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Metabolism Flashcards

1
Q

*** Where does the conversion of pyruvate to acetyl CoA take place?

A

matrix of the mitochondria

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2
Q

What are the 4 fates of acetyl CoA?

A

1) oxidize acetyl groups in the CAC
2) lipgenesis
3) ketogenesis
4) cholesterologenesis - and then cholesterol can be turned into steroids

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3
Q

** preferred fuel of liver?

A

fa, glucose, aa

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4
Q

** preferred fuel of skeletal muscle?

A

resting- fa

exertion- glucose

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5
Q

** preferred fuel of brain?

A

fed- glucose

starvation- ketone bodies + glucose

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6
Q

** preferred fuel of adipose tissue

A

fa

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7
Q

** preferred fuel of heart muscle

A

fa

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8
Q

5 major dietary carbohydrates, where they come from, what breaks them down

A 
amylose- potatoes, rice, corn, bread- maltase
sucrose- sugar, desserts- sucrase
lactose- milk, milk products- lactase
fructose- fruit, honey
glucose- fruit, honey
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9
Q

carb metabolism in RBCs

A
  • lack mitochondria so its only glycoslysis

* glucose - g6p- lactate OR pentose phosphate*

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10
Q

carb metabolism in brain

A
  • absolute requirement for glucose

* glucose - g6p (can do PP pathway)- pyruvate- acetyl CoA- CAC- Co2 ***

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11
Q

carb metabolism in muscle and heart cells

A
  • major store of glycogen (which they can’t mobilize into tissue)
  • glucose- g6p (PP pathway, storage as glycogen)- pyruvate (enter lactic acid cycle)- acetyl CoA- CAC **
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12
Q

carb metabolism in adipose tissue

A
  • main purpose is turn glucose into fat

* glucose- g6p (PP pathway, storage as glycogen)- pyruvate- acetyl CoA- fat *

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13
Q

carb metabolism in hepatocytes

A
  • liver regulates glucose production
  • glucose- g6p (PP pathway, glycurides, storage as glycogen)- pyruvate (enter lactic acid cycle)- acetyl CoA- Fat OR CAC **
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14
Q

what is the main difference between GLUTs and SGLTs?

A

GLUT- down a concentration gradient

SGLT- against a concentration gradient, using co-transport with sodium

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15
Q

difference between SGLT1 & 2

A

1- transports glucose & galactose, found in intestinal mucosa & kidney tubules
2- only glucose, only kidney

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16
Q

what is the main insulin dependent glucose transporter? is it high or low affinity? what tissues is it found in?

A

GLUT4
heart, muscle, adipocytes
high affinity

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17
Q

what is the insulin independent low affinity transporter in liver?

A

GLUT2
low affinity, high capacity - works in both directions
glucose sensor for pancreatic beta cells

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18
Q

what does GLUT5 transport?

A

fructose in skeletal muscle, adipose tissue, brain, sperm, RBCs

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19
Q

definition of glycolysis

A

metabolic pathway where a single glucose molecule converts into 2 pyruvates, 2 ATP, 2 NADH, 2 H20 (happens during hyperglycemia with high insulin)

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20
Q

definition of glycogenolysis

A

breakdown of glycogen to glucose-1-p and glucose in the liver and muscles by glycogen phosphorylase

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21
Q

definition of gluconeogenesis

A

results in the generation of glucose from a non-carbohydrate carbon substance such as pyruvate, lactate, glycerol and glucogenic amio acids (happens during hypoglycemia when there is increase glucagon)

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22
Q

definition of glycogenesis

A

formation of glycogen from glucose (happens during hyperglycemia when insulin is high)

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23
Q

***** what are the 2 main processes that happen during the fasting state? 2 processes during the fed state?

A

fasting: glycogenolysis, gluconeogenesis
fed: glycolysis, glycogenesis

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24
Q

*** where in the cell does glycolysis occur?

A

only in cytoplasm of ALL cell types (NOT mitochondria)

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25
Q

*** what are the 3 key enzymes which have one way reactions?

A
  1. hexokinase/glucokinase (glucose-g6p) (uses ATP)
  2. PFK1- (f6p-f1,6bp) (uses ATP)
  3. pyruvate kinase- phosphoenolpyruvate to pyruvate (makes an ATP!)
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26
Q

what does glycolysis produce energy in the form of?

