and fructose → sweeter

49
Q

Why does the consumption of high fructose corn syrup lead to increased lipogenesis?

A

Fructose metabolised in liver a) Dihydroxyacetone-P→ G3P → Lipogenesis

b) Dihydroxyacetone-P or Glyceraldehyde-3-P → Glycolysis → Acetyl-CoA → Lipogensis

50
Q

Which reducing equivalent is produced in ethanol metabolism?

A

NADH

51
Q

What are 2 ways ethanol is metabolised?

A

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
Q

Acetate produced from the detoxification of acetaldehyde produces ____________ when metabolised.

A

Acetyl CoA and AMP

53
Q

What is alcohol flushing syndrome?

A

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
Q

How does ethanol consumption affect (i) glucose, (ii) lactate and (iii) blood pH?

A

Ethanol metabolism → ↑NADH
→ ↓gluconeogenesis
→ ↓glucose, ↑lactic acidosis

55
Q

Why do alcoholics have increased risk of fatty liver?

A

↑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&raquo_space; VLDL packaging → Fatty liver

56
Q

What are 3 reasons why acetaldehyde is toxic?

A

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
Q

Why are px with gout advised against consuming excessive alcohol?

A

↑Alcohol → ↑Acetate (+ AMP)

AMP→…→Uric acid

(beer also contains purines → uric acid)

58
Q

What is the order of fuel consumption during anaerobic exercise?

A

1) Muscle ATP (1.2s)
2) Creatine phosphate (9s)
3) Muscle glycogen (anaerobic glycolysis)

59
Q

What are 3 ways glycogenolysis is stimulated specifically during exercise?

A

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
Q

What are the fuel(s) consumed during anaerobic exercise?

A

1) Glucose
2) Fatty acid
3) Amino acids

61
Q

What 2 main hormonal control of metabolic events?

A

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
Q

What is the preferred fuel during aerobic exercise. Why?

A

Fatty acid.
ß-oxidation → >ATP per C than glycolysis

63
Q

What are 2 roles of AMP during exercise?

A

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
Q

How does muscle contraction increase the muscle’s sensitivity to insulin?

A

AMP activates AMPK:
→ exocytosis of GLUT4 vesicles

65
Q

What are 3 situations during exercise where lactate/anaerobic metabolism occurs?

A

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
Q

What are 3 types of muscle fibres and how are they different?

A

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
Q

What are the metabolic effects of training?

A

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
Q

What fuels are used by cardiac muscles in descending order?

A

1) fatty acids
2) glucose

69
Q

Glucose transport in the heart is 90% via _____________, but also expresses ____________, despite having ___________ stores.

A

90% GLUT4
express GLUT 1
has glycogen stores

70
Q

How does fuel metabolism in cardiac muscles differ in normal and ischemic conditions?

A

Normal: Aerobic (FA > glucose)
Ischemic: Anaerobic → ↑lactate

Metabolism and Biochem (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions