1. BIOCHEMISTRY LECTURES

2. Figure

3. Stages in the extraction of energy from foodstuffs.

4. Figure 16.24
Triacylglycerol degradation in adipocytes. Epinephrine initiates the activation of protein kinase A, which catalyzes the phosphorylation and activation of hormone-sensitive lipase. The lipase catalyzes the hydrolysis of triacylglycerols to monoacylglycerols and free fatty acids. The hydrolysis of monoacylglycerols is catalyzed by monoacylglycerol lipase.

5. Figure 16.6
Activation of fatty acids.

6. Enzyme is inhibited by malonyl CoA!
Why?
Figure 16.21
Carnitine shuttle system for transporting fatty acyl CoA into the mitochondrial matrix. The path of the acyl group is traced in red.

8. Figure 16.22
Conversion of propionyl CoA to succinyl CoA.

9. Figure 7.24
Cobalamin (vitamin B12) and its coenzymes. (a) Detailed structure of cobalamin, showing the corrin ring system (black) and 5,6-dimethylbenzimidazole ribonucleotide (blue). The metal coordinated by corrin is cobalt (red). The benzimidazole ribonucleotide is coordinated with the cobalt of the corrin ring and is also bound via a phosphoester linkage to a side chain of the corrin ring system. (b) Abbreviated structure of cobalamin coenzymes. A benzimidazole ribonucleotide lies below the corrin ring, and an R group lies above the ring.

10. Figure 16.23
Oxidation of linoleoyl CoA. Oxidation requires two enzymes—enoyl-CoA isomerase and 2,4- dienoyl-CoA reductase—in addition to the enzymes of the -oxidation pathway.

19. heart muscle kidney brain Figure 16.34
Conversion of acetoacetate to acetyl CoA.

20. 1. Synthesis takes place in the cytosol, in contrast with degradation, which occurs in the mitochondrial matrix.
2. Intermediates in fattv acid synthesis are covalently linked to the sulf-hydryl groups of an acyl carrier protein (ACP), whereas intermediates in fatty acid breakdown are bonded to coenzyme A.
3. The enzymes of fatty acid synthesis in higher organisms are joined in a single polypeptide chain called fatty acid synthase. In contrast, the degradative enzymes do not seem to be associated.
4. The growing fatty acid chain is elongated by the sequential addition of two-carbon units derived from acetyl CoA. The activated donor of two-carbon units in the elongation step is malonyl-ACP. The elongation reaction is driven by the release of CO2.
5. The reductant in fatty acid synthesis is NADPH, whereas the oxidants in fatty acid degradation are NAD+ and FAD.
6. Elongation by the fatty acid synthase complex stops upon formation of palmitate (C16). Further elongation and the insertion of double bonds are carried out by enzyme systems of the endoplasmic reticulum with the fatty acyl groups as CoA derivatives.

21. Schematic diagram showing the proposed movement of the biotin prosthetic group from the site where it acquires a carboxyl group from HCO3- to the site where it donates this group to acetyl CoA.

22. Acetyl CoA carboxylase, which catalyzes the committed step in fatty acid synthesis, is a key control site.

24. Figure 16.3
Synthesis of malonyl ACP from malonyl CoA and acetyl ACP from acetyl CoA.

27. Figure 16.5
The elongation stage of fatty acid synthesis. R represents —CH3 in acetoacetyl ACP or [—CH2—CH2]n—CH3 in other 3-ketoacyl ACP molecules.

28. Figure 16.20
Fatty acid synthesis and -oxidation.

29. Citrate transport system
Citrate transport system. The system achieves net transport of acetyl CoA from the mitochondrion to the cytosol and net conversion of cytosolic NADH to NADPH. Up to two molecules of ATP are expended for each round of the cyclic pathway.

30. .

32. All the carbons and all the hydrogens of fatty acids can have come from glucose.
Know how.

34. Figure 16.6
Activation of fatty acids.

35. Figure 16.7
Elongation and desaturation reactions in the conversion of linoleoyl CoA to arachidonoyl CoA.

36. Figure 16.7
Elongation and desaturation reactions in the conversion of linoleoyl CoA to arachidonoyl CoA.

37. Figure 16.7
Elongation and desaturation reactions in the conversion of linoleoyl CoA to arachidonoyl CoA.

38. To make prostaglandins and leucotrienes, animals use
C20 fatty acids with 3,4 or 5 cis
s in key positions.
positions w 6,9 or w 3,6,9 from plants.
We must get fatty acids with
s in

39. D 18 17 15 16 14 13 12 11 10 9 8 7 6 5 4 3 2 1
CH3 w 1 2 4 3 5 6 7 8 9 10 11 12 13 14 15 16 17 18

40. Animals and plants place first cis at D9

41. regardless of the length (C16, C18, C20) of the fatty acid.
by –CH2– from an existing
, towards the –COO- group,
regardless of the length (C16, C18, C20) of the fatty acid.
Animals and plants can place a subsequent
, separated D 6
new 9
existing 9 D
by –CH2– from an existing
, towards the CH3– group.
Only plants can place a subsequent
, separated
existing 12
new

42. In plants
C18:0 D
C18:1 w 9 9 w
C18:2 6 9 w
C18:3 3 6 9

43. In animals or plants w w w w C18:2 C18:3 C20:3 C20:4 PGs1 PGs2 6 9 6 912 w
C20:3
PGs1 6 9 12 w
C20:4
PGs2 6 9 12 15

44. C18:3 w3,6,9
C18:4 w3,6,9,12
C20:5 w3,6,9,12,15 w 3 6 9 12 15
PGs3

45. Figure 16.12
Major pathways for the formation of eicosanoids. The prostaglandin H synthase (PGHS) pathway leads to prostaglandin H2, which can be converted to prostacyclin, thromboxane A2 and a variety of prostaglandins. The lipoxygenase pathway shown produces leukotriene A4, a precursor of some other leukotrienes. The cyclooxygenase activity of PGHS is inhibited by aspirin.

