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MCM mine > MCM Day 2-End > Flashcards

MCM Day 2-End Flashcards

1
Q

which cells carry out glycolysis?

A

all cells

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2
Q

most common fuel for glycolysis

A

fructose and galactose

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3
Q

what is de novo synthesis

A

gluconeogenesis in liver

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4
Q

why can glucose cross membrane so what does it use

A

is polar, needs GLUT

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5
Q

GLUT 1 GLUT2 GLUT3 GLUT4 what is unique about each waht is insulin dependent affinity? regulated?

A

GLUT 1 - ubiquitous but high in RBS;s. high affinity - Glut2 - main transporter in liver - low afinity GLUT3 maintranspoter in neurons - high afinity Glut 4 - present in skelatal muscle heart - adpoose tissue - insulin dependent - only one regulatedf

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6
Q

what type of lipid makes up the lipid rafts

A

cholesterol make up the lipid rafts

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7
Q

where is glut4 sequestered

A

vesicles

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8
Q

what is put in and what are the products of glycolysis

A

1 glucos in 2 molecules pyruvate out generates 2 atp net 2 NADH

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9
Q

what are the 5 steps of glycolysis that are important. what are the enzymes that are used and what are the products

A
  1. Glucose+ATP = glucose 6 phosphate hexokinase/glucokinase (in liver) 3. Fructose6phosphate+atp= fructose 1,6 bisphosphate. pfk1 used. 6. glyceraldehyde 3 phasphate + P +NAD = 1,3 bisphosphoglycerate. G3-P dehydrogenase 7. 1,3 BPG = 3-PG makes ATP phosphoglycerate kinase 10. Phosphenolpyruvate to pytuvate makes atp - pyruvate kinase
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10
Q

3 irriversible phosphoylation steps use which enzymes. eavily influenced by which 2 things. what are the others

A

hexokinase/glucokinase phosphofructokinase-1 (pfk-1) pyruvate kinase insulin and glucagon ATP, AMP, glucose

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11
Q

how is glucokinase different from hexokinase

A

glucokinase - low afinity v max high not inhibited by G6P

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12
Q

what is the rate limiting step and what does it convert to waht? what activates it

A

prk-1. F6P to F1,6BP AMP, F2,6BP PFK2 makes more F26BP. which leads to more PFK1

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13
Q

How does affect does glucagon and insulin have on PFK1

A

High insulin dephosphorylates PFK-2/FBPase-2. makes F2,6BP which activates PFK-1 High glucagon activates protein kinase A, phosphoralates PFK-2/FBPase-2, reduces PFK-1 Activity

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14
Q

How do insulin and glucagon affect pyruvate kinase. what else affects pyruvate kinase and how

A

high insulin causes protine phosphatasewhich activates pyruvate kinase high glucagon increases cAMP, which incrases protin kinase which decreases pyruvte kinase alanine inhibits

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15
Q

what are the fates of glucose-6-phosphate

A

precurosor for Pentose phosphate pathway (becomes ribose and NADPH) glucose pyruvate glycogen

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16
Q

fates of pyruvate, and conditions under why each would happen

A

lactate, when NADH is needed] Oxidized in TCA cycle to Acetyl CoA then CO2 when ATP is needed Alanine for gluconeogenesis fed state or protein synthesis Converted to ethanol. yeast and stuff

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17
Q

What happens to glycolysis when pyruvate kinase is defective

A

causes hemolytic anemia. MOST DISORDERS CAUSE THIS

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18
Q

Why are disorders in glycolsis so detrimental to RBC’s and what are the adverse affects

A

they dont have mitochondia, this is their only source of ATP ATP shortage leads to disruption of ion gradients powered by ATP leads to hemolytic anemia

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19
Q

Why are disorders in glycolsis so detrimental to the brain and what are the adverse affects

A

glucose is the only source of energy that can cross the blood brain barrier brain has to resort to keton bodies or glucose fron liver in starvation

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20
Q

what characterizes diabetes as a whole. what cells are affected to cause diabetes types 1 and 2 what are potentail causes?

A

hyperglycemia characterizes diabetes type one is loss of pancreatic B cells type 2 is loss of funciton of B cells causes: trauma, infections, cancer, all sorts of stuff. mutaions in GK and mitochondrial tRNA leu gens.

