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Biochem 2 > Lectures 19-20: Tissue specific metabolism + diseases > Flashcards

Lectures 19-20: Tissue specific metabolism + diseases Flashcards

1
Q

Glycolysis:
- what substrate (3)
- cellular location
- Number of enzymes
- oxygen needed?
- CO2 produced?
- ATP used?
- NADH/FADH2 produced?
- ATP produced?

A
  • carbohydrates, some AA and glycerol
  • cellular location: cytoplasm
  • 10 enzymes
  • oxygen needed? NO
  • CO2 produced? NO
  • ATP used? YES
  • NADH/FADH2 produced? YES
  • ATP produced? YES
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2
Q

Pyruvate oxidative decarboxylation
- what substrates?
- cellular location
- Number of enzymes
- oxygen needed?
- CO2 produced?
- ATP used?
- NADH/FADH2 produced?
- ATP produced?

A
  • some aa
  • cellular location: mitochondria
  • pyruvate decarboxylase complex (3 complexes)
  • oxygen needed? NO
  • CO2 produced? TES
  • ATP used? NO
  • NADH/FADH2 produced? YES
  • ATP produced? NO
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3
Q

TCA cycle:
- what substrates?
- cellular location
- Number of enzymes
- oxygen needed?
- CO2 produced?
- ATP used?
- NADH/FADH2 produced?
- ATP produced?

A
  • FA and some aa
  • cellular location: mitochondria
  • 8 enzymes
  • oxygen needed? NO
  • CO2 produced? YES
  • ATP used? NO
  • NADH/FADH2 produced? YES
  • ATP produced? YES
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4
Q

oxidative phosphorylation
- cellular location
- Number of enzymes
- oxygen needed?
- CO2 produced?
- ATP used?
- NADH/FADH2 produced?
- ATP produced?

A
  • cellular location: inner membrane mitochondria
  • 4 complexes
  • oxygen needed? YES
  • CO2 produced? NO
  • ATP used? NO
  • NADH/FADH2 produced? NO
  • ATP produced? YES!!
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5
Q

tissue specific metabolism
- skeletal muscle
- adipose tissue
- cardiac muscle
- brain (3)
- liver (3)

A
  • skeletal muscle: uses ATP generated aerobically or anaerobically to do mechanical work
  • adipose tissue: synthesizes, stores and mobilizes TG (BAT carries out thermogenesis)
  • cardiac muscle: uses ATP generated aerobically to pump blood
  • brain: transports ions to maintain membrane potential + integrates inputs from body and surroundings + sends signals to other organs
  • liver: processes fats, carbs and prots from diet + synthesizes and distributes lipids ketone bodies and glucose to other tissues + converts excess nitrogen to urea
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6
Q

liver:
- which cells metabolize all 3 nutrients (which ones?)
- provides energy _________ to all tissues
- maintains balance between _________ supply and _________ demand
- has remarkable metabolic _________ in enzymatic machinery –> rapid _________ of enzymes
- enzymes are sensitive to various hormones (4)

A
  • hepatocytes: carbs, aa, lipids
  • precursors
  • nutrient supply and precursor demand
  • metabolic flexibility –> rapid turnover of enzymes
  • insulin, glucagon, leptin, epinephrin
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7
Q
  • nutrient supply varies with what?
  • precursor requirement varies with (2)
A
  • nutrient supply varies with diet/feeding
  • precursor requirement –> level of activity and health (nutritional state)
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8
Q

2 types of adipose tissue?
- where?
- one or many lipid droplet?
- amount of mitochondria

A

white adipocytes (WAT):
- under skin, around major blood vessels and abdomen
- one lipid droplet (large spherical cell) –> squeezes mitochondria and nucleus to thin layer against plasma membrane
- a few mitochondria
VS brown adipocytes (BAT):
- under skin (chest and back)
- many smaller lipid droplets
- any more mitochondria and high blood supply –> accounts for brown color

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9
Q

White adipocytes:
- energy source = ?
- capable of synthesizing what from energy source?
- sensitive to which hormones (2) –> 2 different roles
- major storage of what?

