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209 Cards in this Set
- Front
- Back
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What are the types of lipids we ingest?
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90% trigacylglycerol, cholesterol, cholesterol esters, phospholipids, free fatty acids
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What is secreted in the saliva and activated in the stomach?
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Lingual lipase (acid stable lipase) activated at low PH
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What are the characteristics of gastric lipase?
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Released in stomach, activated in the duodenum at a neutral PH acts on triacylglycerol w/short and med length fatty acids
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Why do we emulsify fats?
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To increase surface area to volume ratio
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What do we use to emulsify fats?
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Bile salts, derived from cholesterol by the liver, concentrated in the gall bladder
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What is a bile salt made from?
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In gallbladder Cholesterol (hydrophobic) w/ glycine or taurine (both hydrophobic) producing glycocholate and taurocholat (polar molecules)
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What is bile acid?
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Precursor of bile salts made by liver, cholic acid, and chenodeoycholic acid
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What is the most important degrader of lipids in digestion?
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Pancreatic enzymes
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The presence of fat and protein in the duodenum cause the release of what?
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Secretin and cholecystokinin
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What is the function of seretin?
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To stimulate mucosal cells to secrete bicarbonate (HCO3 -) which neutralizes chyme in the duodenum
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What is the function of Cholecystokinin?
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Slowes down gastric emptying, releases bile, and stimulates pancreatic enzymes
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What converts HC03 + H+ go to CO2+ H2O?
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Carbonic anhydrase (is reversible)
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What breaks down triglycerides and into what?
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Pancreatic lipase into 2 fatty acids from C1 and C3 and 2-monoacylglycerol
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What catabolizes cholesterol esters?
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Pancreatic cholesterol esterase into cholesterol and one fatty acid
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What happens in the catabolism of phosphatidyl choline?
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Phospholipase A2 activated by trypsin releases a FFA then lysophospholipase releases another FFA and leaves a glycerylphosphoryl choline
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What makes up a Micelle and where?
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Bile salts and acids, FFA, phosphcholine, and 2-monoacyl glycerol in the lumen of the jejunum
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What happens to bile salts and acids after they are reabsorbed in the ileum?
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They are bound to albumin in the portal system and processed by the liver to be reused all but ~ 3-5% is reused
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How is fatty ACYL CoA produced?
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A FFA is combined with CoA and ATP with Fatty Acyl CoA Synthase (thiokinase) giving off AMP and PPi
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What does acyltransferase do?
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Converts two fatty acyl-CoA and one 2-monoacylglycerol to triacylglycerol + two CoA’s
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Where are micelles absorbed?
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In the jejunum mucosal cells
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What is the fate of long and short tailed fatty acids?
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Long FFA tails are converted to triglycerides using acyl transferase’s Short FFA tails enter the blood and bind to albumin
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What is the function of apoprotein B-48?
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They surround the hydrophobic TG’s, CE’s and phospholipids to form chylomicron’s for exocytosis
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Chylomicrons are made up of what and where?
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Phospholipids, TG’s, CE’s, and apoprotein’s within the jejunum mucosal cells
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How do chylomicrons enter circulation?
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Exocytosis in to the lymphatic system via intestinal lacteal which drain into the L subclavian vein
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Where are the triglycerols in chylomicrons used?
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Mainly muscle and fat, but also heart, lung, kidney and liver
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Lipoprotein lipase does what, where and how? What happens to the products?
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Made in fat cells and skeletal muscle it is bound to the luminal membranes of the circulatory system, it breaks down TG’s within chylomicrons to one glycerol (goes to liver)and three FFA (goes into cells via albumin)
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What is a chylomicron remnant and destination?
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It is CE’s, phospholipids, apoprotein and a little TG’s. It is taken up by the liver and converted into VLDL’s
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What do apolipoproteins do?
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Provide structure, cell recognition and assist in lipoprotein metabolism in lipoproteins
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In order for a chylomicron to mature it must do what?
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It must bump into lipoproteins and pick up apolipoproteins CII and E
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What activates lipoprotein lipase?
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apolipoproteins CII
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Apoprotein B100 is packaged in to VLDL where?
