Biochem Exam 3

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  1. Blood glucose concentration is about ___ millimolar (about ____ milligrams per deciliter)

  2. given that the blood glucose concentration is 5 mM how many grams of glucose are in the blood?
  3. what are the three major sources for blood glucose?
    • alimentary glucose (food glucose)
    • glucose released from storage (glycogen)
    • glucose made from proteins (food but not directly
  4. what is the glucose oxidation equation
    Glucose + 6O2 --> 6CO2 + 6H2O + energy
  5. glycolysis occurs in the cytosol and the products of the two pathways in glycolysis are
    anaerobic: lactate, 2 ATP, water

    aerobic pyruvate, 2 ATP, NADH + H+ and water
  6. where does the TCA cycle occur
    in the mitochondrial matrix
  7. where does the ETC occur
    inner mitochondrial membrane
  8. T/F: the presence of pyruvate at the end of glycolysis makes it anaerobic

    the presence of lactate---pyruvate is aerobic and anaerobic (right before the conversion to lactate happens)
  9. how does glucose get into the cells before glycolysis can occur?
    GLUTs and SGLT
  10. where does the lactate go after anaerobic glycolysis
    it stays in the cytosol
  11. Why do we have an inefficient process (less ATP) such as anaerobic? (2)
    • Easier and less complicated
    • Gives us ATP when we don’t have the resources to do the aerobic route
  12. tissues that use anaerobic glycolysis
    • tissues with few or no mito
    • RBC
    • leukocytes 
    • lens
    • cornea
    • medulla of the kidney
    • testes
    • ischemic tissues (tissues which cannot utilize the blood supplies
  13. what type of fibers are in skeletal muscles in humans?
    type 1 and type 2
  14. aerobic muscle fibers that are rich in mitochondria and myoglobin

    dominant in muscles associated with endurance (legs, back)

    Relatively resistant to fatigue

    slow twitch
    Type 1
  15. Type 1 fibers are ___ twitch
  16. more anaerobic muscle fibers with fewer mito and myoglobin

    dominant in muscle associated with rapid movement, easily fatigued

    fast twitch
    Type 2
  17. Type 2 fibers are ____ twitch
  18. 5 initial steps of glycolysis who's net effect is ____

    they convert glucose (6 C) to ____ (3 C)

    triose phosphates
  19. after the 5 initial steps, the 5 additional steps who's net effect is such that they are ____
  20. what are the three irreversible glycolytic enzymes which are regulatory
    • hexokinase
    • phosphofructokinase
    • pyruvate kinase
  21. the three irreversible glycolytic enzymes are all characterized as being highly
  22. hexokinase and glucokinase are _____ of each other

    not an allele
  23. glucose is converted to G6P by which enzyme?

    does this step use or produce ATP?

    use ATP
  24. G6P is converted to fructose 6 phosphate (ketose) by which enzyme?
    phosphoglucose isomerase
  25. ____ is easily saturated as product inhibition keeps the activity below Vmax
  26. enzyme that functions to removed glucose from the blood
  27. _____ has a high capacity, but a might lower affinity (higher Km)
  28. _____ has a much lower capacity, but a much higher affinity (lower Km)
  29. How do the liver and pancreas respond to glucose being removed from the blood by glucokinase?
    The liver will respond by channeling glucose into storage pathways, while the beta cells of the pancreas will respond by secreting insulin.
  30. Image Upload
    Image Upload
  31. When post-prandial (after a meal) levels of glucose are ____, liver _____- allows the liver to take up circulating glucose and store it as ____.


  32. The absence of product inhibition of ____ serves to ensure that _____ uptake and storage of blood glucose (glycogen) can continue.

