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139 Cards in this Set
- Front
- Back
How do you determining L and D depends on what?
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The position of the hydroxyl group
HC=O #1 C I HC--OH #2 C<---- to the right = D I H2C--OH #3 C |
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Sucrose is...
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a non-reducing sugar
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All mono-saccharides are...
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reducing sugars
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Carbonyl group vs. Aldehyde group vs. Ketose group
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I H R
C=O I I I C=O C=O I I R R |
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What type of sugars can react with alcohol? How?
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-Reducing sugars like glucose
*Carbonyl group can react with itself (which is an alcohol). Aldehyde reacts with # 5-OH group to form a hemiacetal |
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What is a hemiacetal?
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It is formed from a sugar reacting with an alcohol on the #5 OH. This creates an asymmetric carbon which has an -OH branched off of the top and it can be either alpha (drawn on the same side of the D or L) or beta (drawn on the opposite side)
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What would be considered a reducing sugar?
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The carbonyl carbon (the 1st C) is not tied up in the linkage between the disaccharides
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what happens when glucose is put in a solution?
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-It reaches its equilibrium between alpha and beta (equilibrium must be met only if it is passed in the open chain form which is found in very small amounts)
-The solution would then contain 64% beta and 36% alpha |
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What can glucose do in his open chain form?
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It can react with amines
*This causes an in vivo reaction (Mailard Reaction in your body) |
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What is a function of reducing sugars?
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Reduce metal salts (change colors)
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Which is the only for of glucose that can react with hemoglobin?
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D-glucose (not alpha or beta)
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What can hemoglobin A1C be used for?
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-It can be tested for people with diabetes
-Measures glucose levels over a long period of time because it is glycosilated and bound to a sugar *glucose binds irreversibly to hemoglobin and stays with it until hemoglobin turns over (about 3 months) |
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Why is glucose a predominant fuel over galactose?
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-Although the structures are almost identical (C-4 OH is switched), glucose has the lowest % aldehyde
*This means less chances to react with sugars and have free aldehydes floating in the body -Galactose in the open chain form can react with the amine groups of proteins and mess with their structure -glucose is more stable -galactose could become undigestible for plants |
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Which enzymes help in the digestion of carbs?
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-Pancreatic amylase is secreted into the lumen and the stomach
-Enzymes are produced in the brush boarder cells of the small intestine (sucrase) *These break down poly- and disaccharides into monosaccharides |
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How do broken down carbs move thru the epithelial cells into the blood?
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From the apical side to the basolateral side of the membrane
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What helps the monosaccharides across the membrane towards the blood?
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Glucose sodium symport system
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How does the glucose sodium symport system work?
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-Na binds to the transporter protein to create a higher affinity for glucose
-Na is pumped out by an energy dependent system (Na/K ATPase) |
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GLUT 2
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Transports glucose across the basolateral side of the intestinal cell into the blood
*Found in the Liver, pancreatic beta cell, and the kidneys |
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GLUT 5
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-Brings fructose across the apical side of the intestinal cell membrane
(Then brought out of the cell by GLUT 5) |
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Where is GLUT 1 found?
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-Erythrocyte (humans)
-Blood-brain barrier -Placenta -Fetal Tissue |
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Where is GLUT 3 found?
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Brain neurons
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Where is GLUT 4 found?
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-Brown and white adipocytes
-Heart -Skeletal muscles *only GLUT transporter regulated by insulin |
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Where is GLUT 7 found?
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The E.R. of hepatocytes
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How does fructose move best along the cell?
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With glucose
(isolated fructose moves slower and pure fructose can mess with insulin response) |
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What occurs in a GLUT 1 deficiency?
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-Not enough glucose is brought to the brain
*Provide with ketone bodies if caught early -Very rare -Severe symptoms (tremors, low cerebral spinal fluid, mental retardation) |
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How does insulin transport glucose?
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-Insulin binds receptors which signal the cell to produce GLUT 4
-GLUT 4 gets translocated to the surface to facilitate glucose entering the cell *When insulin decreases, GLUT4 stays in the cells as vesicles |
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What is the hexosemonophosphate shunt?
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Glycolysis diverts metabolites to produce ribose sugars (for DNA and RNA synthesis) and NADPH (CP450 and lipid synthesis pathways)
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What can serve as a substrate for gluconeogenesis?