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Liver
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What are the characteristics of HDL, LDL, VLDL and their function?
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VLDL-donate FFA from liver to tissues in the form of FFA LDL-deliver cholesterol to tissues HDL- reservoir of ApoCII they are endocytosed by the liver and recycled
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What does HDL’s do with cholesterol in the blood?
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Trap it as cholesterol esters and transfer it to VLDL in exchange for TG and phospholipids in the liver
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What is the structure of acetic acid, propionic acid and butyric acid?
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2:0, 3:0, 4:0 respectively (common in milk fats)
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What is the structure if palmitic acid, steric acid, and oleic acid?
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16:0, 18:0, 18:1 (they are common in many lipids and in TG’s)
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What is the structure of linoleic acid, linolenic acid
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18:2 and 18:3 (essential fa’s because we cannot make them and they are precursors to arachidonic acids)
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What is the structure of arachidonic acid?
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20:4 (made from linoleate, is precursor of prostaglandins)
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Where does FA synthesis take place and what is the substrate?
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Liver and mammary glands. Carbon from glucose and AA’s
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What is the purpose of citrate translocase?
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To export citrate out of the mitochondrial matrix into the cytosol when there is high citrate levels (due to high atp inhibiting isocitrate dehydrogenase)
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What does acetyl CoA Carboxylase do and how is it regulated?
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It converts AcCoA to malonyl coA using HCO3- and ATP giving off ADP+Pi and H+. It is the key regulatory enzyme for fatty acid synthesis. It is inhibited by malonyl CoA, palmitoy CoA, and epinephrine. Accelerated by citrate and insulin
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What is biotin’s relation to acetyl CoA carboxylase?
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It is a co-factor that hold the activated CO2 for the reaction
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What happens to Malonyl CoA in FA synthesis?
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Malonyl trans acylase uses ACP to convert it into Malonyl ACP giving off CoA
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What does acetyl transacylase do?
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It converts acetyl CoA to acetyl ACP using ACP giving off CoA
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What does acyl-malonyl ACP condensing enzyme do?
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It combines acetyl ACP with Maylonyl ACP producing Acetoacetyl-ACP giving off ACP and CO2
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What are the two enzymes that add 2H+ and 2e- (from NADPH+H+) in fatty acid synthesis?
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_ - ketoacyl – ACP condensing reductase Enoyl-ACP-reductase
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What is the enzyme that removes H2O in fatty acid synthesis?
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3 – hydroxyacyl – ACP – dehydratase
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How many cycles can be run and what is produced?
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7, palmitoyl-ACP which is converted to palmitate
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What is fatty acid synthase?
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It is of all the enzymes if fatty acid synthesis in single enzyme complex
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What if proprional CoA goes through fatty acid synthase?
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It will yield FA’s with an odd # of Carbons
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What is the summary RXN of fatty acid synthase?
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8 AcCoA+7ATP+14 NADPH+7HCO3- = Palmitate + 8CoA+7ADP+14NADP+7CO2+7Pi
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What are the sources for NADPH?
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Pentose phosphate shunt and malic enzyme
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What does malic enzyme (NADP+-dependent malate dehydrogenase) do?
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It converts malate into pyruvate and produces CO2 and converts NADP to NADPH in the cytosol
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How do we make FA longer than 16 C?
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In mitochondria or microsomes on the ER enzymes add Malonyl CoA to COO- of acyl
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Why are Linoleic and linolenic acids essential?
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Because we cannot make them, our oxidases cannot make C=C past C9 and they have C=C beyond
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What is the typical FA arrangement in TG’s?
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C1-saturated, C2-unsaturated, C3-either
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Where does most DeNovo Synthesis of TG’s take place?
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In the liver (little occurs in adipose)
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What does glycerol-PO4 dehydrogenase do?
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It converts DHAP to Glycerol-PO4 using and NADH and giving off NAD
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What does glycerol kinase do?
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It converts glycerol to Glycerol-PO4 using ATP giving off ADP
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What is the simplest Phospholipid?
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Phosphatidate
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Diacylglycerol also acts as?
