Water Soluble Vitamins - B Vitamins, Functions PDF

Water Soluble Vitamins blood formation helping an enzyme do a function Fig. 9.1, p. 323 ...

Water Soluble Vitamins blood formation helping an enzyme do a function Fig. 9.1, p. 323  Thiamin (vitamin B1) Structure: pyrimidine + thiazole Coenzyme form: ________ TDP & thiamin diphosphate _________ TPP thiamin pyrophosphate Sources: yeast, pork, legumes, whole and enriched grains, sunflower seeds through processing it loses the vitamin but it breaks with alkaline not stable whole = has vit. B1 solutions, light/heat enriched = all have Vit. B1 Fig. 9.8, p. 338  Functions of B1 1. Energy Transformation TDP (TPP) functions as coenzyme in catalyzing decarboxylation of pyruvate and α-ketoglutarate B1, B2, B3 and B5 pyruvate to acetyl CoA (pyruvate dehydrogenase complex) α-ketoglutarate to succinyl CoA Both of these reactions are important for release of energy from food in formation of ATP 2. NADPH and pentose TDP needed for _____________________ transketolase reaction which forms pentoses Pentoses used in synthesis of nucleic acids for RNA/DNA 3. Nerve Conduction when there is a nerve stimulation, there is a release of Thiamin B1 Role in Kreb’s Cycle Fig. 9.9, p. 341 PDC NUTR 302 PDC Fig. 9.10, p. 342 NUTR 302  if consuming white rice before B1 was broken down but not it is enriched most products B1 Deficiency only happens when you are extremely deficiency Beriberi (means “I can’t, I can’t” – true deficiency syndrome) Dry: muscle weakness and wasting Wet: heart failure with edema Infantile med.main.teikyo-u.ac.jp/.../ image002.jpg http:// www.nutriweb.org.br/ www.macmed.ttuhsc.edu/ n0201/beriberi.jpg Shen/lecture/Nutrition- Pathology-vitamins-photos-  1.1-1.2 mg/day 100-500 mg/day for this disease B1 Deficiency see this is hospitals Wernicke-Korsakoff syndrome Thiamin deficiency associated with ________________ alcoholism Decreased intake Increased requirement with liver damage May decrease absorption At risk: _____________________ elderly Increased need with elevated metabolism (i.e. fever, hyperthyroidism) increase metabolism need more thiamin because it is involved with energy production  B1 Toxicity Supplementation is quite safe No UL Large doses may be helpful with _________________ MSUD (maple syrup urine disease) Extra Credit: What is MSUD and why do large doses of B1 help this condition?  B1 Assessment RBC HMP shunt enzyme (6C -> 5C) Erythrocyte Transketolase Activity Most sensitive measure, if elevated after thiamin addition, indicates deficiency no enzyme activity = low or no thiamin  Riboflavin (vitamin B2) Structure: Flavin molecule + ribitol Coenzyme forms: FMN, FAD Sources: __________, milk dairy products, eggs, meat, legumes, enriched grains in the US Sensitive to ________ UV light B2 structure & coenzyme forms Fig. 9.14, p. 347  B2 Functions produce 2 ATP 1. Energy transformation FADH2 is riboflavin ETS, pyruvate and succinate dehydrogenase NADH = ? 2. Purine catabolism (xanthine oxidase) when getting rid of these compounds, you need B2 to excrete xanthine oxidase 3. Vitamin ______ B6 activation 4. ________ folate (B9) activation donates H to free radical 5. Reduction of ________________ glutathione 6. Niacin synthesis  B2 Deficiency Symptoms: __________________ Cheilosis – cracking of lips Angular stomatitis – cracking of corner of mouth inflammation ________________ glossitis – inflammation of tongue, magenta tongue www.emedicine.com/.../ www.usc.edu/.../opath/Images/KL/ 2031angularcheilitis.jpg KL075tn.gif www.infocompu.com/.../images/glositis_s.jpg  B2 Deficiency At risk, low intake Elderly Some cancers cancer medication can interfere with the B2 absorption ___________________ alcoholism Elevated metabolism energy reduction  B2 Toxicity: None Reported No UL B2 Assessment: Red Cell Glutathione Reductase FAD important