Term
List the alternative fates for acteyl-CoA |
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Definition
1) TCA cycle 2) Cholesterolgenesis -> cholesterol 3) Ketogenesis -> Ketone bodies |
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Term
Compare the "preferred fuels" of liver, skeletal muscle, heart, adipose tissue, and brain |
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Definition
Liver: glucose, fatty acids, amino acids skeletal muscle: glucose (exertion), fatty acids (rest) Heart: Fatty acids Brain: glucose, ketone bodies (starvation) Adipose: fatty acids |
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Term
Identify the major carbohydrates and the foods in which they are found |
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Definition
Lactose - milk (glc+gal) Sucrose - deserts, table sugar (frc+glc) amylose - corn, bread, potatoes amylopectin - cron, bread, potatoes |
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Term
Explain the consequences of consuming milk by an individual who has lactose intolerance (genetic deficiency of lactase) |
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Definition
- unable to bread down lactose to glucose and galactose
- build up of lactose causing diarrhea, flatulance etc. |
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Term
Compare the pathways of carbohydrate metabolism that are active in RBC's, brain, skeletal muscle, heart, adipocytes and hepatocytes |
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Definition
RBC: Glucose -> pentose phosphate pathway OR glycolysis to lactate
Brain -> pentose phosphate pathway OR glycolysis to TCA cycle
Skeletal muscle and heart: pentose phosphate pathway OR glycolysis to lactate or acetyl CoA (TCA etc)
Hepatocytes: glycolysis/TCA, pentose phosphate, glycogen synthesis, glycolysis/lactate
Adipocyte: glycolysis/acetyl CoA -> fat
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Term
Identify the glucose/monosaccharide transporters that are responsible for: 1) Sodium dependent glucose transport 2) Insulin dependent glucose transport 3) Insulin independent low affinity, high capacity transport in liver |
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Definition
1) SGLUT1 2) GLUT4 3) GLUT2 |
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Term
Identify the three glycolytic reactions that are irreversible under physical conditions |
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Definition
1) Hexokinase/Glucokinase (liver): Glucose -> Glucose-6-Phosphate
2) Phosphofructokinase 1: Fructose-6-Phosphate -> Fructose-1,6-bisphosphate
3) Pyruvate Kinase Phosphoenolpyruvate->pyruvate |
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Term
Compare the tissue localization, kinetic characteristics and regulation of hexokinase and glucokinase |
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Definition
Hexokinase (all cell types): - always in cytosol - high affinity (low Km) for glucose - lower capacity - alosterically regulated by glucose-6-Phosphate
Glucokinase(liver): active in cytosol, tranlocated to nucleus and inactive there - lower affinity (higher km) for glucose - very high capacity, not saturated under physiological conditions - inducible enzyme, insulin upregulates gene expression of glucokinase |
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Term
Compare the allosteric activators and inhibitors of the enzymes that catalyze the irreversible glycolytic reactions |
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Definition
Hexokinase: inhibited by glucose-6-phosphate (its product)
Phosphfructokinase 1: activated by: fructose-2,6-bisphosphate, AMP, ADP inhbited by: ATP, citrate
Pyruvate Kinase: Activated by fructose-1,6-bisphosphate Inhibited by: alanine, ATP
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Term
Identify the pancreatic hormone that leads to the inhibition of hepatic glycolysis
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Definition
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Term
Describe the mechanism by which glucagon exerts its inhibitory effect on hepatic glycolysis |
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Definition
- glucagon works through Gs receptor to increase cAMP.
- cAMP activates phosphokinase A (PKA)
- PKA phosphorylates and thereby inactivates PFK2 (creator of fructose-2,6-phosphate), decreasing activity of PFK1. It also phosphorylates and inhibits pyruvate kinase
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Term
Predict the separate effects of an increased concentration of insulin and glucagon on synthesis of the three irreversible glycolytic enzymres in liver |
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Definition
- insulin increases the expression of the three regulatory glycolytic enzymres
- glucagon decreases the expression of these enzymes |
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Term
Explain the mechanism by which epinephrine inhibits hepatic glycolysis and activates cardiac glycolysis |
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Definition
- Liver: epinephrine increases cAMP, causeing phosphorylation cascade like glucagon (phosphorylation of PFK2, pyruvate kinase)
- Heart: epinephrine inhibits the ability of PFK2 to work backward by causing phosphorylation of its phosphatase domain, which normally catalyzes Frc-2,6-P->Frc-6-P |
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Term
Compare the conditions in whcih the favored end-product of glycolysis is lactate with the conditions that promote formation of pyruvate and acetyl-CoA |
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Definition
-Lactate: anaerobic, no mitochondria
-Pyruvate: aerobic, lots of mitochondria around |
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Term
Predicts the effects of ischemia (partial obstruction of blood flow), caused by a brain tumore, on lactate formation in the brain |
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Definition
- increase lactate formation due to lack of oxygen |
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Term
Identify the allosteric inhibitors of PDH |
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Definition
Inhibitors: 1) NADH 2) Acetyl CoA |
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Term
Predict the effect of covalent modification/phosphorylation on PDH activity |
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Definition
- inhibit it, like other enzymes in glycolysis/TCA pathway |
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Term
Identify the factors that PDH to be phosphorylated and dephosphorylated |
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Definition
Phosphorylated/inhibited: NADH, Acetyl CoA
Dephosphorylated/activated: NAD+, pyruvate, ADP, CoASH |
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Term
Identify the vitamin cofactors that participate in reactions catalyzed by PDH |
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Definition
1) E1 (PDH): Thiamin 2) E2: Pentohenate 3) E3: Riboflavin |
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Term
Predict the effect of thyamin deficiency, a genetic deficiency/abnormality in PDH or arsenic poisoning on circulating levels of lactate and pyruvate |
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Definition
**all three will have same effect: increase pyruvate, increase lactate
Thyamin deficiency: decrease E1 action
Genetic deficiency/abnormality in PDH: less PDH reactions
Arsenic poisoning: inhibits E2 lipoic acid transfering
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Term
Predict the physiological consequences of a genetic deficiency of fructose aldolase, identify the foods the affected individual should avoid |
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Definition
- no conversion of fructose-1-phosphate to dihydroxyacetone or glyceraldehyde
--> get build up of frc-1-P, Pi is tied up to this, so less ATP can be made
- avoid honey and fruit |
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Term
Predict the physiological consequences of a genetic deficiency of either galactokinase or galactose 1-phophate uridyl transferase and identify the food(s) the affected individual should avoid |
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Definition
Galctokinase deficiency: cannot make galactose-phosphate (which is usually convereted to Glucose-1-phosphate then to Glucose-6-phosphate, the glycolytic intermediate) --> Build up in galactose (cataracts, galactosuria)
Galactose 1-phosphate uridyl transferase: Cannot convert galactose-1-phosphate to glucose-1-phosphate --> Much more severe due to build up of galactose-1-phosphate because phosphorylated sugars can be toxic (cataracts, brain dysfunction, hepatic dysfunction)
**avoid milk and other lactose/galactose containing foods |
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