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A second messenger
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What are the caloric values of fat, protein, carbohydrate, and alcohol?
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Fat-9Kcal/g, protein 4kcal/g, carbs-4kcal/g, and alcohol-7Kcal/g
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What do effectors do?
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Produces a second messenger
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What does CAMP activate in Adipose catabolism?
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Hormone-sensitive lipase
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What do lipases do?
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Clip off FA’s
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What does adipose do with glycerol?
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Exports to blood (goes to liver)
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What happens to the FFA in adipose after lipase?
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Exported to blood and attached to albumin (consumed by liver or muscle)
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How are fatty acids use to make energy?
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_-oxidation
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What does carnitine acyl transferase do? Where? Why? What is its regulation?
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It carries Fatty Acyl across the inner mito. Mem. By replacing CoA with carnitine. It is inhibited by malonyl-CoA (enzyme in FA syn)
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What does carnitine acyl transferase II do?
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In the matrix it converts fatty-acyl-carnitine to fatty-acyl-CoA
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What is the 1st energy harvest in _-oxidation?
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Acyl-CoA dehydrogenase converts acyl-CoA (or acyln-2 CoA) to trans-_2-enoyl CoA and produces FADH2 from FAD
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What does enoyl-CoA hydratase do?
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Adds H2O and breaks a C=C double bond in trans-_2-enoyl CoA producing 3-hydroxyacyl CoA
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What is the 2nd energy harvest in _-oxidation?
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L-3-hydroxyacyl CoA dehaydrogenase converts 3-hydroxyacyl CoA to ketoacyl CoA and produces and NADH from NAD
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What does _-keto thiolase do?
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CoA is added to ketoacyl CoA, producing an acyln-2 CoA, and an AcCoA
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Where does Acyl-CoA have to be for _-oxidation?
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In the matrix of the mitochondria
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How many ATP does one palmatate produce?
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Net of 129 (131-2)
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What additional enzymes are needed for _-oxidation of an unsaturated FA?
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Isomerase and epimerase
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What is the cost (loss) in _-oxidation of an unsaturated FA?
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2 ATP per double bond (first energy harvest is skipped)
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What is the end result of _-oxidation on an odd chain length FA?
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The last cycle will produce AcCoA and Propiony CoA
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What happens to propionyl CoA?
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Converted to succinyl CoA and used in TCA
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What is a ketone body?
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A water soluble fatty acid
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What are the three ketones that AcCoA is converted to?
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Acetoacetate, -hydroxybutyrated, and acetone (non-metaboliziable)
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What tissues use ketones, which do not?
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Muscle (skeletal and cardiac) and renal, liver cannot use
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In the liver what does thiolase do?
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It combines two acetyl CoA’s into Acetoacetyl CoA giving off one CoA (in the liver)
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What is the rate limiting enzyme in ketone synthesis, what does it do?
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HMG-CoA synthase(only in liver) it converts acetoacetyl CoA to HMG-CoA by adding an Acetyl CoA giving off a CoA
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How do we get acetoacetate?
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HMG-CoA lyase removes a Acetyl-CoA from MHG-CoA
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What is acetoacetate converted into? How? Where?
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Acetone (spontaneous loss of CO2) and 3-OH-Butyrate (aka _-OH-butyrate) using 3-OH-butyrate dehydrogenase (_-OH-butarat-Dhase) and NADH to NAD in the blood
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How do we get rid of acetone?
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It cannot be metabolized so it is exhaled through the lungs
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What do we do with _-OH-butyrate in the muscle (in the matrix)?
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It is converted to acetoacetate using _-OH-butarat-Dhase producing a NADH from NAD
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What does thiophorase do? What tissue lacks this?
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It converts acetoacetate to acetoacetyl-CoA and succinyl CoA to succunate (not found in liver)
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What does thiolase do in the muscle?
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It adds a CoA to acetoacetyl-CoA to produce two Acetyl-CoA’s
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What is ketonemia, ketonuria?
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High blood ketones and high urine ketones respectively
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What organ controls cholesterol?
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Liver
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How does cholesterol leave the liver?
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Bile salts
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What is cholesterol used for?
