Glycolysis I&ii

Front 1

Starch/Glycogen

Back 1

attached by I, 4 links and 1,6 every 10
broken down by alpha amylase into maltose, isomaltose (1,6), and maltotriose

Front 2

lactose to glucose

Back 2

lactase

Front 3

starch to glucose

Back 3

amylase and then alpha glucosidases

Front 4

sucrose to glucose

Back 4

sucrase makes glucose and fructose

Front 5

Fructose

Back 5

gets in passively by GluT5 and GluT2

Front 6

SGLT-1

Back 6

sodium glucose transporter

Hint 6

helps get in glucose and galactose
energy by Na/K pump

Front 7

GluT-2

Back 7

passive capillary movement of all three sugars

Front 8

SGLT-1 deficiency

Back 8

impaired glucose and galactose absorbtion

Front 9

Step 1
Glucose to
GLU

Back 9

glucose 6 phosphate G6P
by(2)

Hint 9

hexokinase+ATP

Front 10

Step2
Glucose 6 Phosphate G6P to

Back 10

Fructose 6 Phosphate F6P
by

Hint 10

phosphoglucose isomerase PG isomerase

Front 11

Step3
Fructose 6 Phosphate (F6P)
to

Back 11

fructose 1,6 bisphosphate (F16BP)
by(2)

Hint 11

6-phosphofructokinase (PFK!!) and ATP
rate limiting

Front 12

Step4
fructose 1 6 bisphosphate to (2)

Back 12

dihydroxyacetone phosphate(DAP)
&
Glyceraldehyde 3 phosphate (G3P)
by

Hint 12

fructose bisphosphate aldolase FBA

Front 13

Conversion step
dihydroxyacetone phosphate DAP to

Back 13

Glyceraldehyde 3 Phospate (G3P)
by

Hint 13

triose phosphate isomerase (TPI)

Front 14

Step 5
Glyceraldehyde 3 Phosphate G3P to

Back 14

1,3 Bisphosphglycerate(13BP)
by

Hint 14

glyceraldehyde 3 phosphate dehydrogenase (G3PDe)

Front 15

Step 6
1,3 bisphosphoglycerate 13BP to

Back 15

3 phosphoglycerate (3PG)
by

Hint 15

phosphoglycerate kinase (produces ATP)

Front 16

Step 7
3 phosphoglycerate (3PG) to

Back 16

2 phosphoglycerate (2PG)
by

Hint 16

phosphoglycerate mutase

Front 17

Step 8
2 phosphoglycerate (2PG) to

Back 17

phosphoenolpyruvate (PEP!!)
and H20
by

Hint 17

enolase

Front 18

Step 9
phosphoenolpyruvate (PEP) to

Back 18

pyruvate
by(2)

Hint 18

pyruvate kinase and ADP (produces ATP)

Front 19

Cleanup step
pyruvate to

Back 19

lactate
by(2)

Hint 19

lactate dehydrogenase and NADH

Front 20

Regulation of Glycolysis (4)

Back 20

Glucose Transporters
Glucose Phosphorylation
PFK rate limiter
Pyruvate Kinase

Hint 20

PFK PFK PFK

Front 21

Glucose transporter reg

Back 21

Glut4 in muscle is upregulate to cell membrane by insulin

Front 22

Glucose phos regulation(hexokinase)

Back 22

hexokinase is immediately limited by its product G6P-negative feedback
if G6P backs up because PFK is off then it will stop hexokinase from using glucose

Front 23

glucose phos reg (glucokinase)

Back 23

lower affinity for glucose than hexokinase
in liver
higher saturation rate
induced by insulin

Hint 23

F6P turns it off F1P turns it on

Front 24

PFK regulators

Back 24

allosteric inhibitors ATP citrate protons
activators cAMP F26BP
F26BP?

Hint 24

glucagon turns on cAMP which decreases F26BP which decreases glycolysis

Front 25

F26BP regulation

Back 25

dual kinase phosphatase mech
F6P to F26BP by kinase
F26BP to F6P by phosphatase

Front 26

dual kinase phosphatase gene

Back 26

on same peptide, one goes down the other goes up
reg?

Hint 26

glucagon and epinephrine turns off the kinase and thus F26BP by phosphorylating the phosphorylator which increases phosphatase

Insulin increases kinase activity by dephozsing the enzyme and increases F26BP and increasing glycolysis

Front 27

dual kinase F26BP reg in muscles

Back 27

epinephrine seems to stimulate F26BP in muscles is BACKWARDS than the one in the liver
thus by phozsing the dual enzyme by PKA it decreases phosphatase activity and increases F26BP, increasing glycolysis

Hint 27

SO...epinephrine phos both dual enzymes in muscle and liver...
in liver it increases phosphatase which lowers F26BP
in muscle it increases kinase which increases F26BP

Front 28

Pyruvate kinase regulation

Back 28

in liver and muscle it is inhibited by ATP and alanine
in LIVER PK is phozsed by PKA when blood sugar is low. When cAMP is high PKA removes the phosphate and activates pyruvate kinase

Hint 28

LIVER high blood sugar pyruvate kinase is dephozed.

Front 29

RBCs and 2,3BPG

Back 29

RBCs need 2,3BPG to make Oxygen bind
so they take it out of pathway by 1,3BPG with

Hint 29

2,3 BPG mutase and bring it back with 2,3 BPG phosphatase to 3PG but this skips an ATP!!!

Front 30

Fructose entry

Back 30

fructose---F1P by fructokinase
then

Hint 30

F1P to DAP and glyceraldehyde by aldolase B
ten triose kinase makes G3P

Front 31

Galactose entry (2)

Back 31

Galactose to galactose 1 phospate by kinase
then Galactose 1 phosphate gets transferred to UDP and phosphate goes to glucose

Hint 31

the UDP galactose goes to UDP glucose by epimerase and then it continues

glucose 1 phosphate goes to glucose 6 phospate by phosphoglucomutase

Front 32

Glycerol entry

Back 32

glycerol kinase makes glycerol phosphate
glycerol phosphate DH make DAP

Front 33

Disorder in Hexose metabolism (5)

Back 33

Anemia
Warburg Phenomenon
Deficiency in galactokinase and or galactose transferase (uridyl)
Fructose Intolerance
Fructose Toxicity

Front 34

Anemia

Back 34

due to pyruvate kinase deficiency

Front 35

Warburg Phenomenon

Back 35

Tumors like glucose because of low blood supply
Hypoxia inducible factor activates glycolytic enzymes
target for cancer therapy

Front 36

Galactokinase/ transferase actvity deficiency

Back 36

galactokinase deficiency leads to a build up of galactose. galactosemia
aldose reductase converts it galactitol and can cause cataracts
deficiencies in uridyl transferase will cause build up of galactose Galactose 1 phosphate really bad mental damage

Front 37

Fructose intolerance

Back 37

no fructokinase (harmless because other tissues can metabolize fructose)
aldolase B deficiency- more serious accumulation of fructose 1 phosphate ties up inorganic phosphates. Gout. it promotes glycolysis in liver. liver damage

Front 38

Fructose toxicity

Back 38

ingestion of large amounts of fructose
you bypass PFK-1 lots of it goes to fat.
still accumulates like aldolase B deficiencies--increased glycolysis of glucose from sucrose and fat conversion