Everything Metabolism Flashcards
What is the first phase of glycolysis called?
The investment phase
What is NAD+ derived from? What biological reactions does it participate in? How many e- and H+ can it accept, respectively?
Vitamin B3 (niacin). Participates in bio oxidations (it gets reduced). Accepts 2 e- and 1 H+
What is pellagra?
Niacin deficiency - dermatitis, diarrhea, dementia, maybe death (Schaff called it D^3 or D^4)
What is the NAD+/NADH ratio in cells?
High
What enzyme of glycolysis exhibits negative cooperativity? What does that mean?
Glyceraldehyde-3-phosphate dehydrogenase. It means that it is NOT SENSITIVE to changes in substrate concentration
Under anaerobic conditions, how is NAD+ regenerated for glycolysis to continue?
Conversion of pyruvate to lactate.
What is hexokinase inhibited by?
Inhibited by G6P (its product) and 2-F-deoxyglucose
What intermediate do red blood cells take from glycolysis? What do they do with it?
They convert 1,3-BPG to 2,3-BPG (remember that 2,3,-BPG is an allosteric effector that reduces Hb affinity for O2)
What glycolytic enzyme(s) is/are arsenate toxic to?
G3P DH (PDH is also sensitive)
What toxin is enolase sensitive to?
Fluoride
Pyruvate kinase deficiency results in what? Why?
Anemia. Only one isozyme is present in red blood cells. If that one is mutated then that sucks.
What sugar-alcohol can result in retinopathy?
Sorbitol (causes increased ocular pressure - osmotic forces)
What two diseases can result from defective fructose metabolism? Which one(s) are serious?
Essential fructosuria is from fructokinase deficiency (benign b/c hexokinases can kinda do the job)
Hereditary fructose intolerance is from Aldolase B deficiency (SERIOUS b/c phosphates get used up in the phosphorylation of Fructose, then the pathway is stuck)
Which sugar is GALT enzyme involved in metabolizing? What disease results from GALT deficiency? Serious?
Galactose metabolism, disease is called CLASSIC GALACTOSEMIA. Phosphates get used up in the rxn galactose to gal-1-P, then pathway is stuck. Serious disease is in the newborn screen
What is UDP-gucuronic acid used for by cells and where does it come from?
Cells use it to make drugs and blilrubin more soluble for excretion. Comes from UDP-glucose.
What enzyme can combine UDP-glucuronic acid with drugs like benzoic acid to create more soluble substances? What disease results from deficiency of this enzyme?
UGT is the enzyme (UDP-alpha-D-glucuronyltransferase). Gilbert syndrome is the disease - eleveted bilirubin. Peeps usually asymptomatic.
Do obese people get drunk faster?
Yeah
What is the 2nd pathway that alcoholics have to metabolize ethanol?
MEOS Cyt P450 pathway.
What coenzyme is required for alcohol metabolism? What is the clinical significance of this? What disease results?
NAD+ is needed. Alcoholics often don’t eat, so they are deficient in niacin. Alcohol metabolism uses the little NAD+ available so glycolysis is halted as a result. Disease is called Wernickle-Korsakoff syndrome
A high NADH to NAD+ ratio results in the formation of what? (hint: think about what step NAD+ is required in glylcolysis and what side products can be made from the intermediate in the prior step). What population might have a problem with this?
DHAP/G3P can’t go to 1,3-BPG, so instead DHAP is converted into triglycerides. A problem amongst alcoholics
What is the cellular location of the TCA cycle?
Mitochondrial matrix
Thiamine/thiamin is also known as what (Vitamin _____)?
Vitamin B1
Describe pyruvate dehydrogenase, including its coenzymes, and the reaction it is involved in.
E1 (thiamine): Pyruvate comes in, gets decarboxylated (C02 leaves), acetate is the product.
E2 (lipoate): Takes acetate and combines it with CoA, which joins here. S-S bond is reduced. Acetyl CoA is the product and goes to TCA cycle.
E3 (FAD): Regenerates the enzyme (re-oxidizes the sulfur). FAD gets reduced to FADH2, and is oxidized back to FAD by NAD+ to NADH.
Small molecules can inhibit pyruvate dehydrogenase. How?
Small molecules like ATP, acetyl CoA, NADH, and fatty acids activate a kinase, which phosphorylates PDH, making it inactive.