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integration of metabolism Flashcards

1
Q

entrance of hormones (polypeptide (insulin, glucagon); catecholamines (adrenaline); steroids (cholesterol)) into cells

A
  • polypeptide & catecholamines: bind to receptor -> trigger response
  • steroids: diffuse into cell
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2
Q

what is metabolic homeostasis + hormones that regulate it

A

balance between fuel availability and the needs of different tissues for different types of fuels

  • insulin, glucagon, adrenaline
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3
Q

synthesis of insulin

A
  • POLYPEPTIDE
  • synthesis occurs in B cells of pancreas
  • synthesized as inactive precursor (C peptide + A&B chains) -> processing in pancreas forms active insulin (A&B chains)
  • both C-peptide and active insulin are released into blood
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4
Q

metabolic effects of insulin - what does it STIMULATE (2)

A

synthesis and storage pathways
- glycogenesis
- fatty acid synthesis & storage
- protein synthesis

uptake of glucose by GLUT 4 transporters in skeletal muscles + adipocytes

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5
Q

signal transduction process of insulin (5)

A
  • binds to insulin receptor (RTK) -> kinase domain is phosphorylated and activated
  • IRS (insulin receptor substrate) binds to RTK -> gets phosphorylated
  • PI3 kinase docks at
    IRS -> activated & converts PIP2 to PIP3
  • docking of PDK1 and AKT to PIP3 -> cause phosphorylation of AKT by PDK1 and mTOR
  • phosphorylation of AKT makes it active, and it dissociate from PIP3 -> AKT causes effects on metabolism

*key molecules: IRS, PI3-kinase, PIP3, PDK1, mTOR, AKT

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6
Q

synthesis of glucagon

A
  • POLYPEPTIDE
  • synthesized as inactive precursor in a cells of pancreas
  • synthesis inhibited by insulin, upregulated by amino acids
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7
Q

effects of glucagon (2)

A

Liver:
- stimulates GLYCOGENOLYSIS and GLUCONEOGENESIS

Adipose tissue:
- stimulate LIPOLYSIS (triglyceride -> fatty acid acid + glycerol)

**muscles do not express glucagon receptors (glucagon has NO EFFECT on muscle glycogen stores)

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8
Q

signal transduction process of glucagon

A
  • binds to GPCR -> activate glucagon receptor
  • glucagon receptor binds to G protein
  • G protein releases bound GDP and binds to GTP -> a subunit dissociates from BY subunit
  • a subunit bind and activate adenylyl cyclase
  • activated adenylyl cyclase -> converts ATP to cAMP
  • cAMP activate PKA -> PKA cause effect on metabolism
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9
Q

synthesis of adrenaline

A
  • CATECHOLAMINE (synthesized from tyrosine)
  • produced by the adrenal glands, released in response to acute stress
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10
Q

effect of adrenaline (2)

A

binds to B-receptor
- in LIVER, SKELETAL MUSCLES, ADIPOSE
- glycogenolysis in liver and muscles; gluconeogenesis; lipolysis (SAME AS GLUCAGON)

binds to a-receptor
- in LIVER, PANCREAS

inhibit insulin secretion + stimulate glucagon secretion

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11
Q

signal transduction process of adrenaline

A

B-receptor
- binds to B-adrenergic receptor -> dissociation of G protein + activate adenylyl cyclase + cAMP (SAME AS GLUCAGON)
- cAMP directly causes smooth muscle relaxation, vasodilation
- cAMP can activate PKA -> effects on metabolism (glycogenolysis in liver and muscles; gluconeogenesis; lipolysis)

a-receptor
- binds to a-receptor -> activate G protein causing dissociation of a-subunit and BY-subunit
- both a-subunit and BY-subunit activates (PLCB) phospholipase C-B
- activated PLCB cleaves PIP2 -> form IP3 and DAG
- IP3 activates release of Ca2+ from endoplasmic reticulum
- Ca2+ and DAG activates protein kinase C
- protein kinase C -> effects on fuel metabolism + smooth muscle contraction, vasoconstriction in peripheral organs w a-receptors

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12
Q

vibrio cholerae pathogenesis

A
  • produces cholera toxin
  • cholera toxin contains A & B subunit -> B-subunit binds to intestinal cells + processes A subunit -> allows A subunit to enter cell
  • interact with Arf protein -> promote ribosylation of a-subunit of G-protein -> activates G-protein
  • produce cAMP and PKA activation
  • PKA phosphorylates CFTR chloride channel -> efflux of Cl- and water from intestinal cells into intestinal lumen -> diarrhea
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13
Q

what is fed state vs fasting state

A
  • fed: high insulin, low glucagon
  • fasting: low insulin, high glucagon
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14
Q

what are the events in fed starve cycle that a person can undergo (4)