  33. the low km of hexokinase allows tissues
    to efficiently phosphorylate glucose when glucose is in low supply

    because G6P will stay within the cell and won't diffuse out via GLUTs (GLUTs don't recognize g6p)
  34. Mice deficient in glucokinase regulatory protein do not respond rapidly to injected glucose. This metabolic impairment is thought to be due to the absence of a ____ ____ _ _______.
    nuclear reserve of glucokinase 

    If you don’t have the GKRP the GK wont be in a storage place in the nucleus (they will be floating all over the place)—cant easily take it and put it back freely in glycolysis
  35. in the presence of ____ glucokinase will be removed from its inactive form in storage and will be available to use
  36. in the presence of ____ glucokinase will go back into storage (inactive form) and will be unavailable
  37. where are glucokinase and glucokinase regulatory protein located?
    in the nucleus
  38. ATP and citrate turn off the conversion of F6P to F16BP via phosphofructokinase 1

    • ATP—you clearly have enough of ATP so the cycle that makes ATP stops
    • Citrate is a signal that you have enough energy so it turns off the enzyme
  39. AMP and fructose 2,6 BP turn on the conversion between F6P to F16BP via phosphofructokinase 1

    AMP turns on the enzyme because if you have a lot of AMP you don’t have a lot of ATP and you need to continue the pathway to get it
  40. PFK-1 can be regulated allosterically by elevated levels of the following energy-associated signals:

    activated: AMP

    inactivated: ATP, citrate
  41. inhibition of PFK-1 leads to the accumulation of G6P which can be routed towards (3)
    • gluconeogenesis
    • glycogenesis (glycogen synthesis) in musce or liver
    • hexose monophosphate shunt (PPP)
  42. regulatory enzymes of glycolysis in general can be activated by (3)
    • Insulin
    • AMP
    • Substrate
  43. Regulatory enzymes of glycolysis, in general, can be inhibited by (7)
    • glucagon (made in alpha cells)
    • ATP
    • NADH--you have enough of these, don't need more
    • cyclpe AMP
    • Acetyl CoA
    • Citrate
    • Product inhibition
  44. elevated insulin/glucagon ratio promotes ______
  45. elevated glucagon/insulin promotes ______
  46. True/False: ingestion on a regular basis of CHO or administration of insulin can elevate the levels of these glycolytic enzyme transcripts
  47. insulin ___ glucokinase transcription
    glucagon ____ glucokinase transcription

  48. insulin ____ PFK transcription

    glucagon ____ PFK transcription

  49. insulin ____ pyruvate kinase transcription

    glucagon ____ pyruvate kinase transcription

  50. ____ is made as a side product in anaerobic glycolysis 

    able to be used in RBC when there are low oxygen levels
    2,3 BPG

    nAbout 15-25% of glucose converted to lactate in erythocytes is shuttled through BPG shunt, while very minute amounts are shuttled through BPG shunt in other cell types
  51. hypoxia induces synthesis of _____
    2,3 BPG
  52. T/F: pyruvate kinase adds a P to the substrate

    it removed a P from phosphoenolpyruvate to  pyruvate
  53. T/F: pyruvate Can have abnormal Km or Vmax, can show an abnormal response to F16BP
  54. glucagon  indirectly (via a second messenger system) phosphorylates ____ ____ thusly inactivating it
    pyruvate kinase
  55. inhibiting pyruvate kinase inhibits ___ and promotes ____ in the liver and kidney

  56. heredity deficiency of ____ (insulin independent transporter) can lead to seizures in infancy and delayed development
  57. deficiency of a specific isoform aldolase can lead to _____ ____
    hemolytic anemia
  58. deficiency of ___ ___ ____ can lead to hemolytic anemia and neurological symptoms
    triose phosphate isomerase
  59. pyruvate kinase deficiency affects about ___ per ____ individuals and this is considered relatively ____ for a genetic diseases
    1 per 10,000
  60. Phosphofructokinase deficiency is a ___ ____ disease
    glycogen storage

    Will have a problem with glucose-6-phosphate accumulate and therefore you will have problems with glycogen storage
  61. The severity of the disease is a function of both ______ activity and activation of _____ mechanisms

  62. What is the reason that some RBCs are so affected with pyruvate kinase deficiency?
    No redundancy—RBC have no alternative pathways to get from point A to point B—no organelles, etc
  63. _____ deficiency in mince appears to be protective against malaria
  64. why is sodium fluoride generally added to blood samples prior to reading blood glucose levels
    As cells are taking up glucose they are also breaking it down (going through glycolysis) and to stop that process they add fluoride to inhabit enolase (which is an enzyme of glycolysis)
  65. what are the two mechanisms of arsenic toxicity
    Disruption of sulfhydryl-containing enzymes

