Metabolism 2 Study guide Exam 1By: Tony Berardi1. Explain the DRI. The goal of the DRI is to prevent chronic diseases, not to prevent defiencys. The focus is now on malnutrition from over nutrition. DRI started in 1835 with lemons on ships. Then first RDA was in 1949 with the focus to prevent defiency in the military. Changed because it was too broad (focus on healthy people, and too many fat unhealthy people). Now have EAR, RDA, AI, and UP. 2. What are vitamins and difference between fat and water soluble? They are micronutrients that must be supplied from the diet. Needed for normal function and their absence cause certain symptoms with each one. The body can make some, but not in appreciable amounts. Fat soluble is obviously soluble in fat, stored in the body in large amounts so it’s not required every day. Since it’s stored, defiency takes a long time to occur. Most have precursors, and only higher organisms need them. Can be toxic at low amounts (but still way higher than the UL). Water soluble arestored minimally, excreted in the urine, so defiency can happen much faster. Absorbed into blood, sincewater soluble and both simple and complex organisms need. Since they aren’t really stored, they are only toxic at mega doses (100x DRI) Thiamin1. What is the active form of this vitamin? Only active as Thiamin pyrophosphate, which is also known as Thiamin di and triphosphate. So TPP, also TDP, and TTP. Need a phosphate to be active2. What are the source?It’s in most foods. Liver and yeast are the richest sources, followed by meats, and whole grains. Polished rice is a terrible source. There is an enzyme, Thiaminase, present in raw fish and caffeine, that destroy thiamin. It is stable in cooking3. How is it absorbed? It has to be in its free Thiamin to be absorbed. In the blood it travels as a monophosphated form and bound to albumin. Everything vitamin from now on is absorbed by active transport at low concentrations, and passive diffusion at high.4. What are its functions? It is involved in the krebb cycle mainly by decarboxylating pyruvate to Acetyl CoA. Also alpa ketoglutarate to Succinly CoA and the decarboylation of the branch chain amino acids. Also in the synthesis of the pentases and NAPH, which are involved in making nucleic acids. So DNA synthesis. In nerve function too, but mechanism is not clear.5. What is the defiency and the risk groups? Those at risk are the elderly, alcoholics, and people who eat strictly raw fish. Defiency is BeriBeri and there are 4 types. Easy to remember, cause really only two, one affects the cardiovascular and the otheris the nervous system. So have wet beriberi, which is the cardiovascular, then dry beriberi, which are the nerves. Severe is called Wernike’s Korakoff and it happens in chronic alcoholics. There are two possible symptoms to this, Korsakoff phsycosis, and Wernickes encephalopathy. It can cause death if untreated. The DRI is 1.2 mg daily Riboflavin1. What is the active form? Active as Flavin mononucleotide and Flavin Adenine Diphosphate. So FMN and FAD2. What are the sources? Mostly in dairy and milk products, grains, and meats. It is also stable in cooking, and is light sensitive.3. How is it absorbed? Kind of a back and forth thing. Must be free flavin to absorb, so the HCL cleaves out the proteins, it’sthen phosphylated to FMN in the mucosa, then travels to the serosa surface, and is dephosphylated back to flavin, travels to the liver, and phophylated again to FAD. Stored in the liver. 4. What are the functions? FAD, so it’s in glycolysis as an electron transporter. Also in the reduction on glutationin to G5S (reduced form)5. What is the defiency? The risk groups are elderly, alcoholics. People with increased needs, like pregnant and lactating, and trauma patients. Babies with hyperbilurbiemia on photo therapy (I guess the therapy destroys it). Defiency cause oral lesions, glossititis, and stomatitis. 6. How to assess it and what is the DRI?To check the values, look at the activity of the RBC glutathionin reductase. Since need FAD to reduce it, and NADPH is a reactant, meaning if no FAD, then the NAPH won’t be used. And the NAPH is easy to measure Niacin1. What is the active form? Active as nicatinamide and nicotinic acid2. What are the sources? Meats and fish are the best source, since they have free nicotinamide. Corn suck dick as a source, because it’s low in tryptophan. But treating the corn with limewater can release the niacin in it. The liver can also make it with 60mg of tryptophan3. What are the functions? About 200 reactions, but mainly as NAD, NADH, NAP, NAPH. NAD is the electron carrier in glycolysis, NADH is the molecule when its reduced, NAP is involved In the hexose shunt (nucleic acids) NAPH is involved in many pathways= beta oxidation, cholesterol synthesis. Also can be used to lower cholesterol,but side effect is painful (Niacin flush) caused by release of histadine.4. What is the defiency? The risk groups are the people with the higher needs. Some drugs can interfere with absorbtion, such as Izonaid for tuberculosis. There also is a genetic disease where the patient can’t metabolize tryptophan, Hartnup disease. Its autosomal recessive. Defiency is Pellagra. It’s the 4 D’s, Dermatitis, Diarrhea, Dementia, and Death5. What is the DRI? It is 14 NE, or niacin equivalents. 1 NE is equal to either 1mg niacin, 60mg tryptophan, and 6000mg protein.Folic Acid1. What is the synthesis and shit? It’s made from 9 different precursors, such as PABA, glutamic acide, Pterdine. The body can make all, except Pterdine acid.2. How is it absorbed? It must be absorbed as a monoglutamate form, so the polyglutamate is hydrolyzed with a conjugase. The conjugase is also Zinc dependent, so you need Zinc to absorb Folic acid. Some foods have conjugaseinhibitors though, like oranges cabbage, lentin. Then it is reduced in the liver to its active form, THF. Minimal storage of 11-28 mg.3. What are the functions? It is use in one carbon transfers, in the synthesis of the purines and pyridimes (Nucleic acids) and in some AA metabolism, such as the glycine-serin, but the important one is the methionine regeneration. 4. What are the sources? Green, leafy veggies, oranges, yeast. It is destroyed with
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