A
  • glucose
  • synthesize fatty acid from glucose
  • sensitive to insulin (regulated FA synthesis) and epinephrine (hydrolysis of TG to non-esterified FA)
  • of TG
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10
Q

brown adipocytes:
- in children or adults?
- FA undergo what?
- specific protein responsible for what?

A
  • only in children, not in adults BUT preadipocytes can differentiate into BAT in adults during chronic cold exposure (b-oxidation of own FA produces heat)
  • beta oxidation
  • Thermogenin (uncoupling protein 1) responsible for non-shivering thermogenesis –> produces heat but doesn’t involve muscle contraction (that causes shivering) –> to protect vital organs when babies comes out of womb
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11
Q

metabolism in muscle
- uses (3) for energy
- resting vs moderate activity vs vigorous (2)
- which hormone helps in using glucose from blood and glycogen?
- also has what function?

A
  • FA, ketone bodies and glucose
  • resting: FA from adipose and ketone bodies from liver
  • moderate: blood glucose does aerobic glycolysis + FA and ketone bodies
  • vigorous:
    1. stored glycogen gives glucose –> breakdown to lactate bc blood flow can’t give enough O2 to meet high ATP demand = anaerobic glycolysis
    2. phosphocreatine –> creatine produces ATP (creatine from diet or de novo (gly, arg, met))
  • epinephrine
  • shivering thermogenesis (muscle contraction generates heat)
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12
Q

during recovery from physical activity
- accumulation of ________ from anaerobic respiration –> converted to what, where? name of cycle?
- accumulation of _________ from phosphocreatine –> how do we get rid?
(buffer system for _____)

A
  • lactate –> converted to glucose in liver (gluconeogenesis) –> Cori cycle
  • creatine –> converted back to phosphocreatine by creatine kinase
  • buffer system for ATP
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13
Q

each glycogen origin glucose gives how many ATPs during glycolysis?

A

3 ATPs

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14
Q

difference between cardiac muscle and skeletal muscle?

A
  • cardiac = continuously active = completely aerobic metabolism (oxidative phosphorylation)
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15
Q

cardiac muscle:
- small amount or abundant mitochondria?
- source of E? main one vs can also use 2 others
- stored glycogen?
- sensitive to ____ deprivation –> explain

A
  • abundant mitochondria
  • FA, but can also use ketone bodies and glucose
  • less stored glycogen (cannot store adipose tissue or glycogen in big quantity)
  • O2 deprivation –> muscle dies without O2 supply (heart attack)
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16
Q

metabolism in brain:
- main fuel? which type of cells can use smtg else?
- metabolism uses around _____ g of main fuel per day
- can also use _________ as fuel
- ATP used to maintain what through which enzyme
- aerobic or anaerobic metabolism?
- stored glycogen?
- fasting/starvation –> use (2) sources of energy

A
  • glucose but astrocytes can use FA
  • 130g of glucose
  • b-hydroxybutyrate
  • membrane potential (Na+/K+ ATPas)
  • aerobic metabolism
  • no stored glycogen
  • ketone bodies (from FA) and glucose (from muscle protein)
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17
Q

difference btw slow-twitch and fast twitch muscles
- color
- resistant to fatigue?
- low/high tension?
- rich in mitochondria?
- dense vascular system?
- acts fast or slow?

A

SLOW TWITCH:
- red
- highly resistant to fatigue
- low tension
- rich in mitochondria
- dense, lots of blood vessel to bring O2
- slow but steady ox phos
FAST-TWITCH:
- white
- quicker to fatigue
- high tension
- fewer mitochondria
- fewer blood vessels
- acts faster!

