FA biochem 4

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Neda317
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293601
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FA biochem 4
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2015-01-22 22:40:58
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biochem
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  1. Ethanol metabolism reactions and enzymes? and location of each reaction
    • Cytosol:
    •              Alcohol dehydrogenase
    • Ethanol ------------------------->Acetaldehyde
    •                 NAD+ -->NADH
    • Mitochondria:
    •                 Acetaldehyde dehydrogenase
    • Acetaldehyde ------------------------->Acetate
    •                         NAD+ -->NADH  
  2. Alcohol dehydrogenase operates via _____ order kinetics.
    zero
  3. what inhibits alcohol dehydrogenase and is an antidote for methanol or ethyleneglycol poisoning
    Fomepizole
  4. what inhibits acetaldehyde dehydrogenase (acetaldehyde accumulates,  NAD contributing to hangover symptoms).
    Disulfiram
  5. Ethanol metabolism inc NADH/NAD+ ratio in liver, causing:
    • -Pyruvate Ž--> lactate (lactic acidosis).
    • -Oxaloacetate -->Ž malate (preventsgluconeogenesis -->Ž fasting hypoglycemia)ƒƒ
    • -Glyceraldehyde-3-phosphate -->Ž glycerol-3-phosphate (combines with fatty acids to make triglycerides Ž--> hepatosteatosis)

    • Additionally, high NADH/NAD+ ratio disfavorsTCA production of NADH Ž--> inc.   utilization ofacetyl-CoA for ketogenesis
    • (--> ketoacidosis) and lipogenesis (Ž--> hepatosteatosis).
  6. Malnutrition Kwashiorkor
    • MEAL:Malnutrition Edema Anemia Liver (fatty)
    • Protein malnutrition resulting in skin lesions,edema, liver malfunction (fatty change due to apolipoprotein synthesis). Clinical picture is small child with swollen belly
  7. Marasmus
    • Marasmus results in Muscle wasting.
    • Total calorie malnutrition resulting in tissue and muscle wasting, loss of subcutaneous fat, and variable edema.
  8. Metabolism sites
    Mitochondria
    Fatty acid oxidation (β-oxidation), acetyl-CoA production, TCA cycle, oxidative phosphorylation.
  9. Metabolism sites
    Cytoplasm
    Glycolysis, fatty acid synthesis, HMP shunt,protein synthesis (RER), steroid synthesis(SER), cholesterol synthesis.
  10. Metabolism sites in both Mitochondria and Cytoplasm
    HUGs take two (i.e., both).

    Heme synthesis, Urea cycle, Gluconeogenesis
  11. Enzyme terminology 
    Kinase
    Uses ATP to add high-energy phosphate group onto substrate (e.g., phosphofructokinase
  12. Enzyme terminology 
    Phosphorylase
    Adds inorganic phosphate onto substrate without using ATP (e.g., glycogen phosphorylase
  13. Phosphatase
    Removes phosphate group from substrate (e.g., fructose-1,6-bisphosphatase).
  14. Dehydrogenase
    Catalyzes oxidation-reduction reactions (e.g., pyruvate dehydrogenase).
  15. Hydroxylase
    Adds hydroxyl group (-OH) onto substrate (e.g., tyrosine hydroxylase).
  16. Carboxylase
    Transfers CO2 groups with the help of biotin (e.g., pyruvate carboxylase).
  17. Mutase
    Relocates a functional group within a molecule (e.g., vitamin B12–dependent methylmalonyl-CoA mutase
  18. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    Glycolysis
    • -Phosphofructokinase-1 (PFK-1)
    • -AMP (+), fructose-2,6-bisphosphate (+) 
    • ATP (-), citrate(-)
  19. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
     Gluconeogenesis
    • -Fructose-1,6-bisphosphatase
    • -ATP (+), acetyl-CoA (+),
    • AMP (-), fructose-2,6-bisphosphate (-)
  20. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    TCA cycle
    • -Isocitrate dehydrogenase
    • -ADP (+), ATP (-), NADH (-)
  21. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    Glycogenesis
    • -Glycogen synthase
    • -Glucose-6-phosphate(+), insulin(+),
    • cortisol(+), Epinephrine(-), glucagon(-)
  22. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
     Glycogenolysis
    • -Glycogen phosphorylase
    • -Epinephrine(+), glucagon(+), AMP(+),
    • Glucose-6-phosphate(-), insulin(-), ATP(-)
  23. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    HMP shunt
    - Glucose-6-phosphate dehydrogenase (G6PD)

    -NADP+ (+), NADPH(-)
  24. Rate-determining enzymes of metabolic processes
    ENZYME  
    De novo pyrimidine synthesis
    Carbamoyl phosphate synthetase II
  25. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    De novo purine synthesis
    • -Glutamine-phosphoribosylpyrophosphate (PRPP) amidotransferase
    • -AMP (-), inosine monophosphate (IMP) (-),
    • GMP (-)
  26. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    Urea cycle 
    -Carbamoyl phosphate synthetase I

