1. Lipid Metabolism Part 1 Dr. Basima S.Ahmed Jaff Assist.Proffsor
PhD. Clinical Biochemistry

4. 1-Pancreatic secretion enzymes degrade dietary lipids in the small intestine is hormonally controlled .
2-Cells in the mucosa of lower duodenum and jejunum produce peptide hormone, cholecystokinin (CCK), in response to the presence of lipids and partially digested proteins entering these regions of the upper small intestine. CCK acts on the gallbladder (causing it to contract and Release bile. decreases gastric
Motility.
3- secretin, in response to the low pH of the chyme entering the intestine. the pancreas andthe liver to release a solution rich in bicarbonate .

7. Lipid malabsorption
Lipid malabsorption, caused by disturbances in lipid digestion and/or absorption disturbances can result from several conditions, including Cystic Fibrosis (causing poor digestion)

10. TG Biosynthesis

12. FATTY ACID OXIDATION
Sources of fatty acids
(a) Dietary sourcesFatty acids formed from the digestion of dietary lipids are carried to liver. From the liver, they are transported to cell in bound form with albumin.
(b) Endogenous sources As mentioned above, free fatty acids formed from body TG are used for energy production. Though the plasma free fatty acid level is lower than blood glucose level they are rapidly utilized by peripheral tissues. The plasma free fatty acid (FFA) has life of 3-4 minutes.
SiteFatty acid oxidation occurs in the mitochondria of all types of cells like liver, heart, adipose tissue, kidney, lung, skeletal muscle and some extent in brain.

14. 1. Oxidation by FAD
2. Hydration
3. Oxidation by NAD
4-cleavage

16. Regulation of β-oxidation
• Rate limiting step in the β-oxidation
formation of acyl-carnitine which is catalyzed by carnitine-acyl transferase-I (CAT-I). CAT-I is anallosteric enzyme. Malonyl-CoAis an inhibitor of
CAT-I.
– In well-fed state due to increased level of insulin,concentration of malonyl-CoA increases which inhibits CAT-I and leads to decrease in fatty acidoxidation.
– In starvation, due to increased level of glucagon concentration of malonyl-CoA decreases and
stimulates the fatty-acid oxidation

17. β-oxidation of a Fatty Acid with an Odd Number of Carbon Atoms;
final β-oxidation cycle, of odd carbon fatty acids a
3 carbon fragment propionyl CoA is formed
rather than 2 carbon fragment acetyl-CoA.
• Propionyl-CoA is converted to succinyl-CoA a constituent of citric acid cycle.
• Propionyl-CoA is carboxylated at the expense of an ATP to yield the D-methylmalonyl-CoA; catalyzed by propionyl-CoA carboxylase, a biotin enzyme.

19. Pathway of cholesterol biosynthesis

21. THANKS/Dr.Basema