    Substitution of phosphorus anion in phosphate, preventing net ATP and NADH synthesis while allowing glycolysis to proceedGlycolysis will continue, aren't totally killing it but
  66. pyruvate is reduced to lactate by which enzyme?
    lactate dehydrogenase
  67. Structure of pyruvate
    • pyruvate-14443377D60649CEB09
    • (3 carbons--two are present from the splitting of a 6 C glucose molecule)
  68. structure of lactate
    120px-L-Lactat-Ion.svg2 Hs are added from pyruvate --to the O and to the previously carbonyl C
  69. the conversion from pyruvate to lactate serves to
    oxidize NADH to NAD+, prodiving more NAD+ for continuing glycolysis
  70. The reaction of pyruvate to lactate is reversible or irreversible?
  71. Why is the production of lactate in anaerobic glycolysis so important
    NADH in anaerobic glycolysis wont be taken to the mitochondria to be oxidized to NAD+ and therefore it could build up and if there is no more NAD+ glycolysis can stop all together
  72. NADH is oxidized to NAD+ in the _____
  73. In the absence of oxygen, the NAD+ is regenerated by the formation of _____
  74. the following tissues derive their energy from anaerobic glycolysis (6)
    • erythrocytes
    • skeletal muscle in a state of great exertion 
    • lens and cornea of the eye
    • testes
    • leukocytes
    • kidney medulla
  75. After lactate is formed it diffuses for the tissue into the blood and there can be used by the liver for _______
  76. lactate cane be use by the heart or kidney to regenerate ____ which is further oxidize aerobically in the mitochondria
  77. Is lactate responsible for most of the muscle soreness felt on days following physical exertion?

    they used to think that it was the build up of lactate causing this but now people say it due to the tears in muscle
  78. glucose oxidation consists of 3 processes
    • Glycolysis
    • TCA cycle (occurs in mito matrix)
    • Electron transport chain (occurs in inner mitochondrial matrix)
  79. the ETC is involved with (2)
    • electron transport
    • oxidative phosphorylation
  80. glycolysis generates __(1)___ from ___(2)__

    (1) is oxidized to 2 in the mitochondria

  81. the regeneration of NAD+ by the formation of lactate is catalyzed by
    lactate dehydrogenase
  82. Conditions that raise the NADH/NAD+ promote the formation of lactate (7)
    • CO poisoning
    • sickling crisis
    • ischemic tissue
    • myocardial infarction
    • mitochondrial disease
    • warburg effect
    • alcohol intoxication
  83. how does CO poisoning promote lactate formation?
    it causes Hb to hold onto O2 better and it won't release the O2 to the tissues and so your mito won't be working well and the NADH will not be metabolized but he mito and ti will build up and raise the NADH level
  84. how does a sickling crisis promote lactate formation
    sickle cell patents only have this (anemia and crisis) and it is associated with O2 problems in mitochondria won't be working well and you won't be able to metabolize the NADH and it will build up
  85. how does ischemic tissue promote lactate formation
    tissue doesn't have enough oxygen due to cardiovascular issues
  86. how does mitochondrial disease promote lactate formation
    generic disease, and so chronic inability to metabolize NADH bc mito isn't working well
  87. how does Warburg effect disease promote lactate formation
    cancer cells are anaerobic (don’t have to be but they are—so not really explained), thought to be a result of mutation and once it becomes cancerous it starts the warburg effect
  88. If you have more NAD+ you promote the formation of _____

    if you have more NADH you promote the formation of_____

  89. Cancer cells are thought to be due to mutations in the two genes
    Oncogenes—go into over drive and more are made and they make cancer