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Lactate
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What does insulin prefer?
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Glycolysis and glycogenesis
(glucagon favors gluconeogenesis and glycogenolysis) |
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Which pathway is more favored for fructose in glycolysis? Why does is not happen
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Fructose to Fructose-1-P
*Does not really happen because it skips the rate limiting step (PFK-1) -creates a lot of pyruvate and other Krebs cycle substrates -creates a build up of citrate leading to increased FA synthesis **High fructose is lipogenic |
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What is the rate limiting step in glycolysis?
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F-6-P to F-1,6-bisP
*When this is low the gluconeogensis occurs |
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What are the 3 irreversible steps of glycolysis?
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- G to G-6-P
- F-6-P to F-1,6-bisP - Pyruvate to PEP |
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What can the reaction pyruvate to acetyl CoA be used for?
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-FA synthesis
-Krebs Cycle |
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What can initiate the hexosemonophosphate shunt?
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G-6-P
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What do dehydrogenases do in the Krebs cycle?
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Catalyze the removal of H's from FAD and NAD
*Produces NADH (highly negative standard reduction potential = electron donator) and FADH2 to enter the ETC |
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Glucokinase
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-In the Liver and has a high Km (reaction occurs slower and lasts longer)
-Grabs all of the glucose beyond what the muscle can use (liver clears glucose) -Induced by insulin *used for the reaction G to G-6-P |
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Hexokinase
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-In the muscle and lower Km (higher affinity for glucose)
-Will not be able to take up a lot of glucose and cannot clear glucose *used for the reaction G to G-6-P |
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What can insulin stimulate in glycolysis?
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Irreversible steps (G to G-6-P)
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When is glucagon stimulated?
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During fasting
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What allosterically stimulates PFK-1?
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Fructose-2,6-bisP
*positively* |
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What is PFK-2 involved with?
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F-6-P to F-2,6-bisP
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What indirectly regulates PFK-2 activity?
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insulin
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What does glucagon do with regards to gluconeogenesis?
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-Stimulates the 2nd messenger (ATP to cAMP)
-It then activates the protein kinase (a phosphorylating enzyme) protein kinase A which involves ADP to ATP -The bifunctional enzyme is then phosphorylated |
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What will be inhibited when glucagon stimulates the 2nd messenger?
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PFK-1
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What can high levels of fructose cause?
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-Fructose intolerance
-A decrease in the chances of carbonyl compounds binding to hemoglobin A1C (decreases the risk for heart disease) |
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What has increased in consumption over the past 30 years?
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-Fat
-Refined Carbs *sugar consumption has remained unchanged despite increase uses of HFCS |
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Fructose intolerance
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-Deficient in Aldolase B
-Converts F-1-P to dihydroxy acetone phosphate -Can cause hepatic failure and death |
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What happens if pure fructose is consumed in the diet?
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-It is not rapidly absorbed
-Can end up in the G.I. tract and can ferment *not reasonable because no one eats a pure fructose diet* |
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Stable isotope of fructose
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Converted to a fatty acid but mostly converted to glycogen
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HFCS stimulates lipogenesis?
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-Fructose will not end up in the blood
-Can be catazlyzed by glucokinase but mostly by fructokinase -Thought to provide a substrate for lipogenesis |
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High pure fructose = High uric acid production?
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-The reaction converts F-1-P to DHAP and glyceraldehyde
-This reaction uses up ATP (ATP-->ADP-->AMP-->Uric acid) *uses up ATP because glyceraldehyde does not have the phosphate group needed to be used for energy* |
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High Uric acid production = inhibition of nitric oxide-stimulated vascular endothelial function?
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-Inhibition of vascular relaxation = depressed insulin effect on glucose uptake
*insulin increases vasodilation and GLUT4 -Depressed glucose uptake = insulin insensitivity = metabolic syndrome |
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What is an example of a transport protein?
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Albumin-->transports short chained fatty acids in their non esterified form into portal circulation
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What happens to an essential amino acid that is bound to glucose?
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-The amino acid can become unavailable (Mailard reaction)
-This only occurs with non-alpha amines (ex:lysine) -The entire protein quality is reduced |
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Histidine
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-Requirement is low
-Essential for infants with health problems -No proven metabolic synthesis pathway |
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What can Arginine be made from?
