Dietary Carbohydrates I

Front 1

What are dietary carbohydrates?

Back 1

Starch and glycogen

Front 2

Salivary α-amylase

Back 2

Secreted by the salivary glands in the mouth
Only hydrolyzes Internal α-1,4 bonds
Producing di & tri saccharides as well as starch α-dextrins
Action is stopped in stomach

Front 3

Pancreatic α-amylase

Back 3

Secreted in the SI by pancreas
Continues the digestion of dextrins to Maltose & Isomaltose (oligo, tri, di)
Secreted with bicarbonate

Front 4

Enzymes on the brush border of SI

Back 4

Maltase, Iso-maltase, Sucrase & Lactase
Digest the oligo-, tri & di and generate mono-saccharides

Front 5

Enyzme Maltase

Back 5

Breaks down maltose into two glucose molecules

Front 6

Enzyme Isomaltase

Back 6

Uses a α-1,6 glucosidase to break the α-1,6 glycosidic bond

Front 7

Enzyme Sucrase

Back 7

Breaks sucrose down to Glucose and Fructose

Front 8

Enzyme Lactase

Back 8

Breakse lactose down into a Galactose and Glucose

Front 9

Why is cellulose (dietary fiber) not able to be broken down?

Back 9

Because the β-1,4 glycosidic bond is not able to be broken down by the enzyme and passes through

Front 10

How are fructose, Galactose and Glucosd transported after digestion from the SI?

Back 10

By GLUT transporters which are facilitated transporters DO NOT require energy

Front 11

GLUT-1

Back 11

Importatnt for RBC but used in all tissues
Constitutive
LOW Km; Transport prefenentially; High Affinity
Dependent on the concentration on luminal side

Front 12

GLUT-2

Back 12

HIGH Km; Low affinity assures glucose rapidly enters liver in times of plenty
Liver, Pancreatic β cells
Only absorb glucose when there is a high plasma conc.
Participates in INSULIN SECRETION, b/c insulin signals the need to remove glucose from blood

Front 13

GLUT-3

Back 13

Brain, Placenta, Fetal Muscle
Low Km; High Affinity
Constant rate of glucose supplyed to Brain

Front 14

GLUT-4

Back 14

Skeletal/Heart Muscle, Adipocytes
Lower Km (~5)
INSULIN DEPENDENT (Induced)
Mediates insulin-stimulated glucose uptake
Run by INTRAcellular signals
Default in this can result in INSULIN RESISTANCE
Vmax is proportional # of transporters which is dependent on amt. of insulin

Front 15

GLUT-5

Back 15

FRUCTOSE facilitated transport
Small Intestine
Lower Km (~5)
Located on both luminal and baselateral side

Front 16

SGLT-1

Back 16

Na+-Glucose co transport
Intestine (duodenum, jejunum), Kidney
Na+ dependent
Symporter; both Na+ and glucose/galactose move in same direction
Na+ must be reused and transported back out by Na+/K+ ATPase which uses energy

Front 17

What is glycolysis?

Back 17

Degradation of 1 glucose to 2 pyruvates
10 rxns
2 parts
2 ATP consumed
4 ATP & 2 NADH Generated
2 ATP net gain

Front 18

Energy Investing Phase (Steps 1-5)

Back 18

Glucose > 2 Glyceraldehyde-3-Phosphate (G-3-P)
Consume 2 ATP

Front 19

Glycolysis Step 1

Back 19

Addtion of a phosphate
Makes Glucose-6-Phosphate
Uses ATP
Non-reversible

Front 20

Glycolysis Step 2

Back 20

Isomerization = rearrangement
Turns Glucose-6-Phosphate into Fructose-6-Phosphate

Front 21

Glycolysis Step 3

Back 21

Addition of 2nd Phosphase
Phosphofructokinase I
Fructose-6-P to Fructose-1,6-bisphosphate
Uses ATP non-reversible

Front 22

Glycolysis Step 4

Back 22

Aldolase cleaves/splits Fructose-1,6-Bisphosphate to two 3-C molecules; Glyceraldehyde-3-Phosphate (G-3-P)/Dihydroxyacetone Phosphate

Front 23

Glycolysis Step 5

Back 23

Isomerization between 2 molecules

Front 24

Glycolysis Energy Generation Phase (Phase II)

Back 24

G-3-P > Pyruvate
4 ATP Produces
2 Nadh

Front 25

Glycolysis Step 6

Back 25

Removal of Hydrogen & addition of Phophate per G-3-P
Forming 2 NADH
And makes 1,3-bisphosphoglycerate

Front 26

Glycolysis Step 7

Back 26

Phosphoglycerate Kinase Phosphorylates to generate 2 ATP or ADP respectively
Makes 3-phosphoglycerate

Front 27

Glycolysis Step 8 (9)