A

ATP, NADH

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27
Q

** characteristics of hexokinase

A
  • found in all cell types
  • allosterically inhibited by own product
  • non-inducible (found in constant amounts)
  • has low Km
  • saturated easily
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28
Q

*** characteristics of glucokinase

A
  • found in liver & pancreas
  • inhibited by downstream product (f6p) which translocates gk to nucleus
  • synthesis is induced by insulin
  • high km (low affinity- able to handle large amounts of glucose in liver)
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29
Q

what are the allosteric regulators of hexokinase?

A

g6p inhibits

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30
Q

what are the allosteric regulators of PFK1?

A
  • f-2,6-bp major activator (made using PFK2)
  • citrate- major inhibitor (CAC intermediate)
  • ATP- major inhibitor
  • indirectly, glucagon & epinephrine inhibit in liver (phosphorylates kinase domain of PFK2)
  • indirectly, epinephrine actives in heart and skeletal muscle (phosphorylates phosphatase domain of PFK2)
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31
Q

what are the allosteric regulators of pyruvate kinase?

A
  • f-1,6-bp activates
  • ATP inhibits
  • alanine inhibits
  • glucagon & epinephrine inactivate via induced phosphorylation
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32
Q

what is the pancreatic hormone that leads to the inhibition of hepatic glycolysis?

A

glucagon

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33
Q

how does glucagon inhibit hepatic glycolysis?

A

indirectly inhibiting PFK1 (phosphorylates PFK2) and directly inhibiting pyruvate kinase and decreasing synthesis of the 3 irreversible enzymes

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34
Q

relationship between insulin, glucagon, epinephrine; do they increase or decrease synthesis of the 3 irreversible enzymes?

A

increased insulin=
increased cAMP=
decreased glucagon & epinephrine

= increased synthesis of 3 irreversible enzymes!!

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35
Q

what are the differential effects of epinephrine?

A
  • inhibits hepatic glycolysis- phosphorylates kinase domain of PFK2
  • stimulates cardiac/muscle glycolysis- phosphorlates phosphatase domain
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36
Q

when would you expect to see high LDH levels?

A

lactose dehydrogenase is high well cells are damaged- e.g. during myocardial infarction, ishcemic stroke

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37
Q

normal serum ratio of lactate to pyruvate

A

10:1

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38
Q

what are the allosteric inhibitors of PDH (pyruvate dehydrogenase)?

A

it’s reaction products- acetyl CoA and NADH

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39
Q

T/F phosphorylating PDH renders it inactive

A

True

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40
Q

what are some factors that cause PDH phosphorylation? dephosphorylation?

A

phosphorylation- NADH, acetyl CoA

dephosphorylation- coASH, NAD+, ADP, pyruvate

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41
Q

*** vitamin cofactors that participate in the PDH reaction?

A

B1- thiamine
B5- pantothenate
B2- riboflavin
B3- niacin

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42
Q

*** list 3 things that would cause high lactate and high pyruvate in the blood

A
  1. arsenic poisoning (inhibits lipoic acid shuttle)
  2. thiamine deficiency
  3. genetic deficiency in PDH
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43
Q

*** what would a deficiency in fructose aldose cause? what foods should the person avoid?

A
  • get build up in f-6-p, phosphates tied up, can’t generate ATP, can’t power ATP pumps, cells die
  • avoid fruit & honey
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44
Q

*** what would a deficiency of galactokinase or other galactose enzymes cause? what foods should be avoided?

A
  • formation of galactitol- cataracts
  • high blood & urinary galactose
  • high g-1-p levels- hepatic & brain dysfunction
  • avoid lactose
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45
Q

*** what is the range in which fasting glucose levels are maintained?

A

above 60 mg/100mL

below 110 mg/100 mL

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46
Q

** 3 names of important stages for glycolysis

A

priming- ATP investment
splitting- 2 G3ps
oxidoreduction-phosphorylation- ATP earnings

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47
Q

** which reaction requires a steady supply of NAD+? where does it come from in anaerobic respiration? aerobic respiration?