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To make bile salt, steroids, and vitamin D
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Where do the C’s and e- come from for cholesterol synthesis?
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The carbons come from acetate and the electrons from NADPH
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Where in the cell does cholesterol synthesis take place?
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In the cytosol and ER
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What is the rate limiting rxn of cholesterol synthesis?
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HMG-CoA to mevalonic acid using HMG-CoA reductase using two NADPH producing NADP and giving off CoA. It is inhibited by cholesterol and irreversible
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What are lovastatin and metastatin?
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They are anti-cholesterol drugs that inhibit HMG-CoA reductase
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What is squalene?
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It is the first structure that is very hydrophobic and all that follow are too it uses NADPH and O2 giving off H2O and NADP, attached to a carrier protein
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How do we get rid of cholesterol? Why?
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In feces as free or bile acids, it cannot be used for energy
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What is the rate limiting enzyme of all steroid synthesis? What does it do?
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Desmolase it converts cholesterol to pregnenolone using NADPH and O2 giving off NADP
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How do steroids alter target cell behavior?
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By altering gene expression
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What are the characteristics steroids?
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They are lipid soluble, cannot be stored in vesicles, synthesized on demand (regulatory polypeptide hormone) and automatically leave endocrine cells
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What is used to make Eicosanoids, what are they?
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Arachidonate (20:4), intercellular signals ex. Prostaglandins, thromboxanes, and leukotrienes
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What are paracrines? What is there shape?
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They are compounds produced by one cell and alter the behavior of neighboring cells, they are very potent and can cause many different responses in body tissues. They have a bobby pin shape
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What do we use to make Arachidonic acid?
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Linoleic acid, we can also get arachidonic acid from diet
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What is inhibited by corticosteroids?
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Phospholipase A2
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How do we get arachidonic acid?
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Phospholipase A2, an enzyme that takes phospholipids and makes arachidonic acid giving of lysophospholipid
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What 5-lipoxygenase do?
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It is one of the two enzymes that breaks down arachidonic acid in eicosanoid synthasis
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What does cyclo-oxygenase do?
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It turns arachidonic acid in to prostaglandin G2
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What is prostaglandin synthase?
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Is the two enzyme step that converts arachidonic acid into PGH2 the enzymes are cyclo-oxygenase and peroidase
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What does tromboxane synthase do?
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It converts PGH2 to thromboxane A2
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What inhibits cyclo-oxygenase?
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Asprin and other NSAIDs
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What inhibits thromboxane synthase?
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Dipyridamole
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Why can AA be used in the TCA cycle?
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It contains C-C bonds
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What is an _-keto acid?
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An AA with the amine group removed
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Where do we get the AA’s for AA metabolism
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Skeletal muscle proteins
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How do we get rid of amine?
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In the kidneys through the urea cycle
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What is the amino acid pool?
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Total free AA in body from diet and degradation of the body. It is used to make new proteins, energy, and other products
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What is protein turnover?
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Where old proteins are replaced with new proteins during growth synthesis is greater than catabolism. Different proteins have different turnover rates some hours some months to years
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Why do we have turnover?
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It allows for adaptation and increased survival
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What stimulates protein turnover?
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Ubiquitin, and PEST sequences
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How much of our energy comes from protein?
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20%
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How much protein do we need daily?
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50-70g, American diet has ~ 100g
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What is kwashiorkor disease?
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Decrease in essential AA’s because of low protein intake
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How do we get pepsin and what does it do?
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Pepsinogen reacts with HCl both from the stomach and breaks down proteins in the stomach
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What is used to break down protein in the duodenum?
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Pancreatic enzymes:trypsinogen, chymotrypsinogen, proelastase, and procarboxypeptidase
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What activates the pancreatic enzymes?
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On the luminal membrane of the mucosal cells enteropeptidase converts the pancreatic enzymes to trypsin, chymotrypsin, elastase, and carboxypeptidase
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What is used to break down protein in the Small intestine?
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Aminopepstidase
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How do AA get into the cell?
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In single AA or dipeptides through the luminal wall
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What is the length of AA when they leave the mucosal cells?