in reducing glutathione  Niacin (vitamin B3) Structure: Nicotinic acid, nicotinamide Coenzyme forms: NAD, NADH, NADP, NADPH Sources: meat, fish, poultry Food: MFP, enriched grains, legumes Synthesis from _________________________ tryptophan not very efficient Niacin Equivalents calculated to give better indication of intake 60 mg try = 1 mg niacin Fig. 9.17, p. 352 Niacin synthesis from tryptophan Fig. 9.19, p. 354 What two vitamins and what mineral are long and not efficient required for this process to occur? B2, B6, Fe need this to synthesize niacin even if there is typtophan available NAD & NADP Fig. 9.18, p. 353  B3 Functions 1. Energy Transformation through NADH ETS, glycolysis, pyruvate dehydrogenase, Krebs cycle, B-oxidation 2. HMP shunt (NADP) 3. ______________________________ fatty acid synthesis (NADPH) 4. Conversion of vitamin C, glutathione, folate to reduced states 5. Lower __________________ cholesterol 500 mg Nicotinic acid in large doses may decrease VLDL and LDL and increase HDL red face, flushes, heat Side effects: release of histamine (flushing), liver injury, competition with urate for excretion, itching, elevated glucose B3’s role in energy transformation  B3 Deficiency skin burn Pellagra (4 Ds): Dermatitis Diarrhea Dementia Death mark.asci.ncsu.edu/.../NutritionSlides/33.jpg  B3 Deficiency At risk: tubercurosis medication ___________________ isoniazid users (reduce niacin synthesis) Low intake (alcoholics) elevated metabolism Low pro/low tryptophan diet (corn)  B3 Toxicity: like cholesterol treatment Nicotinic acid side effects: release of histamine (flushing), liver injury, competition with urate for excretion, itching, elevated glucose Niacinamide--little known side effects B3 Assessment: Ratio of N’methly-2-pyridone-5-carboxamide to N’methly nicotinamide (urinary metab of nicotinamide)  Pantothenic Acid B5 Structure: usually part of coenzyme A Fig. 9.22, p. 359 An integral part of ____________________ coenzyme A Sources: AI : 5 mg/day Found widely distributed (pantos means everywhere) Liver, meats, egg yolk, whole grains, mushrooms, broccoli, avocados no RDA for this vitamin Structure of coenzyme A Fig. 9.23, p. 361  B5 Functions Acyl group donor as part of coenzyme A Involved in: ________________ Kreb's cycle (acetyl CoA, succinyl CoA) Gluconeogenesis (succinyl CoA) Fatty acid oxidation (fatty acyl CoA, acetyl CoA) Pyruvate and alpha-ketogulatarate decarboxylase Part of ________________________for acyl carrier protein fatty acid synthesis  B5 Deficiency Only seen in severe malnutrition because vitamin spread widely Symptoms: Burning feet, vomiting, fatigue, weakness Populations at risk: Alcoholics (low intake) __________________________ diabetes mellitus (increased excretion) Inflammatory bowel disease (absorption problems) in general compounds we can't really absorb  B5 Toxicity: can happen with everything if consumed in excess Not considered a problem, may cause gastrointestinal distress and diarrhea No UL not enough reports B5 Assessment: Plasma pantothenic acid Urinary pantothenic acid symptoms are vague and can't really tell if they have deficiency The role of B5 in Kreb’s Fig. 9.9, p. 341  Once called vitamin H Biotin B7 referring to haut in German meaning “skin” Structure: Fig. 9.24, p. 364 Sources: Liver, soybeans, egg yolk, cereals, legumes, nuts Also produced by bacteria in colon Absorption: A glycoprotein in raw egg whites called ______________ avidin tightly binds to biotin and can prevent absorption, often called _______________________________ "egg white injury" caused biotin deficiency avidin = most strong covalent bond in nature -> don't have ability to absorb b7  B7 Functions Functions as a Carboxyl group carrier in: Carboxylation reactions _______________________ transcarboxylation involved in fermentation _______________________ decarboxylation involved in fermentation Fig. 9.28, p. 367  B7 Deficiency Populations at risk: Most often caused by ingestion of _________________ raw eggs GI disorders (decreased absorption) Alcoholics (decreased intake) Pregnant women they have higher needs of biotin Symptoms: (lack of appetite) dermatitis, _____________, anorexia depression, hallucination, _______________ alopecia  B7 Toxicity: No known toxic effects in humans No UL no RDA, only AI = 30 microgram/day B7 Assessment: Blood/serum/plasma biotin Urinary biotin excretion  Folate (Vitamin B9 – Folic Acid) Structure: Active forms: Coenzyme tetrahydrofolate In food often as polyglutamate form attached to it most active form in the body Fig. 9.33, p. 371  Folate Sources: Yeast, mushrooms, green vegetables, legumes, liver, fortified foods, citrus fruits – especially strawberries and oranges when cooking, the amount of vitamin is less Easily destroyed due to processing Present mainly as polyglutamate that must be hydrolyzed by _________________ conjugase prior to absorption releases the vit from the polyglut. Inhibitors of conjugase: _________________________, low zinc status alcohol, inhibitors in foods legumes, cabbage, oranges  Folate Functions Functions in single carbon transfers in: Nucleic Acid Synthesis dUMP converted to dTMP (required for DNA synthesis) Carbon donator in ____________________________ purine synthesis Essential for _________________________ cell division to start synthesis of RNA and DNA Amino Acid Metabolism _______________________ homocysteine converted to methionine Glycine converted to serine Interconversions of coenzyme forms of THF Fig. 9.34, p. 374 Resynthesis of methionine NEED TO KNOW AND UNDERSTAND from homocysteine convert back to Fig. 9.37, p. 378 get metyl group from this add to: decrease levels after it loses this is trapped and gets methyl, it untrapped by cobalamin becomes this need cobalamin to remake methylcobalamin for process in right -> using B12 free THF don't want high levels high chances of CVD active form of folate add methyl group to homocysteine to get the vit. B6 enzyme working to convert back dependent important for brain to methionine in egg yolk  Folate Deficiency Megaloblastic Anemia _____________________________________________ immature red blood cells Due to decreased DNA synthesis and improper cell division along with continued RNA production  important for cell division Genesis and maturation of the RBC (left) & RBCs characteristics of microcytic & megaloblastic anemias (right) Fig. 9.38, p. 382 precursor of RBCs sometimes this process doesn't happen low or pale color if you don't have proper heme mature proper RBC no nucleus they haven't matured  Folate Deficiency: Toxicity: At Risk: Supplementation may mask Pregnancy neural tube defects _______ B12 deficiency while Birth defects highly permitting neurological correlated with folate damage caused by B12 deficiency deficiency cause ____________________ alcoholism Megadoses may induce Elderly no proper diet seizures in epileptics Phenytoin users UL: 1 mg/d from (anticonvulsant) supplements and fortified less folate absorption foods folic acid Extra credit: What is phenytoin and 1000 microgram or 1 miligram why can it cause folate deficiency?  Folate Interactions: Assessment: Vitamin B12: Methyl- Plasma, serum, or RBC folate trap folate Without B12, methyl group Deoxyuridine suppression in N5 methyl THF cannot be test (from dUMP to dTMP) removed get blood, RBCs, look at culture for nucleic acid formation Plasma homocysteine Zinc: concentrations Folate may decrease zinc more general, its not specific because B9, B6, B12 deficiency can all be present absorption Zinc deficiency may decrease folate absorption  Vitamin B12 (cobalamin) Structure: Sources: In nature B12 is made by _____________ microbes (ie. in rumen and ileum of some animals), so animal products are the main sources (MFP, egg, milk) if not consuming animals, you have a hard time getting B12 Fig. 9.39, p. 384  B12 Absorption Mechanisms: I. Intrinsic Factor mediated absorption 1) Intrinsic factor (IF, a glycoprotein) is synthesized in the stomach. 