A
  • EARLY REFED state (immediately after a meal)
  • WELL FED state (last a while after a meal
  • EARLY FASTING state (begins after well fed state, usually only during overnight sleep)
  • PROLONG FASTING state (rare)
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15
Q

insulin and glucagon during early refed state

A
  • insulin rises sharply in reaction to sharp increase in blood glucose
  • glucagon begins to fall sharply
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16
Q

what happens during early refed state

A
  • liver remains in GLUCONEOGENIC mode -> generate glucose from lactate & glucogenic amino acids
  • glucose-6-P from gluconeogenesis is used for glycogen synthesis
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17
Q

types of GLUT (glucose transporters) in different tissues (activated during well fed states for uptake of glucose)

A

GLUT 2
- liver & pancreatic cell, LOWEST affinity for glucose (starts taking in glucose at high [glucose])
- always expressed on cell membrane

GLUT 4
- skeletal muscles & adipocytes, moderate affinity for glucose
- location of GLUT 4 INFLUENCED BY INSULIN

GLUT 3
- brain & nerve tissues, HIGHEST affinity for glucose (allow uptake of glucose even at basal [glucose])
- always expressed on cell membrane

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18
Q

main organs involved in well fed state (ie stimulated by insulin)

A

LIVER
- insulin stimulate glycolysis; glycogen synthesis; FA/TG synthesis
- uptake of glucose by GLUT2 (NOT due to insulin)

ADIPOSE
- insulin stimulate GLUT4 expression & uptake of glucose
- insulin stimulate synthesis and secretion of lipoprotein lipase + TG synthesis

MUSCLE
- insulin stimulate GLUT4 expression & uptake of glucose
- insulin stimulate glycogen synthesis

ALL TISSUES
- stimulate protein synthesis

*Cori cycle is inhibited -> lactate is brought to liver and converted to pyruvate -> acetyl CoA instead

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19
Q

specific processes in LIVER during well fed state

A

protein synthesis

glycolysis
- insulin activates phosphofructokinase 1 (PFK1) via fructose-2-6-bisphosphate

glycogen synthesis
- insulin and high levels of glucose leads to the activation of glycogen synthase

lipogenesis (FA synthesis)
- insulin activates acetyl CoA carboxylase (ACC)
- glucose -> pyruvate -> acetyl coA -> malonyl coA -> FA -> TG -> VLDL which is release into the bloodstream

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20
Q

specific processes in ADIPOCYTES during well fed state

A

insulin stimulates glucose uptake by GLUT4 (similar to muscles)
- for synthesis of glycerol-3- phosphate which forms the backbone of TG

insulin stimulates production and secretion of lipoprotein lipase (LPL)
- digestion of TGs in chylomicrons (dietary TG) and VLDL (TG synthesized by liver)
- uptake of FAs into adipocytes
- TG synthesis and storage

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21
Q

specific processes in MUSCLES during well fed state

A

Insulin stimulates the uptake of glucose by GLUT4, glucose is used for:
- glycogen synthesis
- glycolysis -> TCA -> oxidative
phosphorylation (ATP)

Protein synthesis

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22
Q

insulin and glucagon during early fasting state

A
  • high glucagon, low insulin
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23
Q

what happens during early fasting state

A

LIVER
- glucagon stimulates glycogen breakdown and gluconeogenesis -> glucose exported by liver is used mainly be BRAIN and RBC
- uses FA for its ATP needs and excess acetyl coA is used for ketogenesis (ketone bodies later used to supply muscles)

ADIPOCYTES
- glucagon stimulates lipolysis
- glucagon activates hormone sensitive lipase -> breakdown TGs to glycerol and fatty acids
-> release from adipocytes

**glucagon has no effects on muscles (but will hvae some turnover of muscle proteins -> release of amino acids -> glucogenic amino acids will be used for gluconeogenesis in the liver

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24
Q

why do muscles use FA and ketone bodies as a source of energy instead of blood glucose