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18
Q

marathon case study:
1. first 80m: 2 sources of E
2. heart/lung take ___ min to reach what? –> what type of metabolism during this time? (____ ATP)
3. after ___ min, what takes over? (___-___ ATP)
4. by ___ min –> runner’s high = peak in _________
5. glycogen stores (______ g) sufficient for ____km –> after that = runner’s wall = minimal _________
6. so what takes over?
7. what brings him across finish line?

A
  1. ATP and phosphocreatine
  2. 2min to reach max capacity –> during this, not enough O2 so anaerobic glycolysis (2-3 ATP)
  3. after 2min –> aerobic glycolysis takes place (30-32 ATP)
  4. by 45min –> endorphins
  5. 500g –> 30km –> minimal glycolysis = pace slows down
  6. FA oxidation takes over –> slow in ATP yield
  7. motivation!
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19
Q

100m sprint case study:
- O2 demand is so high that what?
1. first 20 m: source of E?
2. 20-60m: 2 sources of E
3. last 40m: source of E?
- breathing required?

A
  • breaking can NOT match
    1. ATP from phosphocreatine
    2. ATP from anaerobic glycolysis (produces lactate) + phosphocreatine
    3. anaerobic glycolysis
  • technically no bc anaerobic –> but after, need breathing for gluconeogensis to replenish glycogen using Cori cycle
20
Q

metabolism during fed-state:
- _________ liver
- everything regulated by which hormone? secreted in response to what? –> role?
- main source of Energy? –> to which tissue? (3)
- excess of main source of energy –> 2 pathways

A
  • lipogenic liver
  • insulin in response to high blood glucose –> role: stimulate glucose uptake by tissues
  • glucose –> to brain! + muscle + adipose tissue
  • to glycogen OR pyruvate –> actetyl-CoA –> CO2 AND TAG –> VLDL –> adipose tissue
21
Q

how are aa and fats metabolized in liver after dietary intake?

A

amino acids:
- enter liver as aa –> a-keto acids: either Acetyl-CoA OR NH3 –> Urea
(acetyl-COA: oxidized for ATP OR to TAG)
Fats:
- moves from intestine to muscle or liver through lymphatic system as chylomicrons
- in muscle: FA oxidized to ATP and CO2
- in liver: TAG –> VLDL –> adipose tissue

22
Q

effects of insulin on blood glucose: INCREASE or DECREASE?
- glucose uptake (muscle, adipose, liver)
- glycogen synthesis
- glycogen breakdown
- glycolysis, acetyl-CoA production
- FA synthesis
- TG synthesis

A
  • INCREASE glucose uptake (muscle, adipose, liver)
  • INCREASE glycogen synthesis
  • DECREASE glycogen breakdown
  • INCREASE glycolysis, acetyl-CoA production
  • INCREASE FA synthesis
  • INCREASE TG synthesis
23
Q

Metabolism during fasting state
- ___________ liver
- decrease in blood glucose triggers release of ___________
- main pathway that will happen in liver?

A
  • glucogenic liver
  • glucagon
  • gluconeogenesis –> to make glucose for the brain
24
Q

fasting-state:
- 3 ways to make glucose
- why need glucose?

A
  1. glycogen –> glucose-6-P –> glucose
  2. proteins from muscle and liver –> aa –> pyruvate –> gluconeogenesis –> glucose 6-P –> glucose
  3. adipose tissue –> TG –> glycerol –> gluconeogenesis –> glucose 6-P –> glucose
    - cause preferred E source of brain
25
Q

fasted state:
- when no more glycogen stores –> synthesis of ________ _________ to fuel the _________
- 2 ways to make?
- what 2 substrates can make E for muscle and liver?