    Tumor suppressor genes—the defense against cancer crumbles and you cannot fight against the cancer
  90. True/False: the mitochondria is involved in apoptosis of cancer cells
  91. how does alcohol intoxication promote lactate formation
    The oxidation of alcohol results in significant amounts of NADH in the liver which raises the ratio of NADH and NAD+
  92. why is NADH produced during alcohol oxidation?
    the dehydrogenases involved in alcohol metabolism take Hs away and add them to NAD+ forming NADH
  93. How is ethanol metabolism related to NADPH
    Alcohol is a xenobiotic and therefore the liver’s cyp system metabolizes it using NADPH

    ^the cyp system being used is very important because alcohol can be very harmful to us
  94. what is MEOS
    microsomal (the smooth ER) ethanol oxidizing system
  95. Lactic acidosis results from the overproduction (or underutilization) of _____ ____
    lactic acid
  96. nemonic device for the steps of the TCA cycle
    CItric Acid Is Krebs’ Starting Substrate For Mitochondrial Oxidation

    C—Citrate (citric acid)


    A—alpha ketoglutarate

    S—succinyl Co-A




  97. Acetyl CoA (acetyl part) has ___ carbons, oxaloacetate has ____ carbons and they combine to form citrate which has ___ carbons
    • TWO 
    • FOUR
    • SIX
  98. The TCA cycle represents the metabolic destination for the oxidation of ____, ___ and ____
    • CHO 
    • proteins
    • lipids
  99. The ____ ____ participates in processes such as transamination, deamination, lipogenesis, and gluconeogenesis.
    TCA cycle
  100. The TCA cycle produces the reduced co-enzymes ___ and ____ that provide substrates for the ETC, which subsequently oxidizes these substrates
    • NADH
    • FADH2
  101. True/False: Few (very little) genetic defects associated with TCA cycle have been identified in humans, as there are none at the present time

    there are none as the severity of these defects might present an overwhelming metabolic challenge--Make a slight change the human cannot survive because these enzymes are so essential so they cannot be tested
  102. is the TCA cycle is anabolic or catabolic?

    it is amphibolic
  103. Almost all of the TCA enzymes are located in the
    mitochondrial matrix
  104. Acetyl CoA can be formed from ___ and ____
    • fatty acids 
    • amino acids
  105. what is the precursor molecule for the synthesis or ketone bodies, fatty acids and cholesterol
    Acetyl CoA
  106. what is the enzyme that forms acetyl CoA from pyruvate
    pyruvate dehydrogenase
  107. What can inhibit the activity of PDH and why?
    Acetyl CoA--negative feedback (product inhibition)

    NADH--this is one of the products of the TCA cycle so don't need more (negative feedback/product) inhibition
  108. Where does the CO2 come from in the production of Acetyl CoA?
    it is from the pyruvate (leaves from the molecule)
  109. activity of pyruvate dehydrogenase complex requires specific nutrients (5)
    • thiamine
    • panthothenic acid
    • niacin
    • riboflavin
    • lipoic acid

    **all B vitamins
  110. how can alcohol affect the activity of pyruvate dehydrogenase complex?
    alcohol depletes the body of certain B vitamins and since the PDH complex requires B vitamins for function it an inhibit the activity
  111. PDC is allseoterically inhibited by elevated levels of ___ ____ and ____
    • NADH
    • ATP
    • Acetyl CoA
  112. ATP, acetyl CoA, NADH will activate the ____ to inactivate PDH complex
  113. T/F: the phosphorylated PDC is inactive
  114. why do ATP, NADH and Acetyl CoA inactivate PDC by activated protein kinase?
    because these are products and we have enough so it inhibits the going forward of the reaction
  115. PDC is activated by what?

    calcium activates phosphoproteinkinase which cleaves the P from PDC and activates it
  116. pyruvate ____ the inactivation of PDC
  117. why does pyruvate inhibit the inactivation of PDC
    Pyruvate inhibits the inactivation of pyruvate dehydrogenase because if there is a lot of it present the reaction will want to go forward and if it is inhibiting the inactivation of it, it will make it go forward
  118. Image Upload
    Image Upload
  119. How many ATP are produced for every NADH molecule
  120. How many ATP are produced for every FADH2 molecule
  121. How many ATP are produced for every GDP molecule

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Biochem Exam 3
2017-11-08 19:38:36

Exam 3 Material
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