Uic Com Biochem Test 2

Front 1

what is gastrin? where is it secreted

Back 1

secreted from G cells in stomach. causes the release of pepsinogen from chief cells and H+ from parietal cells

Front 2

what is the respiration constant? what does it indicate?

Back 2

ratio of CO2 produced / O2 consumed, it is used to calculate energy consumption. carbs = 1, protein = .8, fat = .7

Front 3

what is the energy of ATP - ADP hydrolysis under typical cellular concentrations

Back 3

13.6 kCal / mol

Front 4

does a positive or negative E0 value indicate spontaneity of a redox reaction?

Back 4

positive, delG = -nFdelE0

Front 5

are oxidants electron donors or receivers in redox reactions?

Back 5

receivers - remember that oxidants are reduced - own more electrons after reaction

Front 6

would the ATP/ADP ratio be higher in the cytosol or mitochondria?

Back 6

cytosol, low concentration of ADP drives many ATP coupled reactions

Front 7

are oxidants electron donors or receivers in redox reactions?

Back 7

receivers - remember that oxidants are reduced - own more electrons after reaction

Front 8

would the ATP/ADP ratio be higher in the cytosol or mitochondria?

Back 8

cytosol, low concentration of ADP drives many ATP coupled reactions

Front 9

is glycogen synthetase active when phosphorylated?

Back 9

no

Front 10

how does the debranching mechanism differ from that of removing single non branch sugars from glycogen

Back 10

at the branch sites, glucose is hydrolyzed, at the free ends the bond is phosphorylated

Front 11

what is the cori cycle?

Back 11

lactic acid cycle - lactate from anaerobic respiration -> liver, reconverted to glucose and released back into circulation

Front 12

what carbon of glucose is phosphorylated to begin glycolysis?

Back 12

6

Front 13

what are the differences in liver and muscle isoforms of glycogen phosphorylase?

Back 13

liver isoform is regulated by glucose concentration, muscle isoform is regulated by ATP/AMP and glucose-6-phosphate

Front 14

what carbon of glucose is phosphorylated to begin glycolysis?

Back 14

6

Front 15

what are the differences in liver and muscle isoforms of glycogen phosphorylase?

Back 15

liver isoform is regulated by glucose concentration, muscle isoform is regulated by ATP/AMP and glucose-6-phosphate

Front 16

what reaction does myokinase catalyze?

Back 16

conversion of 2 ADP to one ATP and one AMP

Front 17

what is pompe disease?

Back 17

deficiency in alpha 1-4 glucosidase, a lysosomal enzyme that degrages glycogen. glycogen builds up in lysosomes in all organs, lethal at young age

Front 18

What is SGLT-1 and where is it found?

Back 18

sodium dependent glucose transporter - a glucose Na symporter found in the gut

Front 19

what glucose transporter(s) is associated with normal condition glucose uptake, and what characteristic of its affinity for glucose

Back 19

GLUT1 and GLUT3, both are widely dispersed and have high binding affinity for glucose (low Km)

Front 20

What is GLUT2's function and location

Back 20

low affinity (high Km) transporter which uptakes glucose when it is in high concentration, found in liver, B cells of pancreas, kidney, and intestine

Front 21

What is GLUT4's function and location

Back 21

found in muscle and adipose tissue, they are the insulin sensitive glucose transporters

Front 22

where is vitamin B12 absorbed?

Back 22

in the terminal ileum

Front 23

which glycolysis intermediate is shared with the pentose phosphate pathway?

Back 23

glyceraldehyde - 3 - phosphate

Front 24

what is the total energy investment and expediture from glycolysis?

Back 24

2 ATP and one glucose invested, 4 ATP, 2 NADH, and 2 pyruvate created

Front 25

which three steps of glycolysis are the main control points?

