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Metabolism > :M > Flashcards

:M Flashcards

1
Q

* what is the net gain / loss of ATP during: *

a) glycolysis?
b) TCA cycle?
c) cori cycle?

A

what is the net gain / loss of ATP during:

a) glycolysis: Net 2 ATP gain via susbtrate level phosphorylation
b) TCA cycle: Net 38 ATP gain via oxidative phosphorylation
c) cori cycle: Net 4 loss . Anaerobic

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2
Q

to make glucose, you need a source of energy and carbon units.

what are 3 sources of carbon that can be used in gluceoneogenesis?
what are 2 sources of energy that can be used in gluceoneogenesis?

A
  • *sources of carbon:**
  • lactate (from muscle - glycolysis). exported to liver can be made into pyruvate as a carbon source
  • amino acids - from muscle. (from proteolysis) sent to liver & can be made into pyruvate as a carbon source
  • glycerol (from lipolysis). sent to liver
  • *sources of energy:**
  • ATP (from glycolysis and Krebs cycle)
  • fatty acids (but cannot be used as C source !!)
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3
Q

what are the 3 steps of glycolysis that are metabolically irrervisble and need to be side stepped to in order to produce glucose in gluconeogenesis?

A

3 irreversible steps are in glycolysis:

  • *1. Glucose –> glucose-6-phosphate.
    2. P + fructose-6-phosphate –> fructose-1-6-bisphosphate.
    3. pyruvate -> PEP (complicated)**

enyzmes used to reverse ^^ reactions:

  1. enzyme = gluocse-6-phosphatase (removes the P)
  2. enzyme = fructose, 1,-6-biphosphatase
  3. enzyme = (more complicated -> will come to later)
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4
Q

Acetyl co-A is a product of of fatty acid break down.

how do high levels of acetyl co-a influence gluconeogenesis?

A

high levels of Acetyl Co-A:

activates pyruvate carboxylase (used in step 1 of malate cycle: drives gluconeogenesis from pyruuvate -> PEP & eventually glucose)

inhibits: pyruvate dehydrogenase complex (prevents pyruvate being turned into acteyl co A & sparing it, leaving for gluconeogenesis)

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5
Q

the cori cycle spares pyruvate be ensuring that pyruvate is NOT converted to what?

where is a source of ^ instead?

A

the cori cycle only works if you conserve pyruvate, by removing it from muscle and recycling in the liver. cori cycle has to avoid pyruvate’s conversion to acetyl Co-A

INSTEAD

fatty acid metabolism produces acetyl co-A, creating another source of acetyl co-A & means that cori cycle can go ahead for gluconeogenesis. otherwise the pyrvate from cori cycle would be used to make actetly co-A . good thing !!

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6
Q

gluconeogensis from glycerol:

what is glycerol converted to? what does this get converted to?
where? (2)

A
  • glycerol is converted to dihydroxyacetone phosphate only in the liver & kidneys
  • dihydroxyacetone phosphate then reacts with glyceraldehyde-3-phosphate to produce fructose-1,6, bisphosphate (and from there .. = fructose-6-phosphate -> glucose-6-phosphate -> glucose)
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7
Q

Q

specifically, how is gluconeogensis controlled by:

  • insulin?
  • glucagon?
  • adrenaline?

(.i.e. which enzymes blocked etc)

A
  • *insulin:**
  • inhibits gluconeogensis
  • insulin dephosphorylates pyruvate dehydrogenase. this makes pyruvate dehydrogenase active & converts pyruvate -> acetyl coA, which enters krebs cycle. pyruvate is therefore not available to be made into glucose
  • *glucagon & adrenaline:**
  • promotes gluconeogensis
  • glucagon increases cAMP levels. this causes pyruvate dehydrogenase to be phosphorlayed (by pyruvate dehydrogenase kinase) & inactive. pyruvate is then available for glucose production
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8
Q

explain how diabetes disrupts gluconeogensis pathway ox

A

insulin doesnt work:
SO
- pyruvate dehydrogenase remains phosphorylated & therefore inactive
- = less acetyl co-A to go into krebs cycle from pyruvate
- instead fats are broken down to produce fatty acids & acetyl co-A & goes into krebs cycle instead
- means that pyruvate is available for gluconeogenesis

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9
Q

which a.a are main glucogenic a.a? [2]

which a.a are ketogenic?

