I Thiamin A History Discovered when Japanese sailors whose diet consisted of polished rice were suffering from neurological disease later known as Beri Beri a Food meat especially pork legumes whole and enriched brans breads and B Sources cereals C Stability b Supplements thiamine hydrochloride thiamine monocitrate a Water soluble which means it is excreted in the kidneys b Denatures in alkaline mediums i e cooking in baking soda c Denatures in heat i e overcooking vegetables D Digestion Absorption Transport Storage a Digestion Thiamin is digested in both its free form and its coenzyme form Phosphorlyated thiamin is hydrolyzed by phosphatases to form free thiamin so that it can move into the enterocytes b Absorption i Enterocytes thiamin can be phosphorylated here into its coenzyme form and transported via active transport 1 High concentrations passive diffusion 2 Low concentrations active transport via sodium dependent channels ii Brush boarder thiamin transports across the basolateral membrane via a thiamin H antiport system Ethanol interferes with this transportation 1 Anti absorption factors a Thiminases enzymes found in raw fish that cleave the middle bond of thiamin so that it cannot be absorbed in the body b Polyphenols thermostable organic substance found in coffee tea brussel sprouts blueberries and red cabbage Inactivates thiamin by oxyreductive processes facilitated by Ca2 and Mg2 It can be prevented by citric acid or vitamin C iii Blood 1 Red Blood Cells 90 transported inside RBCs 2 Albumin 10 bound to albumin iv Tissues once distributed to the tissues thiamin can be phosphorylated to its coenzyme form so that it can be used by the cells 1 Thiamin thiamin pyrophosphokinase TPP 2 TPP TDP ATP phosphoryl transferase TTP E Coenzyme Roles a Pyruvate dehydrogenase complex also uses B5 Niacin Riboflavin b Ketoglutarate dehydrogenase complex also uses B5 and Niacin c Branched chain ketoacid dehydrogenase d HMP shunt transketolase produces NADPH and cholosterol for FA synth e Synaptic function TPP released by synaptic cleft after action potential reaches think about biochem mad hatter s disease F Assessment a Urinary b Blood G Deficiency a Beri Beri i Wet enlarged heart edema ii Dry anorexia nausea neurological damage vomiting iii Infant result of deficiency of mother during breast feeding Causes heart failure syanosis dyspenia and aphonia b Wernicke s Encephalopathy often seen with alcoholics causes neurological symptoms like atoxia and delirium i Associated with Korsakoff s psychosis 1 Chronic alcoholism polyneuritis inability to acquire new information confabulation c Prevention avoid polished grains cooking too much or in alkali solutions denatures anti absorption foods avoid high carbohydrate intake Riboflavin II A Sources enriched breads and cereals legumes green vegetables dairy products meat eggs B Forms FAD FMN riboflavin C Digestion a Mouth eaten in all forms b Stomach proteases and HCl degrade coenzyme forms to free vitamin form so that it can be absorbed by the enterocytes a Blood transported by proteins most commonly albumin b Tissues converted into coenzyme form so it can be used by the cells D Absorption normal E Coenzyme Functions a FAD i Pyruvate dehydrogenase B5 niacin riboflavin thiamin ii Succinate succinate dehydrogenase fumarate iii Ketoglutarate succinyl CoA ketoglutarate dehydrogenase complex also uses B5 TPP and Niacin iv Fatty Acyl CoA fatty acyl CoA dehydrogenase Enoyl CoA v Needed for folate B6 and GSSG antioxidant function vi Neurotransmitter function monoamine oxidase vii Needed for the synthesis of niacin from tryptophan viii Drops off electrons to the ETC in the form of hydrogens to produce 2ATP b FMN i Found in the ETC cycle in complex I F Assessment G Deficiency a Erythrocyte glutathione reductase b Urine a Ariboflavinosis b Fatigue weakness anemia glossitis peripheral nerve function dermatitis chleiosis stomatitis H Those at risk heart disease alcoholics cancers thyroid disease diabetes III Niacin A Sources fish enriched cereals and breads meats mostly animal products B Forms NAD NADP niacin C Digestion a Mouth eaten in all forms b Stomach proteases and HCl degrade coenzyme to free vitamin form so that it can be absorbed by the enterocytes D Absorption normal E Coenzyme functions a NAD i Glycolysis glyceraldehyde 3 phosphate glyceraldehyde 3 phosphate dehydrogenase 1 3 bisphosphoglycerate Intermediate pyruvate dehydrogenase thiamin riboflavin and B5 ii iii Krebs 1 Ketoglutarate succinyl CoA ketoglutarate dehydrogenase complex also uses B5 TPP and Riboflavin isocitrate isocitrate dehydrogenase ketoglutarate 2 3 Malate malate dehydrogenase OAA iv Beta oxidation v oxidation of ethanol 1 hydroxyl acyl CoA dehdyrogenase 1 alcohol dehydrogenase and acetaldehyde dehydrogenase found in the ETC NADH dehydrogenase complex I vi vii DNA NAD donates adenosine diphosphate ribose and attaches it to a cyclic ADP ribose b NADP i HMP shunt ii FA synthesis and cholesterol synthesis iii Folate metabolism iv Alcohol metabolism MEOS F Assessment normal G Deficiency a Pellagra i Dementia ii Dermatitis iii Death iv Diarrhea H Those at risk I Toxicity a Alcoholics malabsorptive disorders medications isolazid Hartnup s Disease a High pharmacological doses nicotinic acid niacor advicor i Vasodilation causing flushing itching and headaches ii Glucose intolerance iii GI discomfort heart burn nausea iv Hepatic toxicity liver failure jaundice IV Pentathenic Acid B5 A Sources everywhere B Forms Pentothenoate pentothenol C Digestion then form pantothenic acid D Absorption a Intestine a Mouth eaten in all forms 85 of the time its ingested as coenzyme A which can i High concentrations passive diffusion ii Low concentrations multivitamin carrier biotin b Portal blood i Extracellular free in plasma ii Intracellular RBC c Tissues inside the cell pantothenic acid is converted to CoA i Pantothenate 4 phosphopantothenate pantethiene CoA E Coenzyme Functions a Thioester formation in various metabolic reactions i Intermediate ii Krebs cycle 1 Pyruvate CoA Acetyl CoA CO2 1 ketoglutarate succinyl CoA ketoglutarate complex 2 OAA CoA citrate citrate synthase iii FA synthesis 1 Acetyl CoA Malonyl CoA 2 Fatty acid synthase complex iv Cholesterol synthesis 1 Acetyl CoA Acetoacetyl CoA HMG CoA b Heme formation c Acectylation i Succinyl CoA glycine heme i Acetylcholine neurotransmitter F Assessment normal G Deficiency burning feet vomiting fatigue weakness H At risk alcoholics diabetes
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