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Single AA into blood
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How do AA get inside the destination cell?
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They are transported by AA pumps in to the cell using ATP
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What are the two ways to remove amine groups?
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Transamination and oxidative deamination(in the kidney)
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What are aminotransferases?
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AKA transaminases-a group of specific enzymes that work for a single of a few AA. (lysine and threonine are the exceptions)
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What is the amine acceptor for aminotransferases? What does it become?
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_-ketoglutarate
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What is GPT, what does it do? What direction does run and where?
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Glutamate-pyruvate transaminase, it converts alanine to pyruvate transferring the amine to _-KG making glutamate in the liver, in the muscle it runs in the opposite direction
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What is GOT, what does it do?
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Glut-OAA transaminase, it converts glutamate to _-KG and transfers the amine to OAA forming aspartate
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What else is aspartate need for?
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Urea synthesis
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What is glutamate dehydrogenase? What does it do? How is it regulated?
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The first step in oxidative deamination, It converts glutamate to _-KG and NH3 adding H to NAD or NADP it is regulated in this direction by the presence of ADP and GDP and is slowed (inhibited) by ATP and GTP
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What do we do with D-amino acid?
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We use D-AA-oxidase to convert it to _-Keto acid and NH4+ hydrolyzing FAD
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What are the two direct deaminations?
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Serine dhase and threonine dhase making PYV and keto-butyrate respectively along with an NH4+
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How is urea produced? Where?
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Arginine added w/H2O using arginase produces urea and ornithine in the liver only
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What happens to ornithine?
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It is added to carbamoyl phosphate with ornithine transcarbamylase giving off Pi producing Citrulline (start of the next urea cycle)
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How do we get argininosuccinate?
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Citrulline is added to aspartate using ATP and argininosuccinate synthetase producing Argininosuccinate giving off AMP and PPi (aspartate is the source of the 2nd amine group in urea)
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What does argininosuccinase do?
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Converts argininosuccinate to arginine and fumarate
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What is the rate limiting enzyme for urea formation? What does it do?
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Carbamamoyl-phosphate synthase it adds CO2, NH4+, H2O, and 2 ATP to make Carbamoyl-phosphate giving off 2ADP, Pi, and 3H+
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Where is most of the AA’s coming from for the urea cycle? In what form?
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Muscle proteins, alanine
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What is glutamine? What does it do for in the urea cycle?
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Glutamate with another amine using glutamine synthase and ATP, transports and dumps NH4+ in the kidney to become glutamate using glutaminase
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What is a ketogenic AA?, what are their names?
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They into the glycolsis/tca at AcCoA can be used for ketone synthesis (but not gulconeogenesis), Leucine and Lisine
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What are glucogenic AA?
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Most AA’s they can enter into the TCA cycle and can be used for gluconeogenesis
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Which AA are mixed ketogenic and glucogenic
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Phenylalanine, isolucine, tyrosine, and tryptophan (PITT (mnemonic))
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What are the entry points for carbons in AA catabolism?
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Pyruvate, AcCoA, _-KG, succinyl CoA, Fumarate, and OAA
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What is the key AA that enters at pyruvate?
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Alanine
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What are the AA that enter at AcCoA? Can they be used for gluconeogenisis?
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PITT, leusine, and lysine, No
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Which key AA’s enter at _-KG?
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Glutamate and glutamine
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What key AA enters at OAA?
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Aspartate
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What is significant about PVT TIM HALL?
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They are the ten essential AA (mnemonic)
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What is methionine converted to?
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SAM a methyl donor in the one carbon pool
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What is the one carbon pool?
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It is used to synthesize various compounds (folic acid is another carrier for the pool in the form of TAF
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What are porphyrins? What are they made from?
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Web like structures that bind iron allowing participation in redox Rx’s made from glycine and succinyl CoA Ex- hemoglobin, myoglobin, and cytochromes
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How is HEME broken down?
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It is converted into biliverdin and then bilirubin using hemioxygenase and biliverdin reductase respectively. An NADPH is used in each rx and NADP is given off. It is then bound to albumin in the blood and transported to the liver to be secreted in bile
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What is jaundice? What are the four types?
