907471 properties-of-triacylglycerols
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907471 properties-of-triacylglycerols Presentation Transcript

  • 1. www.Examville.com Online practice tests, live classes, tutoring, study guides Q&A, premium content and more .
  • 2. Properties of Triacylglycerols
    • 1. Hydrolysis
    • triacylglycerols undergo stepwise enzymatic hydrolysis to finally liberate  free FA and glycerols
    • catalyzed by lipases
    • important for digestion of fat in the GIT and fat mobilization from the adipose tissues
  • 3.
    • 2. Saponification
    • hydrolysis by alkali to produce glycerol and soaps
    • Triacylglycerol + 3 NaOH  Glycerol + 3R-CooNa (soaps)
  • 4.
    • 3. Rancidity
    • term used to represent the deterioration of fats and oils resulting in an unpleasant taste
    • fats with UFA - more susceptible
    • occurs when fats are exposed to air, moisture, light and bacteria
  • 5. Metabolism of Lipids
    • Cholesterol, the most feared among the lipids, speaks:
    • “ Consumed through diet and produced in the body;
    • Participate in innumerable cellular functions;
    • Implicated in several health complications;
    • And blamed I am, for no fault of mine!”
  • 6. Cholesterol
    • Best known steroid because of its association with atherosclerosis
    • biochemically of significance because it is the precursor of a large # of equally important steroids
    • 1. Sex hormones 5. Cardiac glycosides
    • 2. Bile acids 6. Sterols
    • 3. Vit. D 7. Sitosterol
    • 4. Adrenal cortical hormones 8. Alkaloids
  • 7. Cholesterol in Perspective
    • Cholesterol has many roles in health and disease, both in its own right, and as a precursor of a variety of biologically, important substances.
    Cholesterol Gallstone Atherosclerotic plaque Lipoproteins Membranes Hormones Adrenal / gonads Bile Acids Acetate    U V light Vit. D
  • 8. ATHEROSCLEROSIS
    • Cholesterol penetrates into the T. interna, narrowing the vessels  decreasing blood supply  causing M I
    • cholesterol must be packaged as part of a LIPOPROTEIN in order to be transported in blood
    • its insolubility makes deposit troublesome especially in atherosclerotic plaques and gallstones
  • 9.
    • A high level of blood cholesterol, especially that contained in LDL is a risk in atherosclerotic  disease, much attention is being given to factors that lower cholesterol levels
    • a) DIET
      • substitute vegetable products for meat and dairy products
      • consume more Polyunsaturated fatty acids that saturated products
      • has a cholesterol lowering effects
  • 10.
    • b) Exercise
      •  HDL / LDL ratio which correlates negatively with Atherosclerosis
  • 11. KETOGENESIS AND THE ROLE OF KETONE BODIES IN ENERGY METABOLISM
    • acetone
    • Ketone bodies acetoacetate
    •  -hydroxybutyrate
    • acetone TRUE ketones
    • acetoacetate
    •  -hydroxybutyrate-does not possess a keto (C=0) group
  • 12.
    • Ketone bodies  are water soluble and energy yielding
    • liver - synthesis occur
    • mitochondrial matrix - where enzymes for ketone bodies synthesis are located
    • oxidation of FA Acetyl CoA
    • pyruvate
    • some AA precursor for ketone
    • bodies
  • 13. Reactions of Ketogenesis
    • 1. Two moles of acetyl CoA condense to form acetoacyl CoA
    • reaction catalyzed by Thiolase (an enzyme involved in the final step of  -oxidation)
    • hence acetoacetate synthesis is regarded as the reversal of thiolase reaction of fatty acid oxidation
  • 14.
    • 2. Acetoacyl CoA combines with another molecule of acetyl CoA to produce  -methyl glutaryl CoA (HMC CoA)
    • HMG CoA synthase, catalyzing the reaction, regulates the synthesis of ketone bodies
    • 3. HMG CoA lyase cleaves HMG CoA to produce acetoacetate and acetyl CoA
  • 15.
    • 4. Acetoacetate can undergo spontaneous decarboxylation to form acetone
    • 5. Acetoacetate can be reduced by a dehydrogenase to  -hydroxybutyrate
    • The C skeletons of some AA (ketogenic, leucine, lysine, phenylalanine, etc.) is degraded to acetoacetate or acyl CoA and to ketone bodies
  • 16. Energy yield from oxidation of ketone bodies
    • 1. Conversion of  -hydroxybutyrate to acetoacetate yields an NADH molecule, yields 3 ATP molecules (by electron transport and oxidative phosphorylation)
    • 2. Each mole of acetyl CoA that is formed yields 12 moles of ATP (via citric acid cycle, electron transport, and oxidative phosphorylation)
  • 17.
    • 3. The activation reactions require 1 mole of ATP.
    • 4. Therefore, oxidation of acetoacetate yields 24 moles (from 2 moles of acetyl CoA) - 1 mole
    • ATP (expended during activation) = 23 moles of ATP
    • oxidation of  -hydroxybutyrate yields
    • 3 moles of ATP (from one NADH molecule) + 24 moles of ATP (from 2 moles of acetyl CoA) - mole of ATP = 26 modes of ATP
  • 18. During prolonged starvation  ketone bodies are the major fuel source for the brain and other parts of the CNS
    • Ability of the brain to utilize FA for energy is limited
    • ketone bodies can meet 50-70% of the brain’s energy needs
    • In N o individuals  constant production of ketone bodies (liver)
      • concentration in the blood  1 mg/dL
      • excretion in urine is very low and undetectable by routine tests (Rothera’s test)
  • 19. Ketonemia  rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in the blood 
    • Ketonuria  follows ketonemia, secretion of ketone bodies in the urine
    • Ketonemia ketosis (overall picture)
    • Ketonuria 
    • (+) acetone breath associated
    • with starvation and severe
    • uncontrolled DM
  • 20. Glucagon  stimulates ketogenesis Insulin  inhibits
    • Ketogenic substances (promote ketone body formation)
    • 1. Fatty acids
    • 2. Amino acids (leucine, lysine, tyrosine)
    • Antiketogenic substances (inhibits ketone body formation)
    • 1. Glucose
    • 2. Glycerol
    • 3. Glucogenic AA (glycine, alanine, serine, glutamate)
  • 21.
    • Acetoacetate strong acids - when in 
    •  -hydroxybutyrate concentration in the blood
    • cause ACIDOSIS
    • Diabetic acidosis  dangerous  coma  death if untreated
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