46. Important eicosanoids
Vascular endothelial cells:
vasdilatory
inhibits platelet aggregation
Platelets:
aggregates platelets
White blood cells,
mast cells
inflammatory,
allergic

48. Aspirin
COX

49. Structure of the active site of prostaglandin H2 synthase (COX)

50. Cyclooxygenases COX 1: constitutive - in plateletts
- in gastrointestinal epithelial cells
COX 2: induced in inflammatory process
Selective inhibitors – non steroidal (NSAIDs) ?
How do steroids reduce inflammation?

52. Figure 16.9
Synthesis of triacylglycerols and neutral phospholipids. The formation of triacylglycerols, phosphatidylcholine, and phosphatidylethanolamine proceeds via a diacylglycerol intermediate. A cytosine–nucleotide derivative donates the polar head groups of the phospholipids. Three enzymatic methylation reactions, in which S-adenosylmethionine is the methyl-group donor, convert phosphatidylethanolamine to phosphatidylcholine.

53. Figure 16.10
Synthesis of acidic phospholipids. Phosphatidate accepts a cytidylyl group from CTP to form CDP–diacylglycerol. CMP is then displaced by an alcohol group of serine or inositol to form phosphatidylserine or phosphatidylinositol, respectively.

54. Figure 16.10
Synthesis of acidic phospholipids. Phosphatidate accepts a cytidylyl group from CTP to form CDP–diacylglycerol. CMP is then displaced by an alcohol group of serine or inositol to form phosphatidylserine or phosphatidylinositol, respectively.

55. Figure 16.11
Interconversions of phosphatidylethanolamine and phosphatidylserine.

56. Figure 16.13
Synthesis of ether lipids. Plasmalogens are synthesized from ether lipids by the formation of a double bond at the position marked with a red arrow.

57. Figure 16.13
Synthesis of ether lipids. Plasmalogens are synthesized from ether lipids by the formation of a double bond at the position marked with a red arrow.

58. Figure 16.13
Synthesis of ether lipids. Plasmalogens are synthesized from ether lipids by the formation of a double bond at the position marked with a red arrow.

59. Figure 16.13
Synthesis of ether lipids. Plasmalogens are synthesized from ether lipids by the formation of a double bond at the position marked with a red arrow.

60. Figure 16.13
Synthesis of ether lipids. Plasmalogens are synthesized from ether lipids by the formation of a double bond at the position marked with a red arrow.

61. Figure 16.13
Synthesis of ether lipids. Plasmalogens are synthesized from ether lipids by the formation of a double bond at the position marked with a red arrow.

62. Figure 16.14
Synthesis of sphingolipids.

63. Figure 16.14
Synthesis of sphingolipids.

64. Figure 16.14
Synthesis of sphingolipids.

65. Figure 16.14
Synthesis of sphingolipids.

66. Figure 16.14
Synthesis of sphingolipids.

69. N-Acetylneuraminate

70. Pathways for the formation and degradation of a variety of sphingolipids, with hereditary metabolic diseases indicated.

71. Pathways for the formation and degradation of a variety of sphingolipids, with hereditary metabolic diseases indicated.

78. Structure of HMG-CoA and two common statins.

79. Figure 16.15
Stage I of cholesterol synthesis: formation of isopentenyl diphosphate. The condensation of three acetyl CoA molecules leads to HMG CoA, which is reduced to mevalonate. Mevalonate is then converted to the five-carbon molecule isopentenyl diphosphate via two phosphorylations and one decarboxylation.

80. Figure 16.16
Condensation reactions in the second stage of cholesterol synthesis.

81. Figure 16.17
Final stage of cholesterol synthesis: squalene to cholesterol. The conversion of lanosterol to cholesterol requires up to 20 steps.

82. All the carbons and hydrogens can have come from glucose.

83. Figure 16.18
Other products of isopentenyl pyrophosphate and cholesterol metabolism.

93. Figure 16.30
Summary of lipoprotein metabolism. Chylomicrons formed in intestinal cells carry dietary triacylglycerols to peripheral tissues, including muscle and adipose tissue. Chylomicron remnants deliver cholesteryl esters to the liver. VLDLs assemble in the liver and carry endogenous lipids to peripheral tissues. When VLDLs are degraded (via IDLs), they pick up cholesterol and cholesteryl esters from HDLs and become LDLs, which carry cholesterol to nonhepatic tissues. HDLs deliver cholesterol from peripheral tissues to the liver.

99. Additional liver enzyme