Back 25

the first two phosphorylations and the final converson of PEP + ADP to pyruvate + ATP (3 steps w/ most - delG)

Front 26

compare and contrast hexokinase and glucokinase

Back 26

both catalyze the C6 phosphorylation of glucose. hexokinase has much lower Km and Vmax, operates under normal conditions and is inhibited by G6P. Glucokinase counters hyperglycemia by rapidly converting under high [glu] and is activated by insulin

Front 27

describe the regulation of phosphofructokinase-1

Back 27

inhibited by ATP, citrate and acidity; activated by AMP. also strongly activated by small concentrations of F-2,6-BP

Front 28

describe PFK-2

Back 28

a bifunction enzyme with kinase and phosphatase domains, phosphatase active when phosphorylated

Front 29

what is the function of ApoCII

Back 29

activates lipoprotein lipases to digest fatty acid contents of lipoproteins

Front 30

what is the difference in ApoB48 and ApoB100

Back 30

ApoB100 from liver has an extra C terminal domain that is recognized by LDL receptors, can deliver fat to any tissure with these receptors. ApoB48 doesnt, only functions to package fats as chylomicrons

Front 31

what is the function of aldolase B, where is it found?

Back 31

found in liver, is able to cleave F1P into DHAP and GA-3-P, bypasses PFK-1 regulation step and overwhelms normal glycolysis in high [fructose]

Front 32

describe galactose metabolism

Back 32

galactose is converted in UDP-gal -> UDP-glu -> glu-1-phosphate -> glycolysis

Front 33

what is the function and regulation of pyruvate kinase. what does deficiency of thus enzyme lead to clinically?

Back 33

converts PEP to pyruvate, activated by insulin inhibited by glucagon and low [glu] through cAMP/PKA -> phosphorylated form inactive. absence leads to hemolytic anemia

Front 34

describe the transport of fatty acids for B oxidation

Back 34

FFA-/. acyl-CoA in cytosol -> acyl-carnitine in intermembrane space -> mitochondria -> acyl-Coa -> oxidation

Front 35

what are the four steps of B oxidation?

Back 35

oxidation with FADH2, hydroxylation (H20), oxidation to carbonyl (NADH), thiolytic cleavage (CoA)

Front 36

which two metabolic reactions require vitamin B12

Back 36

conversion of propionyl-CoA and as a methyl group carrier in the recycling of FH4 through SAM

Front 37

contrast peroxismal oxidation of FAs to B oxidation

Back 37

in peroxisomes, long chain (>20 C) are oxidized with electrons transferred to O2->H2O2, no ATP produced

Front 38

describe the production of ketone bodies

Back 38

2 Acetyl CoAs -> acetoacetyl-CoA -> HMG CoA -> Acetoacetate + Acetyl CoA. Acetoacetate can be converted into B-hydroxybutyrate with NADH as in AKA

Front 39

what regulator is responsible for blocking synthesis of FAs during B oxidation

Back 39

Malonyl CoA, a FA synthesis intermediate, inhibits the Carnitine shuttle system to keep FAs out of the mitochondria

Front 40

what four metabolites can pyruvate directly be converted into?

Back 40

acetyl-CoA (gives off 1 NADH), OAA (requires 1 ATP), lactate (requires NADH), or alanine

Front 41

what are the products of the TCA cycle?

Back 41

3 NADH, 1 FADH2, 1 GTP, 2 CO2

Front 42

how are FA oxidation and glycolysis cross regulated?

Back 42

the body has a natural preference for FA as an energy source, as citrate is developed in TCA cycle, it will inhibit PFK1 in glycolysis, allowing FA oxidation to be the dominant input to the cycle

Front 43

which TCA intermediate can be shunted into gluconeogenesis

Back 43

oxaloacetate. glucogenic AAs enter TCA cycle at leave at OAA, ketogenic AAs are converted into acetyl CoA (these are not glucogenic because they must combine w/ OAA to enter TCA cycle)

Front 44

what are the membrane soluble electron carriers involved in the ETC?

Back 44

Coenzyme Q and cytochrome C