A

glyceraldehyde 3 p dehydrogenase

  • anerobic- lactate/ethanol production (cytosol)
  • aerobic- metabolite shuttle system
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48
Q

** low levels of NADH increase/decrease lactate formation

A

decrease

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49
Q

what are the steps of the citric acid cycle?
* between oxidation steps that produce NADH
# between oxidation steps that produce FADH2
$ by the one that produces GTP
& where C’s are lost via CO2

A 
ACoA
citrate
isocitrate
*&
alphakg
*&
succinyl Coa
$
succinate 
#
fumerate
malate
*
oxaloacetate
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50
Q

which CAC enzyme is in the inner mitochondrial membrane?

A

succinate dehydrogenase

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51
Q

** how many high energy phosphates generated per turn of the CAC? (ATP+GTP)

A

10 (3 NADH, 1 FADH2, 1 ATP)

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52
Q

** types of coarse control for the CAC?

A
  • ATP (needed to make NAD+)
  • acetyl CoA supply
  • oxaloacetate
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53
Q

** fine control- isocitrate dehydrogenase

A

inhibited by NADH and ATP

stimulated by ADP

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54
Q

** fine control- alphaketogluterate dehydrogenase

A

inhibited by ATP, GTP, NADH, succinyl CoA

stimulated by calcium

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55
Q

where does TCA provide precursors?

A 
citrate- FAs & sterols 
alphaKg- AAs/NTs
succinyl coa- heme
malate- gluconeogenesis
oxaloacetate- AAs
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56
Q

*** where can the TCA be replenished?

A
  • alphakg- glutamate from AAs
  • succinyl coa from propionyl coa (val/ile)
  • fumerate- AAs
  • oxaloacetate- aspartate & pyruvate
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57
Q

how does rat poison work?

A

fluroacetate converted to flurocitrate, which inhibits aconitase (transformation of citrate-isocitrate)

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58
Q

2 pathways that form free glucose?

A

1st- glycogen degradation

2nd- gluconeogenesis (NON CARB)

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59
Q

** where in the body does glucogneogenesis primarily occur?

A

liver & kidney- localize it so it doesn’t compete with glycolysis

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60
Q

** what is the major source of ATP for gluconeogenesis? AKA gluconeogenesis REQUIRES ATP

A

oxidation of fatty acids

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61
Q

When you use glucogeneic AA’s as opposed to lactate you need more/less ATPs?

A

need MORE (10 vs 6) b/c energy is needed to dispel amino groups given off via urea cycle

62
Q

*** what are the 4 enzymes that catalyze the 3 irreversible steps of glycolysis? (aka how you do reverse glycolysis to do gluconeogenesis?)

A

1- pyruvate caboxylase
2- PEP carboxykinase
3- Fructose 1,6 bisphosphate
4- glucose 6 phosphatase

63
Q

what factors stimulate glucogenesis as opposed to glycolysis?

A

increase in cAMP caused by high glucagon/epi and increased synthesis of key 4 enzymes

64
Q

what factors stimulate glycolysis as opposed to gluconeogenesis?

A

increased insulin or decreased cAMP, as well as increased synthesis of key 3

65
Q

** how does ethanol ingestion make you hungry?

A

it inhibits gluconeogenesis, causing hypoglycemia via over-production of NADH, converting pyruvate/oxaloacetate to malate/lactate

66
Q

*** which 3 main sources does acetyl CoA come from?

A
  • glycogen/glucose/pyruvate
  • triglycerides/fatty acids
  • protein/amino acids
67
Q

** where are the 3 places acetyla CoA goes?

A

CAC
ketone bodies
fatty acids; sterols

68
Q

** what are some symptoms of children with pyruvate dehydrogenase deficiencies?

A

elevated serum levels of lactate, pyruvate and alanine, which produce a chronic lactic acidosis

69
Q

** what are some examples of substrates that are used in gluconeogenesis to make glucose?

A

NON-CARB: pyruvate, lactate, glycerol, glucogenic amino acids

70
Q

** what is considered the activated form of pyruvate?

A

oxaloacetate- intermediate on the way back to PEP

71
Q

** glucogenic precursors- pyruvate

A

2 lactate, alanine

72
Q

** glucogenic precursors- oxaloacetate

73
Q

** glucogenic precursors- triose phosphates (ga3p)

74
Q

** what are some differences between the cori cycle and the glucose-alanine cycle?

A

cori- muscle/RBCs- lactate goes to liver, makes glucose, costs 6 ATPs
glucose-alanine- muscle- alanine goes to liver, makes glucose, costs 10 ATPs