A

glucogenic amino acids: **alanine & gluatamine

lysine and leucine**
are ketogenic

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10
Q

which cells regulate water contents in the gut?

what is the mechanism of this?

A

secretory cells of the intestinal crpyts:

- CFTR channel within these cells controls this:

a) Cl- moves from ECF via Na/K/CL2 cotransporter (as does Na & K)
b) Cl- enters lumen through CFTR channel
c) Na+ is reabsorbed via Na/K ATPase
d) negative Cl- in lumen attracts Na by paracellular pathway (through cell gaps)
e) water follows the Na into the lumen

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11
Q

how does cholera effect the secretory cells of the crypts?

A
  • Vibrio cholerae releases toxins: has a Part A & Part B
  • Part A incorporated into cell. binds to adenylate cyclase, which in turn makes more cAMP
  • too much cAMP triggers CFTR to be constantly open AND blocks Na/CL symporter (so lots of Cl- is leaving cell and is not being reimbursed)
  • Cl leaves cell into gut = water follows

= secretory diarrhoea

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12
Q

Q

what is MoA for when ORS treats cholera?

A

ORS MoA:

  • ORS has Na, glucose and AA in it.
  • Na & Gluocse transporters are still working with cholera
  • Na prefers to be in ECF: leaves crpyt secretory cells
  • *- pumped out via Na/K ATPase into ECF
  • water follows = save wate**
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13
Q

what is hyperglycemia - why is it bad? explain the mechanism

A

hyperglycemia = high blood glucose

why bad?

  • plasma and interstitial fluid is baso at equilibrium
  • so high blood glucse = high interstitial glucose
  • ECF Na & new glucose has high osmotic power = draws water from ICF (the cell) via aquaporins
  • the water dilutes the Na & bit of glucose = hyponatraemia :( (low serum Na)
  • kidneys: reabsorb Na BUT if too much glucose = excreted in urine.
  • gluocose in urine has osmotic draw -> get osmotic diursesis bc water follows the glucose

= server water loss !

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14
Q

what can the following causes of oedema be caused by?

  1. increased capillary hydrostatic pressure
  2. loss of plasma proteins (2)
A
  1. increased capillary hydrostatic pressure = cirhosis causing portal hypertension
  2. loss of plasma proteins - severe malnutritrion (protein malnutrition like kwashiokor) & liver disease
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15
Q
A
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16
Q

gastric epithelial cells

  • parietal cells produce HCl. But HCl is actually quite toxic. how does the body cell overcome this issue of not causing self harm via the HCl? (2)
A

1. HCl is only produced when food is in the stomach = get unstimualted and stimulated parietal cells:
a) unstimulated parietal cells have H+ ATPase Pumps in the cytosol
b) stimulated parietal cells have H+ ATPase Pumps on apical surface

  • *2. surface mucus cells secrete mucus**
  • without mucus = would directly interact with cells
  • mucus works as:
    a) physical barrier; gel layer
    b) chemical barrier; bicarbonate
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17
Q

which cells produce gastrin?

when do cells produce gastrin?

where are they?

why is gastrin produced?

A

produced by: G cells !! g 4 gastrin xox

located @ atrium of stomach -> bc at the bottom of the stomach. if they sense that there are big proteins - stimulate the formation of more acid.

BUT HOW COMMUNICATE to the other cells?