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-Glutamine
-Glutamate -Proline |
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Chemical score/AA score
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-Don't need animals
-Determines which is in the lowest amount relative to how much is required (limiting AA) -Score = Limiting AA in food protein / content of same AA in reference protein |
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Protein Efficiency Ratio
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-Rats in the study can be messy or eat their own feces (throw off protein count #'s)
-Use 21 day old weanling male rats -Feed diet containing 10% "test" protein -Feed control group 10% casein diet (correct control diet PER = 2.5) -Feed animal for 28 days -PER = gain in body wt (g) / protein consumed (g) *growth assay* -High PER = high quality protein |
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Good quality protein has what effect on the daily value label?
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Daily value on label is low
*basis for labeling requirements |
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Biological value
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-Rats are used
-100 is the best # -BV = I - (F-Fo) - (U-Uo) / I - (F-Fo) -BV = (N retained/ N absorbed) |
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About what % of nitrogen is in protein?
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16%
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What is an equation that can be used to determine the amount of protein in a food?
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Amount of nitrogen X 6.25 (correction factor)
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Nitrogen eliminated in the feces can come from where?
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-Cells coming off of the intestinal lining
-Bacteria |
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Net Protein Utilization
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-NPU = N retained / N consumed
-Accounts for the fact that some proteins aren't absorbed as well as others -NPU = I - (F-Fo) - (U-Uo) / I -Can use total carcass nitrogen -NPU = (TCN on test prot.) - (TCN on prot.-free) / N consumed |
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What is deamination?
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-Remove amine group
-Amine is sent through the urea cycle |
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What is transamination?
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-Remove amine group
-Transfer the amine group to another product *Critical for the body's use of non EAA by converting them from other non EAA or EAA *The transfer of an amine group creates a carbon skeleton (alpha keto acid) |
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How can a carbon skeleton be used once its amine group is removed?
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-In the Krebs cycle
-As a ketone body -As glucose -Converted to FA |
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Alanine aminotransferase (ALT)
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-Catalyzes the transfer of an amine group from alanine to some alpha keto acid (alpha keto glutarate)
-Alanine then gets converted to glutamate *Reaction is reversible |
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What is pyridoxal phosphate's role with ALT?
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-It's a coenzyme necessary for transaminase reactions
-pyridoxal phosphate gets converted to pyrodoxamine (takes the amine from alanine) -pyrodoxamine transfers the amine group to alpha-ketoglutarate to form glutamate which in turn regenerates the pyridoxal |
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Aspartate Amino Transferase (AST) reaction
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aspartate -----> oxaloacetate
AST |
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Heart muscle have more of what transferase?
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AST
(an increase of ALT can show heart damage) |
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What 2 tests can show liver damage?
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-increase of AST
-increase of ALT *can be from lipitor* |
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Glutathione
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-Gamma-glutamyl-cysteinyl-glycine (tripeptide)
-Cystein group deals with function (has disulfide bonds) |
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Glutathione in leukotriene biosynthesis
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-Arachodonic acid enters the eicosanoid pathway from the cell membrane by phospholipase A-2
-Can enter the lipoxygenase pathway (inflammatory mediators) *Activated by injury or inflammation of the cell |
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GSH and it's effect on peroxides
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-Reduced form = GSH-peroxidase
-Selenium containing enzyme -Breaks down peroxide -GSH + H202 ------->2H20 + GSSG GSH- peroxide *GSSG = 2 glutathione's bound together |
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Peroxides
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-Can be used to kill microorganisms (biproducts of metabolism)
-Found in lipid peroxidation -Can be formed by free radicals |
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Glutathione reductase
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-Riboflavin (Vit. B2) containing enzyme
-Converts GSSG back to GSH |
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How does glutathione eliminate toxins?