A
  • low insulin -> NO GLUT4 transporters (exocytosis) -> cannot take up glucose
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25
will there be chylomicrons present in blood test after overnight sleep
- no -> all converted to remnant chylomicrons and taken up by liver
26
will there be VLDL/ VLDL remnants in blood test after overnight sleep?
- no -> all converted to IDL or LDL
27
what happens during conversion of early fasting (overnight sleep) to prolonged fasting (starvation >3 days)
- decrease liver glycogenolysis to 0; increase gluconeogenesis (MAIN SOURCE OF BLOOD GLUCOSE) - rate of proteolysis decreases (initially high in early fasting) -> PROTEIN CONSERVATION - brain progressively uses more ketone bodies for source of glucose (rather than glucose)
28
hormonal levels in prolonged fasting state
- high glucagon and cortisol; low insulin
29
what happens in prolonged fasting state
increased release of cortisol MUSCLES - cortisol activates proteolysis -> glucogenic amino acids -> used for gluconeogenesis in liver ADIPOCYTE: - glucagon and cortisol activate lipolysis -> FA + glycerol -> both are transported to liver LIVER - glycerol used for gluconeogenesis - FA used for ATP production and for production of ketone bodies (ketogenesis) - gluconeogenesis, production of ketone bodies
30
how is cortisol released by cells
- low blood glucose -> detected by hypothalamic regulation center -> release ACTH from pituitary -> induce cortisol release from ADRENAL GLAND
31
Marasmus pathogenesis
- severe MALNUTRITION (prolonged fasting state) -> inadequate caloric intake - BW < 60% of normal, severe muscle wasting - no edema
32
Kwashiorkor pathogenesis
- inadequate PROTEIN intake but caloric intake is sufficient - BW 60-80% of normal, some muscle wasting - EDEMA -> lack of serum albumin (insufficient protein) -> decrease colloid osmotic pressure - HEPATOMEGALY -> lack of lipoprotein synthesis (insufficient protein) -> liver cannot transport fats out -> deposit in hepatocyte -> fatty liver
33
cachexia pathogenesis
- UNINTENTIONAL muscle wasting and severe weight loss (despite adequate nutrition) - associated with cancer
34
what happens in obesity
- body is continuously in WELL FED STATE -> metabolism driven by insulin - glucose, aa, lactate converted to FA, stored as fats (accumulates)
35
how does obesity lead to Type 2 diabetes
- constant secretion of insulin by pancreas -> insulin resistance over time -> pancreas secrete more insulin -> type 2 DM
36
types of adipose tissues
- subcutaneous adipose tissue (SAT) - visceral adipose tissue (VAT)
37
subcutaneous vs visceral obesity
subcutaneous obesity - SAT can expand through hyperplasia (generation of new fat cells) - storage of excess fat in SAT is safe and the adipocytes remains normal visceral obesity - when storage in SAT becomes saturated, excess fats are stored in VAT - enlargement of VAT (hypertrophy) -> pathological situation
38
what are the adverse effects of visceral obesity
- Accumulation of visceral fat -> enlargement of adipocytes -> macrophages: switch from anti inflammatory (M2) to pro inflammatory (M1) - Enlarged adipocytes & M1 macrophages -> increased production of pro- inflammatory cytokines and release of free fatty acids (FFA) - Pro-inflammatory cytokines + FFA -> negatively affect insulin signaling pathway -> insulin resistance - insulin resistance -> reduced uptake of glucose by GLUT4 in skeletal muscles and adipocytes + increase gluconeogenesis in liver -> high blood glucose
39
how is visceral obesity measured
- waist circumference
40
what is metabolic syndrome (commonly associated with obesity)
group of characteristics (at least 3 of 5 = metabolic syndrome) - large waist circumference - HDL-cholesterol - fasting blood triglyceride - fasting blood glucose - fasting BP *metabolic syndrome -> GREATLY increase chance of developing DIABETES & HEART DISEASES
41
what happens after a low carbs diet
- no significant increase in blood glucose level -> LOW INSULIN, HIGH GLUCAGON - liver remains in glucogenic & ketogenic mode
42
why is a person with low carbs diet lean
- low carbs diet -> muscles continue to undergo proteolysis (not inhibited due to low insulin) to provide glucogenic aa for gluconeogenesis -> loss of muscle protein -> lean *to prevent excess loss of muscle -> ensure HIGH PROTEIN diet
43
what happens after a low carbs, HIGH PROTEIN meal
- significant increase in glucagon -> stimulate gluconeogenesis in liver, lipolysis at adipose tissue + ketogenesis in liver - small increase in insulin -> enough to enable protein synthesis (due to high aa intake) but will NOT inhibit gluconeogenesis -> excess aa not needed for protein synthesis will be used for gluconeogenesis & ketogenesis
44
why is a high protein meal not suitable for pts with renal problems
- metabolize aa -> produce urea -> renal problems cause urea accumulation
45
how does fructose lead to synthesis of lipid (ie TGs)
broken down to form dihydroxyacetone-P and glyceraldehyde - dihydroxyacetone-P can form glycerol-3-P (glycerol backbone) - glyceraldehyde-3-P undergo glycolysis -> pyruvate -> acetyl coA -> FA FA + GLYCEROL = TG
