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biochem test 3

  1. what are the five monosaccharides?
    Ribose, glucose, fructose, mannose, galactose
  2. What are the three polysaccharides?
    Starch, glycogen, fiber
  3. What are the three disaccharides?
    Sucrose, maltose, lactose
  4. What is amylose?
    non-branched polysaccharide, alpha 1,4 bonds
  5. What is amylopectin?
    • Branched polysaccharides
    • alpha 1,6 bonds
  6. What is retrograde amylose?
    • Resistant to small intestine digestion
    • causes reformation of polysaccharides, disaccharides, etc...
    • reason why beans give gas
  7. Is insulin required for the uptake of glucose by intestinal cells?
    No
  8. Is carbohydrate an essential nutrient?
    No
  9. what is the RDA for carbohydrate?
    130 g/day
  10. What happens to blood glucose if there is a high glycemic index?
    Glucose rises faster after ingestion
  11. What two sources can decrease glycemic index?
    • Fat
    • Fiber
  12. What is the AI (adequate intake) of fiber for men/women?
    38 g/day / 25 g/day
  13. Does a high fiber diet help reduce the risk of colon cancer?
    No
  14. Does eating fiber help with hyper- or hypotension?
    Hypertension (although not clinically proven)
  15. If a child is constipated, what would be required in a juice to relieve the constipation?
    • High fructose, low glucose
    • Even better if the high fructose is accompanied by sorbitol
    • This works because of the glucose dependent fructose transporter
  16. What are waste products given off from metabolism?
    H2O, Heat, CO2
  17. What are the five phosphotases that can release energy during hydrolysis of metabolism?
    • PEP
    • Carbamoyl phosphate
    • Creatine phosphate
    • Acetyl phosphate
    • ATP
  18. What are the two methods for carrying energy during metabolism?
    • Chemical
    • Electrons
  19. What are the four reducing equivalents?
    • NADH
    • FADH2
    • FMNH2
    • NADPH
  20. Which water-soluble energy carrier is kept higher in the cell, NAD+ or NADH, NADP+ or NADPH?
    • NAD+ helps to act as an oxidizing agent to accept electrons
    • NADPH helps to act as a reducing agent for FA synthesis
  21. What are the five methods of metabolic control?
    • Allosteric
    • Hormone control
    • Enzyme concentration
    • Compartmentalization
    • Specific control of individual tissues
  22. What are the two stages of lipogenesis?
    • Fatty acid synthesis
    • TAG synthesis
  23. What is the difference b/t synthase and synthetase?
    Synthetase requires ATP
  24. What inhibits isocitrate DH? What activates isocitrate DH?
    • Inhibit: NADH and ATP
    • Activate: ADP
  25. In their prospective order, after fasting, what are the skeletal muscles, liver, brain and RBCs using for energy?
    • FA
    • FA
    • Glucose
    • Glucose
  26. Where are the GLUT -1/3 located?
    All tissues
  27. Where is the GLUT-2 transporter located?
    • Liver
    • Pancreas (beta cells)
  28. Where is the GLUT-4 transporter found?
    • Skeletal muscles
    • adipose tissue
  29. What are the two shuttles NADH uses to pass its electrons across the mitochondrial membrane?
    • G3P shuttle = 2 ATP b/c of FADH2 used through complex 2
    • MA shuttle = 3 ATP because straight NADH
  30. What are the two sources of NADH and FADH2?
    • TCA cycle to the ETC
    • Beta Oxidation
  31. What is the rate limiting enzyme of the TCA cycle?
    Isocitrate Dehydrogenase
  32. Is the TCA cycle considered aerobic or anaerobic and why?
    It is aerobic because NADH and FADH2 would accumulate in anoxic environments so there would not have to be any production of NADH and FADH2 from the TCA cycle.