  • gastrin produced and excreted into blood. = therefore a hormone ! (endocrine activity)
  • goes to ECL and parietal cells
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18
Q

what are 3 medical options for GORD?

why do u have to be careful if taking NSAIDS with GORD / GERD? (2)

A
  1. inhibited by PPI
  2. block the H2 receptor: (cant target others bc the receptors are so common)
  3. neutralised by antacids: form a protective raft over acid pockets
  • NSAIDs: block the prostoglandins from binding to prostaglandin receptors on the parietal cells = means that body’s natural inhibitor is blocked :(.
  • *- will cause less mucous and bicarbonate secretion :(**
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19
Q

how does Helicobacter pylori cause a peptic ulcer? (4)

A
  • H. pylori produces urea in stomach.
  • urea turns into NH3: as a result: 1. raises acid. 2. degels the mucin (lose mucous layer)
  • builds up
  • eventually mucin layer removed and mucosal damage is caused by the pepsin and H+ of HCl :(
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20
Q

which cells do you find in the body of stomach? [3]
which cells do you find in the antrum of stomach? [3]

A

which cells do you find in the body of stomach: parietal cells, chief cells, D cells
which cells do you find in the antrum of stomach: G cells, mucous cells, D cells

21
Q

* MESS NOTES *

describe the differences of pH within the stomach and why they occur

A

cell surface = pH 7: HCO3- layer neutralises stomach acid = chemical barrier
then
mucous layer: physical barrier
then
stomach acid = pH 2

22
Q

explain a) hormonal control of intestinal stage of stomach acid secretions xo
b) nervous control

A

Primarily inhibits gastric acid secretion when FOOD AND ACID ENTERS THE INTESTINES

NERVOUS CONTROL:

  • *It signals the sympathetic system to stop gastric secretions**
  • Inhibition of parietal and chief cells

HORMONAL CONTROL:

  • *- Cholecystokinin, secretin and GIP (gastric inhibitory protein) produced by duodenum –> inhibit gastric secretions**
  • Cholecystokinin and GIP released by presence of lipids and carbohydrates
  • Secretin released when pH decreases (due to entrance of acidic chyme into the duodenum)
23
Q

How can you diagnose H. pylori presence? (4)

A
  • urea breath test: urea C13 is given to patient and H. pylori ​converts urea C13 to NH3 + C1302
  • CLO test (Campylobacter-like organism test) : biopsy placed in media with urea and pH indicator conversion of urea to ammonia raises pH - changes colour
  • blood antibody test
  • stool antigen test
24
Q

Acetyl Co-A is one of the starting molecules needed for TCA. But what is the equation for the formation of Acetyl Co-A from pyruvate?

what is the enzyme used to catalyse this reaction?

what nutrition is needed for this reaction?

A

- pyruvate + CoA + NAD+ –> acetyl Co-A + Co2 + NADH

  • enzyme: pyruvate dehydrogenase (PDH)
  • co-enzymes are members of the B-vitamin family. uses TPP (aka vitamin B1)
25
Q

when is PDH blocked for TCA? [2]

A
  • PDC / PDH is blocked when:
  • *a) levels of Acetyl CoA levels are high
    b) If reduced NAD levels are high**
26
Q

what happens (overview) to acetyl co-A during the TCA?

A

Acetyl CoA combines with oxaloacetate to form Citrate.

(Citrate is a tricarboxylic acid, hence the name TCA)

This enters the cycle and is progressively oxidised, each time producing NADH/FADH2, until finally forms oxaloacetate again and the cycle can begin again.

27
Q

Q

PDH is regulated in two ways:

  1. PDH is de/-phosphorylated by which enzymes? what do they add / remove? what is their effect?

which substances control 1.?

A

:)

  • PDH Kinases inhibit PDH by adding PO4
  • PDH Phosphatases activate PDH by removing PO4

//

  • *control of PDH kinases**
  • PDH kinases are activated: by ATP, acetyl Co-A and NADH (last two are products of PDH) = switch off PDH.
  • Pyruvate & insulin inhibits PDH Kinasese (as pyruvate wants PDH to be active to break pyruvate down) = switch on PDH.

control of PDH phosphatases
- Ca2+ ions activate PDH phosphatises - increases PDH. occurs in muscle -> eventually get more ATP production = switch on PDH
- insulin activates PDH phosphatases - actives PDH

28
Q

to put simply - insulin has what effect on PDH?
what effect does insulin have of kinases & phosphatases?

what do adrenaline and glucagon do to PDH? - why?