A
  • ketone bodies
    1. proteins from liver and muscle –> aa –> ketone bodies
    2. TAG from adipose tissue –> FA –> ketone bodies
  • ketone bodies can make ATP for muscles too
  • FA –> b-oxidation to make ATP in liver
26
Q

effects of glucagon on blood glucose: INCREASE or DECREASE
- glycogen breakdown
- glycogen synthesis
- glycolysis
- gluconeogensis
- FA mobilization
- Ketogenesis

A
  • INCREASE glycogen breakdown
  • DECREASE glycogen synthesis
  • DECREASE glycolysis
  • INCREASE gluconeogensis
  • INCREASE FA mobilization
  • INCREASE Ketogenesis
27
Q
  1. immediately after meal: glucose increase/decrease –> what 2 pathways increase (what hormone)
  2. 2 hours post-prandial: glucose levels increase/decrease –> what happens? (what hormone)
  3. 4 hours post-prandial: what hormone? what becomes the major fuel?
A
  1. glucose increases –> increase glycolysis and glycogenesis (insulin)
  2. glucose begins to drop –> liver glycogen releases glucose (glucagon)
  3. more glucagon –> FA becomes major fuel (more TG hydrolysis)
28
Q

main difference btw fasting and prolonged fasting metabolism?

A

similar pathways –> in prolonged fasting, end-products like ketone bodies accumulate = bad

29
Q

proteins containing (5 aa) sequence are preferentially depleted in liver and heart

A

Lys-Phe-Glu-Arg-Gln sequence

30
Q

fuel reserves in body:
- normal weight 70kg man –> how many kg of adipose tissue –> estimated survival months?
- obese 140kg man –> how many kg of adipose tissue –> estimated survival months?

A

70 kg man:
- 15kg
- 3 months
140kg man:
- 80kg
- 14 months

31
Q

2 forms of diabetes mellitus?
1. ______________ = what?
- due to what?
- usually develops when?
2. ______________ = what?
- due to what?
- usually develops when?
- what signaling is affected?
- what is sequestered in cytoplasm? why?

A
  1. Type 1 diabetes = insufficient production of insulin
    - due to autoimmune destruction of b-cells
    - early life
  2. Type 2 diabetes = insulin resistance
    - cells do not respond appropriately to insulin (insulin response system is defective)
    - late adulthood
    - INSR signaling is affected –> IRS proteins are dephosphorylated
    - GLUT4 is sequestered in cytoplasm bc IRS is dephosphorylated
32
Q

diabetes symptoms:
- blood glucose is elevated = increased ___________ –> excessive (2) + proteins get ___________
- in type 1, ____ breakdown is accelerated –> leads to high _____A___ ___A___ –> raises [ __ ], which leads to ___________
- what buffering system is activated? leads to what?
- breakdown of ___________ (a type of A) produces ___________, which is expelled via what?
- untreated diabetes leads to dramatic _______ _______

A
  • osmolality –> excessive urination and thirst –> proteins get glycosylated
  • fat –> high ketone bodies –> raises [H+] –> ketoacidosis
  • bicarbonate buffering system is activated –> leads to altered breathing pattern
  • ketone body acetoacetate produces acetone –> expelled via breath
  • dramatic weight loss
33
Q

why does accelerated breakdown of fat leads to high ketone bodies?

A

because there is an incomplete fat oxidation bc of high NADH/NAD+ radio –> inhibits TCA cycle –> leads to accumulation of acetyl-CoA –> this accumulation favorises synthesis of ketone bodies –> can’t be used as fast as they are produced = accumulation

34
Q

adipose tissue is also an __________ organ bc releases what?
- these released things have what role?
- 2 examples of these things

A

endocrine organ
- bc it releases peptide hormones called adipokines
- carry information about fuel stores in adipose tissue to brain
- leptin, adiponectin

35
Q

2 types of neurons that control eating behavior?
- example
- 2 levels of neurons
- 3 effectors?