  33. At what regulatory enzyme do the ETC and TCA cycle link?
    Succinyl CoA through complex II of the ETC
  34. What regulatory enzyme from the TCA cycle allosterically inhibits PFK-1?
    Citrate
  35. In what organelle is the ETC found in metabolism?
    Mitochondria (inner mitochondrial membrane)
  36. In what part of the mitochondria does PDHC, Beta oxidation and the TCA cycle occur?
    Matrix
  37. What is an inhibitor of complex IV in the ETC?
    Cyanide and CO
  38. How to you treat the ETC if CN or CO are inhibiting complex IV?
    • Nitrites: convert hemoglobin to methemoglobin to bind Cyanide
    • Oxygen: Administer enough to compensate for inhibition
  39. What is an ETC uncoupler?
    Molecule that causes a charge gradient so H+ leaks back into the matrix before the ATP synthetase so ATP is not produced.
  40. Name an artificial ETC uncoupler?
    DNP
  41. Name the natural uncoupler of the ETC?
    Brown fat cells
  42. How does ADP for ATP production enter the mitochondrial matrix?
    ATP-ADP voltage gradient channel. It is an antiport system, 1:1.
  43. What inhibits the ADP-ATP antiport in the mitochondria?
    Atractyloside
  44. What is the RLE of glycogenesis?
    Glycogen synthase
  45. What is the coenzyme of glycogen phosphorylase in the glycogenolysis process?
    Pyridoxal phosphate (vitamin B6)
  46. Does glucagon play a role in the liver, muscles, or both?
    Liver only
  47. When does the body want to produce lactate from pyruvate?
    When there is low Oxygen or a lack of NAD+
  48. How much glucose is required for the brain daily?
    130 g
  49. How much glucose required for the human body?
    160 g
  50. Can gluconeogenesis occur in the muscle?
    No, only in the liver
  51. What are the three precursors for gluconeogenesis?
    • Lactate
    • amino acids
    • glycerol
    • ***they all come from catabolic rxns. during a fasting state
  52. How much pyruvate, ATP, GTP and NADH are utilized during gluconeogenesis?
    • Pyruvate = 2
    • ATP = 4
    • GTP = 2
    • NADH = 2
  53. How is OAA sent to the cytosol during gluconeogenesis?
    Malate-Aspartate Shuttle
  54. What are the two rxns. that OAA has to go through in order to make PEP?
    • Decarboxylated
    • Phosphorylated
  55. What is the RLE of gluconeogenesis?
    FBPase-1
  56. What activates FBPase-1 in gluconeogenesis?
    low levels of F2,6BisP (from phosphorylatd FBP-2/PFK-2)
  57. What is protein sparing?
    Utilizing other body resources for energy instead of spending energy on gluconeogenesis.
  58. What molecules participate in protein sparing and what absorption state are they found?
    • Fed = carbohydrate
    • Short-term fasting = liver glycogen
    • Long-term fasting = ketone bodies
  59. In the HMP shunt, what is NADPH used for?
    Anabolic pathways
  60. In the HMP shunt, what is Ribose5P used for?
    Biosynthesis of nucleotides
  61. In the HMP shunt, what is created from the RLE G6PD?
    • G6P
    • NADPH
  62. How is NADPH produced for tissue with no Mitochondria?
    • Use the HMP Shunt
    • NADPH is produced from G6PD and sent out to those tissues
  63. What is cytochrome P-450 system?
    • Part of the HMP shunt, oxidative branch
    • NADPH offers a hydrogen to help make drugs more soluble so they can be excreted through the kidneys
  64. What is the pathway to reduce hydrogen peroxide?
    Oxidative HMP shunt: G6PD - NADPH - Reduce oxidized glutathione - reduced glutathione offers H+ to H2O2 to make H2O - NADPH then reduces glutathione again since it is toxic (GSSG > GSH)
  65. Is fructose insulin dependent?
    No
  66. What happens if galactokinase is deficient in galactose metabolism?
    Aldose reductase will convert the extra galactose to galctitol and cause neuronal problems and cataracts