A

insulin caueses the activation of PDH & eventual production of acetyl co-A

insulin = -ve effect on kinases (which inhibit PDH)
+ve effect on phosphatases (which activate PDH)

adrenaline and glucagon: want pyruvate untouched, so it can be used to make glucose via gluconeogenesis = inhibit PDH

29
Q
A
  • protons flow back to matrix through ATP synthase. This drives phosphorylation of ADP:
    ATP produced by oxidative phosphorylation:

ADP + P –> ATP at ATP Synthase

30
Q

* acetyl co-A is the input for TCA. acetyl co-A can be produced by three ways. What are they? *

A

1.Glycolysis of glucose to pyruvate
•Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)
•Produces 2 reduced NAD molecules per glucose
•1 reduced NAD per pyruvate

2.Transamination of glucogenic amino acids to pyruvate
• Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)

3.Beta-oxidation of fatty acids directly to acetyl-CoA
•Produces 1 NADH and 1 FADH2 per acetyl-CoA

31
Q

how many acetly Co-A enter the TCA (from one glucose molecule)
what are the end products of TCA cycle? (3)

A
  • TCA end products:
    a) 1 GTP / ATP
    b) 3 NADH
    c) 1 FADH
    BUT BECAUSE HAVE 2 ACETLY CO-As GOING INTO TCA:
    a) 2 GTP / ATP
    b) 6 NADH
    c) 2 FADH
32
Q

what is produced if hypoxia occurs at TCA?

A
  • during hypoxia: formation of reactive oxygen species (ROS) -> highly damagin to lipids / proteins / DNA
  • oxygen is not there to mop up the electrons at complex 4. electrons are abcked into the ETC
33
Q

during ox. phosph H+ are pumped across the inner mitochondrial matrix at which complexes?

  • complexes 1, 2 & 3
  • complexes 1, 2 & 4
  • complexes 1, 3, & 4
  • complexes 2, 3 & 4
A

during ox. phosph H+ are pumped across the inner mitochondrial matrix at which complexes?

  • complexes 1, 2 & 3
  • complexes 1, 2 & 4
  • *- complexes 1, 3, & 4**
  • complexes 2, 3 & 4
34
Q

where is insulin produced?
where is glucagon produced?
where is somatostatin produced?

A

pancreatic islets of Langerhans

  • alpha cells: produce glucagon
  • beta cells: produce insulin
  • delta cells: produce somatostatin
35
Q

what does insulin cause to happen to glucose in muscles?

what does Akt do in muscle?

A

glucose –> glucose-6-phosphate –> glucose-1-phosphate –> UDP-glucose –> glycgoen. aka glycogenesis

Akt: phosphorylates and inactivates glycogen synthase kianse = activates glyocgen synthase

36
Q

effect of insulin at:

muscles [2]

adipose tissues: [2]

liver: [2]

protein synthesis? [2]

A

effect of insulin at:

muscles:

  • *i) activates glycogenesis
    ii) inhibits glycogenolysis**

adipose tissues:

i) activates lipogenesis
ii) inhibits lipolysis

​liver:

  • *i) glycogensis Activated
    ii) lipogenesis activated
    iii) GNG inhbiited**

​protein synthesis:

  • *i) activates protein synthesis
    ii) inhibits protein catabolism**
37
Q

effect of insulin of gluconeogenesis?

A

insulin inhibits gluconeogenesis !

38
Q

how is the TCA cycle controlled in response to exercise?

(3)

A

1.

  • Ca2+ is an allosteric keeps the pyruvate deyhyrogenase complex activated.
  • therefore causes **quicker conversion of pyruvate -> acetly co-A
  • increases TCA to occur more**

(PDH controls the entry to the TCA, it’s activity is regulated. The enzyme is phosphorylated and dephosphorylated depending on whether it is active or inactive. The calcium is promoting essentially the active state of PDH, by influencing PDH phosphatase (this PDH phosphatase will remove phosphates from the PDC and activate it)

2:
calcium and ADP drive activity of two dehydrogenase enzymes in the TCA to maintain high ATP production

3.