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21
Q

what is hemolitic anemia what causes it

A

when there is premature destruction of rbs many things cause it. infections, inhereted defects, nutritional deficeniceis

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22
Q

what disease does a deficient PFK-1 cause what characterizes this

A

Tarui disease least common GSD excersied induced muschle cramps and weakness hymolytic anemia juandice

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23
Q

how much glucose does the body need per day and how much does the brain need. how much available from glycogen

A

160 g per day 120 g for brain 20 present in body fluids 190 availabe from glycogen have enough in store for 1 day

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24
Q

where does gluconeogenisis occur, what are the precurosrs

A

occurs in liver, kidney and small instestine lactate, amino acids and glycerol

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25
Q

what are the steps of gluconeogdenesis and the enzymes it uses to bypas the 3 irrivirsible steps of glycolysis?

A

pyruvate to OAA, uses Pyruvate carboxylase OAA to Posphoenolpyruvate (PEP) uses PEP carboxykinase Fructose 1,6 -BP to Fructos 6-P uses Fructose 1,6-bisphosphatase Gructose 6P to glucose Glucose-6 phosphatase Named for what it sated out as, except the second one

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26
Q

what are the enzymes in glycolosys with their correspoining gluconeogenesis enzymes that get around them

A

hexokinase/glucokinase - Glucose -6 phosphatse PFK1 - fructose1,6- bisphosphatase PK - Phosphoenolpyruvae (PEP) carboxykinase and Pyruvate carboxylase

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27
Q

regulation of of gluconeogenesis first step

A
  1. pyruvate corboxylase (PC) mitochondial enzyme, biotin is cofactor. CO2 dependent.
28
Q

what hepes to gtaet oxaloacatete of of mitochondia

A

converted to malate through malate dehydrogenase, then leaves and converted back

29
Q

rate limiting step of gluconeogenesis, regulation of last step regulation of other step that circumvents irrivirsible step of glycolysis

A

fructos 1,6 bisphosphatase -rate limiting -activates : cortisol and citrate -inhibited: AMP and F26BP Glucose 6-Phosphatase -dephosphoraltion to make glucose -activated by cortisol, only in liver, kidneys, SI and pancreas PEP carboxykinase (CK) - transcription activated by cortisol, glucagon, thyroxine

30
Q

where does glucose 6- phosphatase operate? How does G6P get to the ER

A

in the lumen of the ER G6P transporter

31
Q

Cori Cycle links what to what

A

links lactate from anaerobic glycolysis in RBS and convertes it back to glucose through gluconeogenesis in the liver

32
Q

precursors or gluconeogenesis

A

carbs, lipids, protiens fructose, galactose glycologen, glycerol propionate lactate alanine amino acids

33
Q

Glycerol, propionate, alaine and amino acids are precurors of gluconeogenesis, what are theri sources and points of entry

A

glycerol - source - lipid degredation - enters - DHAP via phosphorylated glycerol intermediate propionate - source is degradation of odd numbered fatty acid - enders - TCA cycle intermediate converted to malate alaine - source, easy enter - pyruvate amino acid - TCA cyle intermeida for amino acid entry

34
Q

Von Gierke disease

A

Dificeincey in glucose 6-phosphatase. can’t regenerate that glucose

35
Q

What are GLUT5 and SGLT1 responsible for what in the blood cell

A

GLUT5 - fru uptake SGLT1 - Gal/Glc Na

36
Q

What is Fanconi-Bickel syndrome, what is it

A

Glut 2 defect. (mutations) cant bring in Glactose, fructose, glucose autosomal recessive disorder fasting hypoglycemia and postprandial hyperglyemia

37
Q

how to get from glucose to fructose

A

glucose reduces to sorbitol by aldose reductase frucose oxidized by sorbitol dehydrogenase.

38
Q

where does sorbitol accumulate

A

kidney lens, retina, schwann cells

39
Q

why can fructose be bad,

A

avoid PFK-1, rate limiting step. converted easily to fat

40
Q

galactosemia what is it

A

deficient in glucose 1p uridyltransferase (GALT) Deficeincy in Galactokinase - accumulation of galactitiol in lense of eye, leads to cataracts in early life

41
Q

What is the purpoose of the PPP. where does it occur? what gets converted to what

A

make sugars for DNA and RNA formation makes NADPH no energy produced occurs in cytosol oxidation of G6P to ribulose 5-P

42
Q

PPP oxidative phase what is being oxidized what is the rate limiting step, what happens with defienceny of the rate limiting enzyme what is regenerated and what is regenerated by?