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-Can bind to Leukotriene A4 (non-polar)
-This forms LTC4 which is more water soluble because a peptide is added to it by being bound to the sulfur part of glutathione *LTC4 helps to eliminate toxins |
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Carnitine
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-Carnitine acyl transferase 1 and 2 help fatty acyl CoA get across the mitochondrial inner membrane to generate energy
*It is structurally an amino acid |
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Creatine
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-Can be a quick source of additional ATP(energy) when ATP is depleted from the muscle during strenuous exercise(exhaustion is reached)
-Should be constant in the muscle -Can be a crude measurement used to determine muscle mass (more muscle = more creatine excreted in the urine) *Structurally an amino acid |
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The conversion of Creatine to phosphocreatine
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-Exothermic reaction (releases about -10,300 calories)
-Non-enzymatic (chemical breakdown) |
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Phenylalaine and tyrosine metabolism
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-Uses a monoxygenase
*An oxygen added to it to form the hydroxyl group on the benzene ring of phenylalanine to create tyrosine *The other oxygen used in the reaction used to form H2O |
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Which micronutrients are used in phenylalaine and tyrosine metabolism?
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-Enzyme contains Fe and Copper
*Vit C (a H2O soluble reducing agent) is used to reduced the metals to the -ous form (2+) |
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What can phenylalanine be metabolized to make?
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-Catacholamines (epinepherine and nor epinepherine)
-Acetyl CoA (for energy or FA synthesis) |
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What does the adrenal cortex make?
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Steroid hormones
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What does the adrenal medulla make?
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Catacholamines
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PKU
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-Deficient in phenylalanine monoxoygenase (no conversion to tyrosine)
-Creates a build up of phenylalanine |
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What can tyrosine amino transferase do?
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Can form glutatmate
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Tryptophan metabolism
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-Tryptophan serves as a substrate for seritonin (controls blood flow around the intestine)
-Seritonin can form melatonin (sleep regulation) -Conversion occurs mostly in the intestinal tract |
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What can tryptophan dioxygenase be used to generate?
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-Acetyl CoA
-NAD+ -NADP+ *Can be used for energy or FA synthesis |
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Methionine and Cysteine Metabolism
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-Meth. converted to homoC
(Rarely, some people are deficient in the enzyme that converts homoC back to Meth.) |
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Homocysteine
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-Intermediate of the conversion of methionine to cysteine
-Possibly a risk factor for heart disease -Excess can lead to death of atherosclerosis (toxic to blood vessels) |
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What are micronutrients involved in Methionine metabolism?
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-Vitamin B12 (homoC to meth.)
-Folate -Vitamin B6 |
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What can the metabolism of cysteine do?
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-Create taurine to make bile acids
*Cysteine can also make glutamate |
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Where is insulin excreted from?
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The beta cells of the pancreas from a rise in plasma amino acids
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What does insulin stimulate?
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-The entry of AA into the cells
-Protein synthesis *Anabolic hormone |
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What does glucagon increase the uptake of?
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-AA in the liver (provides carbon skeletons for gluconeogensis)
*Secreted from the alpha cells of the pancreas *Catabolic hormone |
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what does the EPA deal with?
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Pesticide control
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What does the FTC deal with?
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Advertising
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Difference between a food and a drug
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-Food = Cholesterol lowering (not a disease)
-Drug = Prevents heart disease |
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When can a food have prevention against disease claims?
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Congress allows heart disease prevention claims on foods high in oat fiber under strict guidelines
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What does a drug have to proven in order to be placed on the market?
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-Safety
-Efficacy |
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Label
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Refers to what is on the product
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Labeling
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What is on the product and anything associated with the producr
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What prevents a food additive from being allowed on the market?
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If it is found to cause cancer in humans or animals (Delaney Cause)
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What is not considered a food additive?
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-Pesticide
-Color additive -New animal drug *F.A.'s should be GRAS |
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What is the federal register?
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A daily publication of the executive branch which states enforced laws
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What does not have to be considered GRAS?
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Dietary Supplements
|
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FDA inspections
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-Refusing entry to an inspection violates the law
-Don't need a warrant (4th amendment) |
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Crepe Label
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-Stated that dietary supplements must contain a label stating that vitamins and minerals can be supplied by the diet
-FDA never got it finalized in 1973 |
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FDA and its minimum and maximum of nutrients (1973)
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-Dietary supplements should have more than 50% of a nutrient and less than 150% or considered a drug
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What happened in 1976 to the FDA?
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-They had to stop trying to consider dietary supplements as drugs
-The vitamin and mineral amendment which got congress involved |
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Implicit claim vs. Explicit claim
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High fiber vs. Contains high fiber and low fat which decreases the risk of heart disease
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What happened in 1985?