75
Q

** what does a genetic deficiency in pyruvate carboxylase cause?

A

failure to thrive, developmental delay, recurrent seizures, and metabolic acidosis; elevated serum levels of lactate, pyruvate and alanine, which produce a chronic lactic acidosis

76
Q

** what are the different uses for muscle & liver glycogen? what are the different effects you would see if their activities were impaired?

A

muscle- production of ATP via g6p in cell- decreased ability to exercise
liver- maintenance of blood glucose- decreased blood glucose levels

77
Q

** what is the key enzyme lacking in muscles with regard to glycogen storage?

A

glucose 6 phosphatase- glycogen can’t be converted all the way back to glucose

78
Q

**what is the rate limiting enzyme for glycogen degredation? what enzyme regulates it?

A
  • glycogen phosphorylase a (-PO4)

- regulated by phosphorlyase kinase a

79
Q

** what is the rate limiting enzyme for glycogen synthesis? what enzyme regulates it?

A
  • glycogen synthase a

- phosphoprotein phosphatase (activates) and calmodulin dependent protein kinase (inhibits)

80
Q

** in both cases, phosphorylation of both glycogen phosphatase and glycogen synthase promote the storage or breakdown of glycogen?

81
Q

** what are the actions of insulin on the glycogen cycle?

A
  • synthase: stimulates phosphoprotein phosphatase, removes the phosphate from synthanse converting it from B to A, makes glycogen
  • phosphorylase: stimulates the removal of a phosphate from a, get inactive b form, no storage
82
Q

** what are some allosteric regulators of the phosphorylase/synthase pathways?

A

phosphorylase:
- b: activated by AMP
- a: inhibited by ATP, activated by glucose

synthase:
- b: activated by G6P

83
Q

** what are the actions of cAMP on the glycogen cycle?

A
  • cAMP produced by glycogen/epi stimulation
  • increases the activity of phosphorylase kinase, activates glycogen phosphorylase, degrade glycogen
  • inhibits the activity of phosphoprotein phosphatase, don’t activate glycogen synthase
84
Q

** what are the actions of Ca2+ on the glycogen cycle?

A
  • Ca2+ released with sustained muscle contraction
  • activates phosphorylase kinase, which activates glycogen phosphorylase (glycogen degradation)
  • activates calmodulin dependent protein kinase which inactivates glycogen synthase (no storage)
85
Q

what two hormones increase the concentration of blood glucose?

A

glucagon & epinephrine

86
Q

what are the specific functions glucagon & epinephrine inhibit and activate?

A
  • inhibit glycolysis (inhibits PFK2, reducing PFK1 function, inhibits pyruvate kinase)
  • activates hepatic glucogenogenesis (increases fructose 1,6,bp, inhibits pyruvate kinase)
  • inhibits glycogen synthesis
  • activates hepatic glycogenolysis (breakdown of glycogen by activating glycogen phosphorylase and phosphorylase kinase)
87
Q

** what is the main system that uses the pentose phosphate pathway?

88
Q

** what does the metabolism of glucose in the pentose phosphate pathway produce?

A
  • NADPH- lipid biosynthesis; maintains glutathione in a reduced state that helps protect the RBCs against oxidative damage
  • ribose 5 phosphate- DNA/RNA synthesis
  • glycolysis intermediates
89
Q

** what is the rate limiting enzyme in the pentose phosphate pathway? what does a deficiency in this enzyme cause?

A

glucose 6 phosphate dehydrogenase (g6dp)

- causes hemolytic anemia b/c RBCs can’t reduce NADPH (which maintains glutathione in a reduced state)

90
Q

what is the physiological condition that favors fatty acid biosynthesis?