A

oxidation of G6P G6P dehydrogonase is the rate limiting step. produces NADPH G6P dehydrogenase deficiency causes hemolytic anemia NADPH regenerates gutathionie

43
Q

PPP Oxidative phase 3 steps

A

Oxidation of G6P, to 6-phosphoglucono lactone lactone to 6- phosphogluconate 6-phosphogluconate to ribulose 5P

44
Q

PPP non oxidative whatcha need to know

A

reversible end products shunt to glycolytic, gluconeogenic or nucleotide synthesis pathways

45
Q

When is the PPP needed

A

when there is a high demand for ribose 5P, when cells are rapildy dividing WHen there is a high demand for NADPH - non oxidative producs channeled inot gluconeogenesis for re-entry into PPP

46
Q

branching and links of glycogen non reducing vs reducing end what is glycogenin, what purpose does it serve

A

branching is a-1,4 glycosidic bonds a-1,6 glycosidic bonds for branching non-reducing ends each gontain a terminal glucose with a free hyrdoxly group at carbon 4 reducing end consists of clucose monomer connectd to a protein called glycogenin glycogenin on reducing ends. is primer for more glycogen to be added

47
Q

how and where is glycogen stored

A

liver muscle in granuales. granules also conatin enzymes needed for glycogen metabolism

48
Q

liver glycogen vs muscle glycogen what does this mean in terms of glucagon

A

liver - regulates blook glucose levels muscle - provides resivoir of fule glucose for physical activity glucagon does not act on muscle

49
Q

stargint with glucose, what is the initial pathway to glycogenesis what are the first 3 enzymes

A

glucose to G6P (hexokinase)(glucokinase) G6P to G1P (Phosphoglucomutase) G1P to UDP-Glucose (UDP-glucose prrophosphorylase)

50
Q

Glycogenesis enzyme that elonges

A

glycogen Synthase (GS)(RATE LIMITING)

51
Q

branching enzyme of glycogenesis

A

glucosyl (4:6) transferase

52
Q

two major steps of gycogenolysis 1, shorteing . name of shorteing enzyme cofactor? 2? enzyme used? name of de-branching enzyme

A
  1. glycogen phosphorylase (GP) cofactor-vitamin B6 2. transferer. transferase debranching enzyme is the name
53
Q

ration of glucose and G1P generated

A

10-1

54
Q

Lysosomal glycogenolysis is a thing disease that happens when you cant?

A

small amount. Prompe disease

55
Q

fate of glu1P in liver vs muscle

A

in liver can go back to GLU 6 P suinging glucose 6 phosphatase in muscles cant go to GLU-6-P so it is used in glycolysis and TCA Cycle

56
Q

regulations steps for 1. glucogenesis 2. glycogonlysis what regulates both? when is each activive

A
  1. synthase 2. phosphorylase synthase active when dephosphorylated phosphorylation active when phosphorylation
57
Q

regulation by insulin 4 key proteins involved in signaling cascake

A

Glut4 Protien kinase b (PKB) protein phosphatase 1 (PP1) glocogen synthase Kinase 3 (GSK3) Insulin activates PKB PKB activates PP1 PKB deactivates PP1 activates glycogen synthase, PP1 deactivtes glycogen phosphorylase

58
Q

Type 2 blood levels

A

70-100 normal fed <140 100-125 pre fed >140 125+ diabetus fed >199

59
Q

regulation of glycogenolysis signaling cascade key enzyme and second messengers

A

g Protein adenylate cyclase (AC) and cAMP Protein kinas A (PKA) Prtein phosphotase 1 (PP1) Phosphorylase Kinas (PK) Glucagon to receptor turns on G protein Activates AC which froms cAMP activates PKA phosphorylates GS (inactivating itn phosphroylates PK (activates) PK phosphorylat3es GP

60
Q

GSD 0 enzyme, pathway effected

A

glycogen synthase deffective

61
Q

CORI disease ENzyme pathwaye effected

A

a-1,6, glucosidase (debranching enzyme

62
Q

Andersen disease

A

glucosyl 4:6 transferase branching enzyme

63
Q

McArdle disease

A

glycogen phosphorylase breaking down glycogen

64
Q

Hers Disease

A

liver glycogen phosphorylase

65
Q

way to treat Pompe disease and what is it

A

defect in acid maltase (a-glucosidase) used in lysomal glycogen pathway accumuation of glycogen in lysosomes Enzyme replacement therapy - recombinant human a-glucosidase delivered via intravenous

66
Q

Liver vs muscle glycogen phosphorylase mutations in each cause what disease what does AMP do to both

A

differ in sentsitivites to regultory molecules. mutations in liver cause HErs disease mutaions in muscle cause McArdle synderom Muscle activated by AMP Liver anaffected by AMP

MCM mine (11 decks)

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