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-Kelloggs did not wait to change the regulation
-Made explicit claims to violate the law (promoted themselves as a drug) to make the FDA take action -Got the National Research Counsel involved to endorse their ad |
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Who has the "Burden of Proof"?
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FDA
*Determines safety for dietary supplements after they are placed on the market |
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NLEA of 1990
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-Congress included authority for the FDA to decide which explicit health claims were allowed on foods
-FDA gets to determine the wording on the label and which foods qualify *Did not allow dietary supplements to make explicit claims* |
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What are 2 health claim exceptions allowed on pills?
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-Folic acid (neural tube defects)
-Ca (osteoporosis) |
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How did the DSHEA of 1994 changed the NLEA for dietary supplements?
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-Created a new category of food substances (dietary supplements)
-Created a new "safety standard" (significant or unreasonable risk of illness or injury) -Defined what can be a dietary supplement -Can use 3rd party materials to inform consumers about health benefits -Use of nutritional support statement (bodily function not disease) -Must include "has not been evaluated by the FDA" |
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What happens if the advertisment is misleading?
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The FTC can get involved
|
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Acetalaldehyde
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-Toxic
-Mutagenic (interacts with amine groups by effecting the normal structure and function of DNA) and carcinogenic |
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Disulfiram
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-Blocks aldehyde dehydrogenase
-Decreases the sickness from alcohol (no conversion to acetate) |
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What type of tests are used to determine if something is mutagenic?
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In vitro tests (easy and takes 48 hrs)
*Carcinogenic = doses to animals and have to wait a lifespan (time consuming and expensive) |
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CP450
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-Inducible enzyme
-Heme protein -Uses oxidation reactions (binds to a substrate [R-H] to create a hydroxyl group [R-OH] -Reduces Fe to -rrous state (+2) |
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What induces CP450?
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Alcohol
*It changes the metabolism processes of the liver |
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Where do most oxidation reactions occur?
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Smooth E.R. (microsomal fraction)
*can be non-microsomal (alcohol DH) |
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Hydrolysis rxn
|
-Split with water
*structural modification |
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Reduction rxn
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-Azoreductase can split azo bond (R-N=N-R) to form 2 separate amines
-Common in colon because lots of bacteria *structural modification |
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Conjugation rxn
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-Addition of a side chain to a molecule
(Ex:methylation-->does not necessarily make the compound water soluble) *phase 2 structural modification |
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What is the 1st metabolic reaction a toxic is exposed to?
|
CP450
*found in the lungs, liver ER (highest), skin, and intestinal lining |
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What do PCB's induce?
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CP450
|
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What is a proximate carcinogen?
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A cancer causing substance (can be activated by gut flora)
*found in the environment as a pre/pro carcinogen (stable) |
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What can the cell do when it is affected by a carcinogen?
|
-Try to repair the DNA
-Die -Mutate |
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Metabolism of toxins
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-Host defense=immune response and encapsulation
-Elimination of the chemical in an "unchanged form" = Expire air, vomit, urine, sweat, feces -Structural modification = metabolize the toxin by altering the structure to make it less toxic and easily excreted |
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What is impermeable to many toxins?
|
The skin
|
|
What can be used for joint pain?
|
DMSO on the skin
*Can easily carry material in the body and can taste within minutes of putting on the skin |
|
What are cruciferous vegetables high in?
|
-Glucosinolate
-Isothiocyanate |
|
Sulforaphane
|
-A glucosinolate / metabolic enzyme
-Potent inducer of phase 2 metabolism -Suppresses CP450 -Induction of apoptotic pathways -Suppresses cell cycle progression (cell division) -Inhibition of angiogenesis -Anti-inflammatory activity |
|
Formation of Indole-3-Carbinol
|
-Glucosinolate
-Glucobrassicin is affected by myrosinase (when Indole-3-Carbinol is eaten or broken up, this is released) -Myrosinase cleaves off the S-glucose and sulfate group -A cyanide group is left over, Isothiocyanate (Indole-3-Methylcyanate) -The isothiocyanate is unstable so it loses the cyanide to form the Indole-3-Carbinol |
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What does Indole-3-Carbinol induce?
|
CP450 which increases production of estrogens because of an increase of hydroxylases
|