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When bilirubin accumulates in blood, hemolytic, obstructive, hepatocellular, undeveloped liver in premature newborns
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What is creatine made from?
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Glycine and arginine. It is broken down into creatinine (if high in urine=kidney malfunction
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What is histamine?
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It is histidine with the COO- removed (regulates H+ secretion by stomach)
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What is serotonin?
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Made from tryptophan is and neurotransmitter in the CNS and Gut
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What are catecholamines?
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They are made from tyrosine. They are neurotransmitters in the CNS and autonomic nervous system (dopamine, norepinephrine and epinephrine) they are broken down by monoamine oxidase and catecholamine-O-methyltransferase
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What is melanin?
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Made from tyrosine. Provides pigmentation (when low or absent=albinisim)
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What are the two main polypeptide hormones in metabolism? What do they do?
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Insulin and glucagon. They coordinate the actions of adipose, liver, muscle, and brain
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What is insulin? What does it do?
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An anabolic hormone, it promotes the synthesis of glycogen, triglycerides, and protein, it is produced by the pancreatic _-cells in the islets of langerhans (present in the fed state)
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What stimulates insulin? Which is strongest?
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An increase of glucose, AA, secretin, and Glucagon. Glucose
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What inhibits insulin secretion?
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Epinephrine
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What does insulin cause the liver, muscle, and adipose to do when carbohydrates are present?
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In the liver it decreases gluconeogenesis and glycongenolysis and increases glycogen synthesis Muscle- increases glycogen synthesis and glucose uptake Adipose-increases glucose uptake
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Why does the liver not increase glucose uptake when insulin is present?
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It has insulin independent glucose transporters
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What is the function of insulin when lipids are present?
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Adipose-decreases triglyceride catabolism and increases TG synthesis Blood-increase lipoprotein lipase
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What is the effect of insulin when proteins are present?
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All cells increase AA uptake and protein synthesis
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Why can insulin produce so many different effects?
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By binding to specific receptors it causes the phophorylation of certain enzymes in target cells
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What causes glucose transporters to increase in the cell membranes, How?
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Insulin binding to insulin receptors cause stored glucose transporters to be exocytosis into the cell membrane, the opposite happens when insulin is not present
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What types of tissues have insulin independent transporters?
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Brain/neurons, hepatocytes, erythrocytes, intestinal mucosa, renal tubules, cornea
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What is insulin receptor down regulation?
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It occurs when insulin is present and the bound receptor is endocytosed and degraded with lysosomes (many of the receptors are recycled) if it occurs over a long period the #of membrane receptors is decreased can eventually lead to type II diabetes
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What can happen with long term exposure to insulin?
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It can cause long term effects like increased synthesis of glucokinase, PFK, and pyruvate kinase (changes in gene expression)
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What is the major effect of glucogon? What stimulates it? What inhibits it?
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To stimulate glycogenolysis and gluconeogenesis in the liver, stimulated by decreased blood glucose, increased in AA w/out carbs, increase in epinephrine. Inhibited by blood glucose
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What is post-prandial hypoglycemia?
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When there is a lot of protein but no carbs (from a meal) causeing a drop in glucose levels
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What does glucagon cause the liver to do in the presence of each of the following; carbs, lipids, and proteins?
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Carbs- increase in glycogenolysis and gluconeogenesis Lipids-increase FA _-oxidation and ketone synthesis Proteins-increase AA uptake for gluconeogenesis
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In the fed state how much of the carbs are taken up by the liver? How much goes to pentosphospate shunt?
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60%, 5-10%
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How long do you have to be unfed for the brain to begin to use ketones?
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10-14 days
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What is diabetes mellitus? What are the forms?
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It refers to sweet urine and is characterized by excessive urine production. Insulin dependent (type I) and Insulin independent (type II)
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What are the characteristics of type I diabetes mellitus?
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20% of all diabetes, absolute insulin deficiency due to autoimmune destruction of _-cells can be caused by genetics or virus, require insulin injections to prevent fatal ketoacidosis. Symtomes are polyuria, polydipsia, polyphagia, fatigue, weight loss, and weakness. Causes body to behave in fasting state even when fed. There is more glucose than can be reabsorbed so it excreted in the urine, causes increased VLDLS (hypertriglyceridemia)
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What are the characteristic of type II diabetes mellitus?
