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MCM mine > MCM Day 2-End > Flashcards

MCM Day 2-End Flashcards

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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
what are the steps of gluconeogdenesis and the enzymes it uses to bypas the 3 irrivirsible steps of glycolysis?
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
26
what are the enzymes in glycolosys with their correspoining gluconeogenesis enzymes that get around them
hexokinase/glucokinase - Glucose -6 phosphatse PFK1 - fructose1,6- bisphosphatase PK - Phosphoenolpyruvae (PEP) carboxykinase and Pyruvate carboxylase
27
regulation of of gluconeogenesis first step
1. pyruvate corboxylase (PC) mitochondial enzyme, biotin is cofactor. CO2 dependent.
28
what hepes to gtaet oxaloacatete of of mitochondia
converted to malate through malate dehydrogenase, then leaves and converted back
29
rate limiting step of gluconeogenesis, regulation of last step regulation of other step that circumvents irrivirsible step of glycolysis
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
where does glucose 6- phosphatase operate? How does G6P get to the ER
in the lumen of the ER G6P transporter
31
Cori Cycle links what to what
links lactate from anaerobic glycolysis in RBS and convertes it back to glucose through gluconeogenesis in the liver
32
precursors or gluconeogenesis
carbs, lipids, protiens fructose, galactose glycologen, glycerol propionate lactate alanine amino acids
33
Glycerol, propionate, alaine and amino acids are precurors of gluconeogenesis, what are theri sources and points of entry
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
Von Gierke disease
Dificeincey in glucose 6-phosphatase. can't regenerate that glucose
35
What are GLUT5 and SGLT1 responsible for what in the blood cell
GLUT5 - fru uptake SGLT1 - Gal/Glc Na
36
What is Fanconi-Bickel syndrome, what is it
Glut 2 defect. (mutations) cant bring in Glactose, fructose, glucose autosomal recessive disorder fasting hypoglycemia and postprandial hyperglyemia
37
how to get from glucose to fructose
glucose reduces to sorbitol by aldose reductase frucose oxidized by sorbitol dehydrogenase.
38
where does sorbitol accumulate
kidney lens, retina, schwann cells
39
why can fructose be bad,
avoid PFK-1, rate limiting step. converted easily to fat
40
galactosemia what is it
deficient in glucose 1p uridyltransferase (GALT) Deficeincy in Galactokinase - accumulation of galactitiol in lense of eye, leads to cataracts in early life
41
What is the purpoose of the PPP. where does it occur? what gets converted to what
make sugars for DNA and RNA formation makes NADPH no energy produced occurs in cytosol oxidation of G6P to ribulose 5-P
42
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?
oxidation of G6P G6P dehydrogonase is the rate limiting step. produces NADPH G6P dehydrogenase deficiency causes hemolytic anemia NADPH regenerates gutathionie
43
PPP Oxidative phase 3 steps
Oxidation of G6P, to 6-phosphoglucono lactone lactone to 6- phosphogluconate 6-phosphogluconate to ribulose 5P
44
PPP non oxidative whatcha need to know
reversible end products shunt to glycolytic, gluconeogenic or nucleotide synthesis pathways
45
When is the PPP needed
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
branching and links of glycogen non reducing vs reducing end what is glycogenin, what purpose does it serve
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
how and where is glycogen stored
liver muscle in granuales. granules also conatin enzymes needed for glycogen metabolism
48
liver glycogen vs muscle glycogen what does this mean in terms of glucagon
liver - regulates blook glucose levels muscle - provides resivoir of fule glucose for physical activity glucagon does not act on muscle
49
stargint with glucose, what is the initial pathway to glycogenesis what are the first 3 enzymes
glucose to G6P (hexokinase)(glucokinase) G6P to G1P (Phosphoglucomutase) G1P to UDP-Glucose (UDP-glucose prrophosphorylase)
50
Glycogenesis enzyme that elonges
glycogen Synthase (GS)(RATE LIMITING)
51
branching enzyme of glycogenesis
glucosyl (4:6) transferase
52
two major steps of gycogenolysis 1, shorteing . name of shorteing enzyme cofactor? 2? enzyme used? name of de-branching enzyme
1. glycogen phosphorylase (GP) cofactor-vitamin B6 2. transferer. transferase debranching enzyme is the name
53
ration of glucose and G1P generated
10-1
54
Lysosomal glycogenolysis is a thing disease that happens when you cant?
small amount. Prompe disease
55
fate of glu1P in liver vs muscle
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
regulations steps for 1. glucogenesis 2. glycogonlysis what regulates both? when is each activive
1. synthase 2. phosphorylase synthase active when dephosphorylated phosphorylation active when phosphorylation
57
regulation by insulin 4 key proteins involved in signaling cascake
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
Type 2 blood levels
70-100 normal fed \<140 100-125 pre fed \>140 125+ diabetus fed \>199
59
regulation of glycogenolysis signaling cascade key enzyme and second messengers
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
GSD 0 enzyme, pathway effected
glycogen synthase deffective
61
CORI disease ENzyme pathwaye effected
a-1,6, glucosidase (debranching enzyme
62
Andersen disease
glucosyl 4:6 transferase branching enzyme
63
McArdle disease
glycogen phosphorylase breaking down glycogen
64
Hers Disease
liver glycogen phosphorylase
65
way to treat Pompe disease and what is it
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
Liver vs muscle glycogen phosphorylase mutations in each cause what disease what does AMP do to both
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

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