907471 properties-of-triacylglycerols


Published on

  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

907471 properties-of-triacylglycerols

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