Back 27

Rearangement of P from 3rd C to 2nd C by Mutase makes 2-Phosphglycerate

Front 28

Glycolysis Step 9 (8)

Back 28

Makes PEP by Enolase and generation of super highway energy compound (and water)

Front 29

Glycolysis Step 10

Back 29

Removal of P to generate 2 ATP and 2 Pyruvate

Front 30

Substrate level phosphorylation

Back 30

ATO generated in the cytosol

Front 31

Hexokinase

Back 31

All tissues
Constitutive glycolysis regulation
Very Low Km
Inhibited by its product G-6-P
High conc. signals that cell does NOT need glucose and it is left in the blood

Front 32

Glucokinase

Back 32

Liver
Inhibited by Fructose-6-Kinase
Isoenzyme of hexokinase
INDUCIBLE by insulin; only active under high Glucose levels
Provides G-6-P for synthesis of glycogen
Usually coupled with GLUT-2

Front 33

PFK-1

Back 33

Key enzyme in Glycolysis regulation at Step 3
PFK is the rate-limiting enzyme in all tissues
Allosteric Inhibitors: ATP, Citrate
Allosteric Activators: AMP, F-2,6-P

Front 34

What regulates Production of F-6-P?

Back 34

PFK-2 and F-2,6-Pase and therefore regulate PFK-1

Front 35

F-2,6-P

Back 35

In Liver regulates Glycolysis and gluconeogenesis
Adipose regulates glycolysis

Front 36

Pyruvate Kinase

Back 36

Regulates at 10th step
Turns PEP to Pyruvate
Allosteric Inhibitors: ATP, Alanine
Allosteric Activators: F-1,6-P
Hormonal Induced by insulin dephorphrylation (MORE active)

Front 37

Alanine Generation (Pyruvate)

Back 37

Via Alaine Aminotransferase
Connect to protein synthesis

Front 38

Oxaloacetate Generation (Pyruvate)

Back 38

Via Pyruvate Carboxylase
Carboxylation rxn for gluconeogenesis

Front 39

Lactate Generation (Pyruvate)

Back 39

Via Lacate Dehydrogenase
During Anaerobic Conditions
Reduces NADH to NAD+
Can be reversably oxidized to pyruvate via Cori Cycle requires 6 ATP (net loss 2)

Front 40

Acetyl CoA Generation (Pyruvate)

Back 40

Via Pyruvate Dehydrogenase
Condition: Mitochondria, low: ATP:ADP
Pyruvate transported into mitchondira via Anti-Porter
Decarboxylated generating CO2
Acetyl CoA eneter TCA for formation of reducing equivalents

Front 41

Whats happens and why under anaerobic conditions in Glycolysis?

Back 41

Either due to lack of mitochondria or limited O2
Pyruvate is reduced to lactate in cytosol (via LDH)
Utilizing the reducing equivilants in NADH
2 ATP generated for every 1 glucose degrading into 2 lactate

Front 42

What happens to lactate in skeletal muscle?

Back 42

Will be oxidized back to pyruvate and used for different pathways

Front 43

What can happen to Lactate through the Cori Cycle?

Back 43

Can be translocated to the liver where it is converted to glucose.
6 ATP are needed for synthesis of glucose here resulting in a net lose

Front 44

What happens to Pyruvate under aerobic conditions?

Back 44

Enters mitchondira via antiporter MONOCARBOXYLATE with exchange of OH-
Decarboxylated in acetyl-CoA catalyzed by PDH
This is ultiately oxidized to CO2 and H20 through TCA with generation of ATP

Front 45

Regulatio of TCA

Back 45

Can only go as fast as electrons from NADH FADH2 enter
Rate is adjusted to the rate of Oxidative Phosphorylation
Thus it is controled by the ratios of ATP/ADP and NADH/NAD+

Front 46

Citrate Synthase E1

Back 46

Regulatory Enzyme TCA
Regulates Acetyl CoA > Citrate
Inhibited: Citrate, Succinyl CoA
Activated: Ocaloacteate, Acetyl CoA

Front 47

Isocitrate Dehydrogenase E3

Back 47

Regulatory Enzyme TCA
Regulates: Isocitrate > α-Ketoglutarate
Inhibitited: NADH
Activated: ADP, Ca2+

Front 48

α-Ketoglutarate Dehydrongenase E4

Back 48

Regulatory Enzyme TCA
Regulates: α-Ketoglutarte > Succinyl CoA
Inhibited: NADH, Succinyl CoA, GTP
Activated: ADP, Ca2+

Front 49

Overall from TCA Cycle

Back 49

Oxidation of Acetyl CoA generates 10 ATP
3 x NAD+ > NADH (3 x 2.5 = 7.5)
1 x FAD > FADH2 (1 x 1.5 = 1.5)
1 x high energy CoA > GTP =ATP