    -N-acetylglutamate(+)
  27. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    Fatty acid synthesis
    • - Acetyl-CoA carboxylase (ACC)
    • -Insulin (+), citrate(+), Glucagon(-),
    • palmitoyl-CoA(-)
  28. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    Fatty acid oxidation
    • - Carnitine acyltransferase I
    • -Malonyl-CoA (-)
  29. Rate-determining enzymes of metabolic processes
    ENZYME  
    Ketogenesis 
    HMG-CoA synthase
  30. Rate-determining enzymes of metabolic processes
    ENZYME and REGULATORS
    Cholesterol synthesis
    • - HMG-CoA reductase
    • -Insulin(+), thyroxine(+), Glucagon (-), cholesterol(-)
  31. NADPH is used in
    • ƒƒ Anabolic processesƒƒ
    • Respiratory burstƒƒ
    • Cytochrome P-450 systemƒƒ
    • Glutathione reductase
  32. where do u find Glucokinase
    Liver, b cells of pancreas
  33. where do u find Hexokinase
    Most tissues, but not liver nor β cells of pancreas
  34. Feedback-inhibited by glucose-6-P
    what enzyme?
    Hexokinase
  35. Gene mutation associated with maturity-onset diabetes of the young (MODY)
    Glucokinase
  36. which one of these two Induced by insulin Hexokinase or Glucokinase
    Glucokinase
  37. Pyruvate dehydrogenase
    Mitochondrial enzyme complex linking glycolysis and TCA cycle. Differentially regulated in fed/fasting states (active in fed state).
  38. Pyruvate dehydrogenase Reaction:
    pyruvate + NAD+ + CoA -->Ž acetyl-CoA + CO2 + NADH
  39. Pyruvate dehydrogenase Activated by
    Activated by exercise, which: inc NAD+/NADH ratio, inc ADP, inc Ca2+
  40. Arsenic inhibits
    arsenic poisoning findings
    • lipoic acid.
    • Findings: vomiting,rice-water stools, garlic breath.
  41. Pyruvate dehydrogenase complex deficiency
    Causes a buildup of pyruvate that gets shunted to lactate (via LDH) and alanine (via ALT).
  42. Leucine—the onLy pureLy ketogenic amino acids.
    Lysine and Leucine
  43. Electron transport inhibitors and func
    • Rotenone, cyanide, antimycin A, CO.
    • Directly inhibit electron transport, causing a dec proton gradient and block of ATP synthesis.
  44. ATP synthase inhibitors and func?
    • Oligomycin.
    • Directly inhibit mitochondrial ATP synthase,causing an  proton gradient. No ATP is
  45. Uncoupling agents
    2,4-Dinitrophenol (used illicitly for weight loss), aspirin (fevers often occur after aspirin overdose), thermogenin in brown fat.

    inc permeability of membrane, causing a dec protongradient and inc O2 consumption. ATP synthesis stops, but electron transport continues.Produces heat.
  46.  Glucose-6-phosphatedehydrogenase deficiency
    3 main features
    • Heinz bodies
    • immune def
    • hemolytic anemia
  47. Essential fructosuria Involves a defect in
    Symptoms:
    • fructokinase. asymptomatic
    • fructose appears in blood and urine
  48. Fructose intolerance Hereditary deficiency of
    and Symptoms:
    tx:
    • aldolase B.
    • hypoglycemia, jaundice, cirrhosis, vomiting.
    • Treatment: dec intake of both fructose and sucrose (glucose + fructose).
  49. Galactokinase deficiency Hereditary deficiency of
    Symptoms:
    • galactokinase. 
    • Symptoms: galactose appears in blood and urine, infantile cataracts. May initially present as failure to track objects or to develop a social smile.
  50. Classic galactosemia  Absence of
    Symptoms
    Treatment:
    • galactose-1-phosphate uridyltransferase
    • Symptoms: failure to thrive, jaundice, hepatomegaly, infantile cataracts, intellectual disability.
    • Treatment: exclude galactose and lactose (galactose + glucose) from diet.
  51. Classic galactosemia can lead to
    can lead to E. coli sepsis in neonates.
  52. what enzyme makes sorbitol from glucose?
    Aldose reductase w NADPH
  53. sorbitol -----?---> fructose?
    Sorbitol dehydrogenase and NAD+
  54. both Aldose reductase & Sorbitol dehydrogenase are found in
    Liver, ovaries, and seminal vesicles have both enzymes
  55. Aldose reductase found in
    Schwann cells, retina, and kidneys have only aldose reductase. Lens has primarily aldose reductase.
  56. tissues with an insufficient amount of this aldose reductase & Sorbitol dehydrogenase are at risk for
    at risk for intracellular sorbitol accumulation, causing osmotic damage (e.g., cataracts, retinopathy, and peripheral neuropathy seen with chronic hyperglycemia in diabetes).
  57. High blood levels of galactose also result in
    conversion to the osmotically active galactitol via aldose reductase.
  58. Lactase deficiency Stool demonstrates
    low pH and breath shows inc hydrogen content with lactose tolerance test. Intestinal biopsy reveals normal mucosa in patients with hereditary lactose intolerance.

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