2) B12 combines with ____________in R protein stomach and travels to small intestine 3) B12 releases R protein and complexes with IF 4) B12-IF is absorbed in the _____________ ileum through receptor 5) B12 is released once complex is in the enterocyte II. Diffusion Not of importance with normal intakes With large doses, some non-intrinsic factor mediated absorption takes place B12 shots could be helpful for people with stomach problems B12 Absorption Fig. 9.40, p. 385 binds as soon as it gets to stomach enter cells with IF receptor  B12 Functions Converts homocysteine to methionine by transfer of methyl group from folate to homocysteine Converts methylmalonyl CoA to succinyl CoA which can be used in ____________________________ energy metabolism __________________________________through nucleic acid synthesis methionine formation and possibly through reduction of ribonucleotides to deoxyribonucleotides Resynthesis of methionine from homocysteine Fig. 9.37, p. 378  B12 Deficiency: Megaloblastic Anemia Symptoms: At risk: lack of food sources? Large immature red blood Elderly cells, neuropathy, increased Diseases/Surgery of the mean corpuscular volume ileum can't absorb B12 (MCV) looks at size of RBCs if high = deficiency or B9 or B12 Alcoholic Vegans Usually due to decreased absorption secondary to Stomach surgery recipients part of stomach removed or there is issues lack of IFas opposed to decreased intake, called pernicious anemia specific for IF give them injections instead?  B12 Toxicity: Assessment: None known Serum B12 No UL _______________________ Schilling test Used to test B12 tracer compounds absorption/presence of given and sees if it is absorbed IF plasma homocysteine ✽ Often done in conjunction with folate assessment  Pyridoxine (Vitamin B6) Structures: Coenzyme forms: PL, PM, PN, ______, PLP PMP, PNP Sources: Liver, nuts, bananas, legumes, meat, whole grains, salmon, sirloin steak, white meat chicken also from fortified cereals Pyridoxine Fig 9.42, p. 390 B6 Metabolism in liver Fig. 9.43, p. 392  B6 Functions need PLP/B6 !!!!! 1) Amino acid metabolism ▪ Transamination coenzyme (ie. AST/GOT, ALT/GPT) ▪ Decarboxylation (ie. serotonin production) ▪ Transulfhydration/desulfhydration (ie. methionine to cysteine or cysteine to pyruvate) ▪ Cleavage (ie. serine to glycine in folate metabolism) can lead to anemia = hypochromic anemia = not enough color 2) ______________________ heme formation 3) ______________________ niacin synthesis 18 carbon chain 4) Arachidonic acid production from lineoleate 20 carbon chain with 4 double bonds 5) Glycogenolysis (glycogen phosphorylase)  B6 Functions Potential Effects: homocysteine high levels Coronary Heart Disease  low levels may play role in etiology Premenstrual Syndrome (PMS)  beneficial effects of high doses is controversial _____________________________________  carpal tunnel syndrome research needed but high doses seem to decrease symptoms  B6 Deficiency Symptoms: Lethargy in adult Seizures in infants ____________________________________________ hypochromic, microcytic anemia Depression At risk: Breastfed infants of mothers with deficiency Elderly poor intake Alcoholics because of liver (conversion happens here) Oral contraceptive users  B6 Toxicity: Neuropathy UL: 100 mg/day B6 Assessment: Plasma PLP ___________________________________ transaminase activities Tryptophan load-B6 required to convert to niacin, deficiency leads to build up of xanthurenic acid = not enough B6 look at how much niacin is being synthesized dependent on B6 availability