Low levels of ATP/NAD pushes PDH into its active state.

39
Q

- during exercise, ATP runs low & AMP levels start increasing

how does AMP regulate exercise? (3)

A
  • during exercise, ATP runs low & AMP levels start increasing

AMP stimulates:

  • increases recruitment of GLUT4 tranpsorter to membrane of muscle cells
  • allosterically activates inactive glycogen phosphorylase
  • allosterically activates phosphofructokinase-1 (PFK-1) (drives glycolysis)
40
Q

Q

what is the common pathway used to break down alcohol?

* what is an important product of alchohol break down? *

A

most common pathway:

i) ethanol ⇌ acetaldehyde (via enzyme alcohol dehydrogenase (ADH))
ii) acetaldehyde –> acetate (ketone body - so can be used to make energy !) via enzyme ALDH2
iii) acetate can then be converted into (acetyl co-a

important product: NADHs produced !! remember

41
Q

what are the step changes in metabolism that undergo during starvation? (5)

A
  1. glucose starts falling; insulin goes down, glucagon up
  2. glycogen can keep brain alive for 2/3 days / 30 hrs
  3. swith to FA break down = energy for 2-3 days due to gluconeogenesis
  4. FA then switches to ketone bodies. (ketone bodies can go into brain - important !)
  5. final resource = break down proteins to release amino acids for gluconeogenesis
42
Q

extremes of met:

high levels of AMP also activates an important kinase anzyme: AMPKinase.

AMP kinase has 3 major effects. what are they?

A
  1. promotes the recruitment of GLUT4 tranporters to the membrane of muscle cells. important: insulin-independint effect !!

2. Activates phosphofructokinase 2, (PFK2). PFK2 strong allosteric activator of PFK-1 (to make fructose 1,6 BP -> glycolysis). only happens in cardiac muscle !!!

  1. shifts from glucose to fatty acid break down as a source of ATP:
    i) phosphorylase acetyl co-A carboxylase (which makes FAs)
    ii) stops the production of malonyl-CoA (normally inhibits carnitine shuffle. cartinine shuffle is needed in FA break down)
43
Q

explain how two pathologies occur from xs alchohol consumption !

A
  • excess alchohol consumption leads to excess acetyl co-A
  • excess acetyl co-A:
    i) produces lots of ketone bodies: acidic –> metabolic acidosis
    ii) gets converted to fats -> fat & obese
  1. fatty liver:
    - XS acetly co-A converted to fat & stays in liver.
    - often have low food intake - poor protein intake = low albumin. = fat not transported
    - get scar tissue forming
    - results in cirrhosis
44
Q

immune cells have an increased requirement for the co-factor WHAT?

what is used for this to occur? ^

A
  • immune cells have increased requirement for co factor: NADPH
  • glucose is taken from glycolysis to pentose phosphate pathway to make NADPH
45
Q

what specifically do neutrophils and monocytes produce to kill bacteria from NADPH?

A

hypochlorite

46
Q

Q

NADPH is a co-factor created by immune cells.

Name 2 functions of NADPH

A

NADPH functions:

  • as a reducing agent (like NADH)
  • to generate ROS: immune cells use NADPH oxidase to reduce O2 to free radical and the H202. H202 then used to kill engulfed pathogens = respiratory burst
47
Q

Q

cancer cells have different metabolism to normal cells - what is it?

A

A

cancer cell metabolism: high metabolic rate

  • *Warburg Effect / Hypothesis**
  • cancer cells use glucose for aerobic glycolysis rather than oxidative phosphorylation even in the prescence of oxygen
  • leads to build up of lactate & lactic acid
48
Q

what is the space in peritneal sac / fluid:

a) before the stomach
b) behind the stomach?

A

a) before the stomach: greater sac
b) behind the stomach: lesser sac

49
Q
A

Metabolism (35 decks)

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