  67. Why are cataracts not a result of hereditary fructose intolerance (aldose B deficiency)?
    Fructose is not an aldose sugar and cannot be changed by aldose reductase
  68. What are the two general causees of enzymopathies?
    • 1) Increased substrate
    • 2) Not enough product produced
  69. What causes PKU and is it autosomal dominant or recessive?
    • PKU - caused by lack of PAH
    • Autosomal Recessive
  70. What causes hereditary fructose intolerance?
    • Aldolase B Deficiency
    • This means that Fructose 1-P builds up and ties up free phosphate
  71. What are the results of hereditary fructose intolerance?
    • Jaundice
    • Hypoglycemia
    • Hemorrhage
    • hepatic failure
  72. What are the two GSD diseases caused by defective glycogenesis?
    • Type 0 (no glycogen synthase)
    • Type IV (no branching enzyme)
  73. What are the two GSD diseases caused by defective glycogenolysis?
    • Type VI (lack of hepatic glycogen phosphorylase)
    • Type V (McArdle disease, lack of muscle glycogen phosphorylase)
  74. What is type III GSD in glycogenolysis?
    • Cori disease
    • lack of debranching enzyme
  75. What is Type I GSD in glycogenolysis?
    • von Gierke disease
    • lack of G6Pase
  76. What is Type II GSD in lysosomal degradation?
    • Pompe disease
    • lack of breakdown of glycogen in lysosomes
  77. In lipogenesis, what is necessary to synthesize palmitate?
    • Acetyl CoA
    • 7 Malonyl CoA
    • 14 NADPH
  78. 1) How are 8 of the fourteen NADPH necessary for lipogenesis created?
    2) How are the other six NADPH formed?
    • 1) Malic enzyme: from ATP citrate Lyase that produced OAA
    • OAA reacts with NADH to become Malate and then everything continues

    2) NADPH from HMP shunt
  79. How many carbons must be linked in a fatty acid to become a palmitate?
    16 carbons
  80. What types of tails are added to the Glycerol-P backbone to form TAG?
    • #1 = saturated
    • #2 = PUFA (polyunsaturated)
    • #3 = either
  81. How is TAG released into the blood stream?
    • package into VLDL particles
    • shipped via calcium exocytosis
    • APO cII is transferred from HDL to VLDL for lipoprotein recognition
    • (smaller than CM)
  82. Where does lipolysis occur?
    Adipose tissue
  83. What activates and inhibits HSL in lipolysis?
    • Activate: epinephrine (not glucagon), low insulin (allows for phosphorylation of HSL)
    • Inhibit: high insulin, Niacin
  84. When and where does beta oxidation occur?
    • When: low oxygen environment
    • Where: mitochondria
  85. What are the steps of the carnitine shuttle for beta oxidation?
    • 1. entrance of long chain FAcoA through OMM
    • 2. CoA cleaved by CPT-I and carnitine attached
    • 3. entrance into IMM
    • 4. Cleavage by CPT-II to produce FACoA and Carnitine
    • 5. Carnitine shipped out by CANT
  86. What are the three products from Beta Oxidation?
    • FADH2
    • NADH
    • Acetyl-CoA
    • (No ATP)
  87. What are the products from palmitate after Beta oxidation (7 rounds)?
    • 7 FADH2
    • 7 NADH
    • 8 Acetyl-CoA
  88. How many ATP are released when AcetylCoA passes through the TCA cycle?
    12 for each Acetyl-CoA
  89. What inhibits Beta oxidation of fatty acids?
    Malonyl CoA from high insulin and lipogenesis
  90. What is produced from Beta oxidation in Peroxisomes?
    • FADH2 - hydrogern peroxide to be destroyed
    • Short Fatty acids move into mitochondria
  91. What is formed from ketogenesis?
    • Beta-hydroxybutyrate
    • acetoacetate (ketone)
    • acetone (ketone)
  92. Why are fatty acids shunted into the ketogenesis cycle?
    • OAA is being used in gluconeogenesis
    • extra acetyl CoA and less citrate for lipogenesis
Author
kepling
ID
38212
Card Set
biochem test 3
Description
biochem test 3 random questions
Updated

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