HNF 462 1st Edition Lecture 21Outline of Last LectureI. Vitamins/Minerals Needed for Exercise and Sports PerformanceII. ExerciseIII. Ergogenic PotentialIV. Vitamin DV. MagnesiumVI. IronVII. Fluid and ElectrolytesVIII. ACSM GuidelinesIX. HyponatremiaOutline of Current LectureI. Sources of Vitamin KII. Digestion and Absorption of Vitamin KIII. Transport and Storage of Vitamin KIV. Excretion of Vitamin KV. Blood Clottinga. Importance of Vitamin Kb. Role of Calciumc. Formation of the ClotVI. Anticoagulantsa. Heparinb. Warfarinc. Calcium ChelatorsVII. Bone Mineralizationa. Osteocalcinb. Calcium ParadoxThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.VIII. Other Functions of Vitamin KCurrent Lecture: Vitamin K and Blood Clotting1. Sources of Vitamin Ka. Plants: phylloquinone (K1)b. Animals: menaquinone (K2)c. Synthesis of K2 via colonic bacteria—doesn’t produce enough to satisfy needs of the body2. Digestion and Absorption of Vitamin Ka. No digestion needed for absorptionb. Intestinal Absorptioni. Micelle absorption via passive diffusion in colon, incorporated into chylomicrons, and then transported to liverc. Cellular Absorptioni. Chylomicron remnants are absorbed into the liver, and then vitamin K is distributed into VLDL and HDL (follows cholesterol)d. Enhancers: fat with meale. Inhibitors: fat malabsorption diseases3. Transport and Storage of Vitamin Ka. Transport:i. In fasting states, vitamin K is distributed into VLDL LDL/HDLii. After a meal, will be transported via chylomicronsb. Storage:i. Very low storage in the liver because vitamin K has a very short half life and ismetabolized very quickly4. Excretion of Vitamin Ka. Degraded in the liver at a fast rate—involves oxidation of side chains and the attachment to a sugar residue to make more water-solubleb. Mainly excreted via feces, but some via urine5. Blood Clotting: bleeding would go unchecked without blood clottinga. Importance of Vitamin K: Vitamin K1 drives the gamma-carboxylation of protein-bound glutamic acid residues, which is required in order for calcium to be able to bindb. Role of Calcium: binds to the two carboxyl groups on protein-bound glutamic acid residues; when this occurs, clotting factors can bind to the cell surface of the injured tissuec. Formation of the Clot: Clotting factors (II, VII, IX, and X) bind to the injured cell surface; the binding occurs in a cascade-like manner. When clotting factors bind, thrombin activates fibrin, which forms the mesh network to bind plateletsi. Plasmin will inhibit clotting by breaking down fibrin mesh6. Anticoagulantsa. Heparin: activates antithrombin enzymes (blocks thrombin) so fibrin doesn’t formb. Warfarin: antagonizes vitamin K functionc. Calcium Chelators: clotting factors can’t bind to cell surface, so clotting process cannot occur7. Bone Mineralization: requires vitamin K2a. Osteocalcin: osteoclasts produce osteocalcin (contains gamma-carboxyl glutamate sowill bind to calcium). Osteocalcin recruits calcium from the blood and deposits it intothe bone tissue.i. With vitamin K deficiency, there is a decrease in gamma-carboxylation, so protein will lose ability to bind to calcium, and bone formation will be less effectiveb. Matrix Gla Protein (MGP): prevents calcification of blood vessels by extracting the calcium out of vessels and depositing it into bone tissuec. Calcium Paradox: a person needs calcium to build bone, but too much calcium (ex. supplementation) can increase risk of CVD8. Other Functions of Vitamin Ka. Apoptosisb. Signal transductionc. Growth
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