46
effect of caffeine on fuel metabolism
- caffeine inhibit PDE -> cAMP not broken down -> enhance metabolic effects of epinephrine & glucagon
47
how is alcohol metabolized
metabolized to form acetate (2 pathways): - ethanol metabolized by ADH (alcohol dehydrogenase) in cytoplasm to form acetyldehyde -> converted to acetate by ALDH - ethanol metabolized by microsomal ethanol oxidising system (MEOS, CYP2E1) in endoplasmic reticulum acetate is then converted to acetyl coA (by acetyl coA synthetase & CoASH) -> fed into TCA cycle
48
what causes flushing syndrome
- deficient hepatic ALDH2 (acetyldehyde not converted to acetate) -> accumulate -> cause flushing
49
blood concentrations of glucose, lactate, pH in alcohol intoxication
glucose: - NADH builds up from alcohol metabolism to acetate -> inhibit gluconeogenesis -> LOW GLUCOSE lactate - pyruvate converted to lactate to oxidise excess NADH to NAD+ -> lactate builds up -> HIGH LACTATE pH - acidosis from lactate -> LOW pH
50
why do alcoholics have fatty liver
- high NADH levels -> reduce rate of beta oxidation of FA -> FA accumulates in liver - high NADH also favours glycerol-3-P pdn from dihydroxyacetone phosphate -> combine with FA for resterification - acyltransferase (catalyse resterification, ie combine glycerol & FA) -> inducible by ethanol - when rate of TG formation > rate of VLDL packaging -> fatty liver
51
adverse effects of acetaldehyde pdn and accumulation
- binds to glutathione -> reduce antioxidant capacity of liver - inhibits tubulin polymerization -> decreased microtubules formation, OR binds directly to and damage microtubules -> prevent secretion of VLDL from the liver
52
why are gout pts not allowed to consume alcohol
- acetate is produced from alcohol -> converted to acetyl-coA -> results in production of AMP - AMP -> metabolized to uric acid - beer also contains purines which are absorbed and metabolised to uric acid - increase uric acid production -> worsen gout
53
why is there little organ cooperation during intense exercise
- peak contraction, blood vessels are compressed, and muscle is isolated from the rest of the body
54
fuel used during anaerobic exercise by muscles
Muscle ATP – can last for about 1.2s Creatine phosphate (lasts about 9s if not regenerated) - high energy source for ATP synthesis until glycogenolysis and glycolysis sets in - Creatine phosphate + ADP -> Creatine + ATP (creatine kinase, reaction is reversible) Muscle glycogen -> glucose-1-phosphate -> glucose-6-phosphate for anaerobic glycolysis (main source of ATP) -> lactate
55
3 ways to activate muscle glycogen phosphorylase (breakdown glycogen) DURING EXERCISE
- AMP produced during muscle contraction -> allosteric activator of glycogen phosphorylase - Ca2+ produced in sarcoplasmic reticulum -> form Ca-calmodulin complex -> activate phosphorylase kinase -> phosphorylate & activate glycogen phosphorylase - adrenaline produced -> activate cAMP -> activate PKA -> activate phosphorylase kinase -> activate glycogen phosphorylase
56
key metabolic events during AEROBIC EXERCISE (all stored fuel are mobilized for the run)
Low blood glucose -> high glucagon / low insulin -> glucagon will activate: - lipolysis in adipose tissues -> release of FAs - hepatic glycogenolysis and gluconeogenesis -> release of glucose Adrenaline released during the run will activate: - lipolysis in adipose tissues -> release of FAs - glycogenolysis and gluconeogenesis in liver -> release of glucose - glycogenolysis in skeletal muscles -> G1P -> G6P for glycolysis Blood glucose (released from liver) can be used by the muscle -> glycogenolysis in muscles provide G1P -> G6P for glycolysis FAs released by adipose tissues -> used directly by the muscle or used by liver to produce ketone bodies -> then exported for use as fuel by muscle *PREFERRED FUEL: FA -> MORE ENERGY PER MOLECULE)
57
function of AMP in exercise (produced in large amounts during muscle contraction, 2ADP -> ATP + AMP) (2)
- activate glycogen phosphorylase - activate PFK-1
58
how is AMPK (AMP dependent protein kinase) activated
- activated by AMP - inhibited by ATP
59
effects of activated AMPK
skeletal muscles: - increase glucose uptake by exocytosis of GLUT4 transporters on muscle cell surface - increase fatty acid oxidation liver: - inhibition of gluconeogenesis (so that glycolysis can take place) - inhibition of fatty acid and cholesterol synthesis so fatty acid oxidation can occur *metformin (diabetes med) activates AMPK
60
types of muscle fibres
Type 1: - low glycogen stores, high blood capillaries - for aerobic respiration Type 2b: - high glycogen stores, low mitochondria - for anaerobic respiration, easily fatigued Type 2a: - intermediate of 1 & 2b
61
types of fuel used by cardiac muscles
- 60-80% FA - 20-40% glucose *cardiac muscles contain glycogen stores
62
how is glucose transported to cardiac muscles
- 90% GLUT 4 - RESPONSIVE to insulin - also express GLUT1
63
normal metabolism vs ischemic metabolism of cardiac muscles
normal: aerobic ischemic: anaerobic -> lactate build up

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