A

fed state, high insulin

91
Q

** what is the rate limiting enzyme in fatty acid biosynthesis?

A

acetyl-CoA carboxylase

92
Q

** what are the hormones that activate/inhibit aCoA carboxylase?

A

activate- insulin

inhibit- *epinephrine & glucagon

93
Q

** what are the allosteric activators and inhibitors of aCoA carboxylase?

A

activate- citrate & biotin

inhibit- palmitoyl-CoA, AMP

94
Q

what are some factors that increase/decrease the synthesis of aCoA carboxylase?

A
  • increased: carbs, insulin, thyroid hormone

- decreased: high fat, fasting, glucagon

95
Q

** what is the product of the acetyl CoA caboxylase reaction? what does it inhibit? what cofactor serves as a carrier of activated CO2?

A

malonyl CoA
inhibits beta oxidation
biotin

96
Q

what is the name of the 7 enzyme complex that catalyzes the formation of fatty acids? what is it’s allosteric activator?

A

fatty acid synthase

activated by fructose 1,6, bisphosphate

97
Q

what are some things that increase/decrease the synthesis of fatty acid synthase?

A
  • increased by high carbs/free fat

- decreased by high glucagon, hight fat diet

98
Q

what are the two essential fatty acids?

A

alpha linolenic acid & linoleic acid

99
Q

how are fatty acids stored?

A

as triacylglycerols (TAGs)

100
Q

what are the 5 things fatty acid biosynthesis required?

A 
1- acetyl coa groups transported as citrate 
2- acetyl coa caboxylase
3- biotin
4- FA synthase complex
5- NADPH
101
Q

**which glucose transporter do you see on hepatic cells for glycogen production? on muscle cells?

A
  • hepatic: glut 2, works both ways, insulin independent

- muscle- glut 4, only takes glucose in after a meal (insulin dependent)

102
Q

** pathway for glycogen synthesis

A

glucose __> g6p __> glucose1-p __> UDP-glucose __> glycogen

103
Q

** what factors cause reactive oxidative species to rise?

A

oxidative drugs, infections, favism (lots of fava beans)

104
Q

which hormone mobilizes FA from adipose TAGS?

A

HSTL- hormone sensitive triacylglycerol lipase

105
Q

what is a major activator of the hormone that mobilizes FAs and via which pathway? lesser activator?

A
  • epinephrine via PKA, cAMP pathway

ACTH

106
Q

which are some inhibitors of the hormone that mobilizes FAs?

A 
insulin via dephosphorylation
and PGEs (prostaglandins)
107
Q

what three factors are required for normal HSTL activity?

A

thyroid hormones & adrenal cortical hormones & perilipin to coat surface of fat droplets

108
Q

what are the two products of TAG breakdown?

A

fatty acids and glycerol

109
Q

what does the released glycerol stimulate?

A

gluconeogenesis in liver

110
Q

what do the released fatty acids stimulate/inhibit?

A
  • inhibit fatty acid synthesis
  • stimulate beta oxidation (no malonyl coa)
  • stimulate the production of ketone bodies and ATP
  • ATP inhibits glycolysis, stimulates gluconeogenesis
111
Q

what are some good users of fatty acids?

A

liver, kidney cortex, heart, skeletal muscle

112
Q

tissues that cannot use fatty acids directly

A

brain, RBCs, nervous system, adrenal medulla, lens

113
Q

what does each cycle of mitochondrial b-oxidation generate?

A

1 acetyl-COA
1 NADH
1FADH2

114
Q

what is the comparison of phosphates produced from beta oxidation of palmitate and metabolism of glucose?

A

106 ATP vs 36-38 ATP

115
Q

what is the name of the protein that transports long chain fatty acids into mitochondrial matrix for beta oxidation?

116
Q

what is the rate limiting enzyme for beta oxidation? what is it inhibited by?

A

CPT1; malonyl CoA

117
Q

when are ketone bodies formed?

A

when beta oxidation production of acetyl CoA > utilization (high beta oxidation, high activity of HSTL, high levels of fatty acids)

118
Q

why is liver the only tissue in which ketone bodies can be synthesized?

A

b/c rate limiting enzyme is only in liver- HMG-COA synthase

119
Q

can livers use ketone bodies as fuel?

A

NO- don’t have acetoacetate:succinylCoA CoA transferase

120
Q

what is the end product of ketone body utilization?