A
  • anorexigenic neurons –> suppress appetite: eat less, metabolize more (ie: a-MSH)
  • orexigenic neurons –> stimulate appetite: eat more, metabolize less (ie Neuropeptide Y (NPY))
  • arcuate neurons –> second order neurons –> effectors
  • muscle, adipose tissue, liver
36
Q

3 types of signals (which produce what hormones) impact eating behavior

A
  1. adiposity signals:
    - leptin (adipose)
    - insulin (pancreas)
  2. Satiety signals:
    - PYY (gut)
    - GLP-1 (gut)
  3. hunger ginal:
    - ghrelin (stomach)
37
Q

which signal activate anorexigenic neurons? vs orexigenic neurons

A
  • leptin activates a-mSH –> eat less, metabolize more (anorexigenic)
  • ghrelin activates NPY –> eat more, metabolize less (orexigenic)
38
Q

which signals inhibit orexigenic neurons? anorexigenic neurons?

A
  • insulin, PYY and GLP-1 inhibit NPY –> eat more, metabolize less (orexigenic neurons)
  • NPY inhibits anorexigenic neurons (second order)
39
Q

leptin –> increases/reduces appetite
- first identified in what? –> homo/heterozygous ob/ob mice –> 7 symptoms –> when leptin was injected, what happened? VS in humans?

A
  • reduces appetite
  • obese mice
  • homozygous ob/ob
  • ate continually, obese, elevated cortisol, shivered, infertile, insulin resistance and died early
  • mice lost weight, temp returned to normal
  • leptin administration to most obese people does NOT restore normal body mass –> they have high levels of leptin and maybe have leptin resistance
40
Q

db/db mice are (2)
- db gene encodes what receptor in brain?
- expressed mostly where?

A
  • obese and diabetic
  • leptin receptor in brain
  • hypothalamus
41
Q
  • ghrelin is a short term ___________ peptide from the ___________
  • where are the ghrelin receptors (3)
  • signaling mechanisms well understood?
  • works via which signalling pathway to decrease/increase sensation of hunger
  • injection of ghrelin immediately increases/decreases appetite?
A
  • orexigenic peptide from the stomach
  • brain (hypothalamus), heart and adipose tissue
  • not well-understood
  • GPCR –> increase sensation of hunger
  • increases appetite
42
Q

PYY is an _______-suppressing hormone
- peptide of ___ aa with 2 ____ residues at the end
- secreted from (2) in response to what?
- inhibits release of what from orexigenic/anorexigenic neurons
- results in increased/reduced hunger

A
  • appetite-suppressing hormone
  • 36 aa with 2 Tyr residues
  • small intestine and colon in response to food entering to stomach
  • inhibits release of NPY from orexigenic neurons
  • reduced hunger
43
Q

microbes in the gut influence what?

A

obesity

44
Q

some microorgs create ___________ products that affect ___________ tissue
- most bacterial products are short/long chain FA (3 ex)

A

fermentation products that affect adipose tissue
- short chain FA (acetate, propionate, butyrate)

45
Q
  • propionate acts through which signalling pathway?
  • stimulates and inhibits what? leading to increase in what?
A
  • GPCR 43 and 41
    1. stimulates preadipocyte differenciation to adipocytes
    2. inhibits lipolysis
    leading to increase in white adipose tissue (obesity)
46
Q

lipid toxicity hypothesis link between obesity and type 2 diabetes
1. normal person
2. overweight person
3. pro-inflammatory state
4. chronic inflammation
5. 6. 7.

A
  1. TG diet = TG catabolized –> small adipocytes
  2. TG diet > TG catabolized –> larger adipocytes
  3. enlarged adipocytes produce macrophage chemotaxis protein (MCP-1)
  4. macrophages infiltrate adipose tissue in response to MCP-1
  5. macrophages in adipose tissue produce tumor necrosing factor (TNF) which favors export of FA
  6. adipocytes export FA to muscle, where ectopic lipid deposits form
  7. extopic lipid interferes with GLUT4 movement to myocyte surface, producing insulin resistance
47
Q

counter hypothesis to lipid toxicity/obesity linking to T2DM?

A

counter hypothesis: insulin resistance leads to obesity

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