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Most common form of diabetes, develops gradually, _-cells function normally, genetic predisposition, caused by obesity and alchoholism, receptor downregulation is cellular cause, weight reduction and dietary changes help more than insulin
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What percent of the body is mineral? What are their main functions?
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7%, structure, cofactors, acid/base balance, nerve conduction, muscle excitation, signaling
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What are the functions of Na+, K+, and Cl-?
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They are the major inorganic ions in the body, NA is concentrated in extracellular fluid, and K in concentrated in intracellular fluid, Cl is the anion of the two
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What are the most abundant minerals in the body and there uses?
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Ca++, PO4-3 much in crystallized form in bone and teeth, Ca is a 2nd messenger and regulates threshold for AP generation, phosphate is involved in metabolism in many places
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What is osteoporosis?
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Can happen when dietary calcium is not processed appropriately
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What is the function of iron in the body? What can deficiency lead to?
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It is found in hemoglobin, myoglobin, and cytochromes. It is transported by transferring in the blood and can be stored bound to ferritin. Iron deficiency anemia. Excess (hemochromatosis) can damage the liver, heart, pancreas, and spleen
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What is the function of Mg++?
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Stabilizes ATP, can depress CNS, and slow heart rate, and cause cardiac arrest
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What is the function of sulfur?
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It is in CoA and connective tissue most comes for diet
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How is iodine used in the body?
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It is concentrated in thyroid and used to make thyroid hormones, deficiency can cause goiter, we get most from iodized salt
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What is the function of fluoride?
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Not essential, less soluble and makes stronger teeth and bones
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What are vitamins and their major characteristics?
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“vital amine” serve as cofactors in many enzymatic reactions
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What are the water soluble vitamins?
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C (ascorbic acid), B1 (thiamine), B2 (riboflavin), B3 (niacin), Biotin, panthothenic acid, folic acid, B12 (cobalamin), B6 (pyridoxine)
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What are the fat soluble vitamins?
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A (retinol, _-carotene), D (cholecalciferol and ergocalciferol), E (_-tocopherol) and K (phylloquinone and menaquinone)
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What are the general characteristics of water soluble vitamins?
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Many of them are precursors of cofactors, they are non-toxic and are not stored, excreted in urine
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What is the active form of thiamine, what does it do, what happens if deficient?
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Thiamine pyrophosphate TTP, it is a cofactor in decarboxylation of keto acids and transketolose. If deficient can cause beriberi and wernicke-korsakoff syndrome
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What is the active form of riboflavin, what does it do, what happens if deficient?
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FMN and FAD they are activated with an ATP (to make FMN) then another ATP giving off a AMP to make FAD. they are involved in redox rx. Deficiency is rarely seen alone (vegans beware - sun degrades in leafy vegetables)
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What are the active forms of niacin, what are their functions, what happens if it is deficient?
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NAD+ and NADP+ they serve as coenzyme e- acceptors in redox rx for energy production, if it is deficient it is called pellagra
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What does biotin do, what happens if it is deficient?
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It is a coenzyme in carboxylation rx’s it holds the CO2 until it is bound to the substrate deficiency is rare
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What is the active form of pantothenate, what is its function?
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It is a component of CoEnzymeA along with ADP
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What is the active form of folate, what is its function, what happens if it is deficient?
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Tetrahydrofolate is made from folate using dihydrofolate reductase and two NADPH, it is used to make purine’s, AA, thymidine (sulfonamides limit bacterial growth by stopping dihydrofolate synthasis)
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What can produce a deficiency of cobalamin?
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A lack of intrinsic factor (which is made in the stomach and binds to B12 to get it out of the gut in the ileum into the blood. B12_ is a cofactor in the production of menthionine and the metabolism of methylmalonyl CoA
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What is the active form of pyridoxine, what is its function?
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Pyridoxal phosphate, it is a cofactor in many reactions of AA metabolism
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