A

2 acetyl CoA

121
Q

3 key regulatory steps for the break down of fatty acids

A

1- HSTL- inhibited by epi, stimulated by insulin
2- acetyl CoA carboxylase- stimulated by citrate/insulin, inhibited by glucago/epi
3- CPT1- inhibited by malonyl CoA

122
Q

in which way is dietary cholesterol packaged and where?

A

with TAG, in chylomicrons (least dense transport molecule) in intestinal cells

123
Q

in which way is synthesized cholesterol packaged and where?

A

with TAG, in VLDL molecules in liver cells

124
Q

how is cholesterol used?

A
  • cell membranes
  • bile acids
  • steroid hormones
125
Q

what vitamin is made from cholesterol?

126
Q

what are some steroid hormones that come from cholesterol?

A

progesterone, 17 beta estadiol, testosterone, cortisol, aldosterone, dehydroepiandrosterone

127
Q

what is the cholesterol biosynthesis pathway?

A

acetyl CoA –> mevalonate –> C15 –> squalene –> lanosterol –> cholesterol

128
Q

what is the rate limiting enzyme in cholesterol biosynthesis?

A

HmG-CoA reductase

129
Q

what factors regulate HmG-CoA reductase?

A

statins (lipitor)
cholesterol (transcription/enzyme stability)
AMP, glucagon (phosphorylation)
mevalonate (translation/enzyme stability)
- insulin activates

130
Q

what is the rate limiting enzyme in bile acid synthesis?

A

7 alpha hydroxylase

131
Q

what does an excess of cholesterol lead to

A

inhibits HMG CoA (bio-synthesis of cholesterol)
Activates ACAT (storage)
activates 7 alpha hydroxylase (bile)

132
Q

ratio of esterified to free cholesterol

A

70 esterified :30 free

133
Q

T/F esterifying cholesterol makes it more soluble for storage

A

F- cholesterol already is hydrophobic, adding the ester group makes it MORE hydrophobic

134
Q

which enzyme catalyzes the esterification of cholesterol for storage?

A

ACAT

acyl-CoA cholesterol acyl transferase

135
Q

What are lipoproteins made of?

A

apolipoproteins + TAGs, cholesterol, cholesterol esters

136
Q

what are the 5 major class of lipoproteins?

A

chylomicron, VLDL, IDL, LDL, HDL

137
Q

Chylomicrons are a good indicator of ____ because they are formed in the ______

A

dietary fat, intestines

138
Q

VLDLs are a good indicator of ____ because they are made in the ______

A

dietary carbohydrates; liver (endogenous TAG)

139
Q

which apolipoprotein activates LPL?

140
Q

which apolipoprotein clears remnants of VLDL/chylomicrons after TAGs have been hydrolyzed

141
Q

which apolipoprotein activates LCAT and turns cholesterols into cholesterol esters?

142
Q

T/F Apoproteins are made in the adipose tissue

143
Q

What does b-48 do? b-100?

A

b48- chylomicron secretion

b100- LDL receptor binding

144
Q

what does LDL do?

A

delivers fat/ cholesterol to liver & other cells (steroid-making)

145
Q

what does HDL do?

A

accepts cholesterol, esterifies it & transports to liver for excretion; carries apolipoproteins

146
Q

how is cholesterol taken up into cells?

A

B100s bind to LDL receptors in clathrin-coated pits, are endocytosed

147
Q

how does a defect in LDL receptors affect serum cholesterol, intracellular cholesterol, cholesterol biosynthesis

A

increases serum cholesterol
decreases cholesterol biosyntheses
decreases intracellular cholesterol esters

148
Q

two mechanisms of reverse cholesterol transport (mature HDLs)

A

a) CETP (transfer protein) mediates transfer from HDL - VLDL/IDL/chylomicron
b) HDLs taken up by liver by receptor mediated endocytosis

149
Q

LDL or HDL is highly sensitive to oxidation?

150
Q

major apoproteins for each of the 5 classes

A
  1. chylomicron- B48, ACE
  2. VLDL- B100, ACE
  3. IDL- B100, CE
  4. LDL- B100
  5. HDL- A’s (CE)

Physiology (22 decks)

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