Академический Документы
Профессиональный Документы
Культура Документы
LACTOSE: beta-Galactose-1,4-Glucose.
1. It is a disaccharide of glucose and galactose.
2. It is considered a reducing sugar because it still has the free
aldehyde group on C1 of glucose.
3. It hooks from the 1-carbon of galactose to the 4-carbon of
glucose.
SUCROSE: alpha-Glucosyl-1,2-beta-Fructose
1. A disaccharide of glucose and fructose.
Return to top
GLYCOLYSIS / FERMENTATION
1. Catalyzed by Glyceraldehyde-3-Phosphate
Dehydrogenase.
2. An aldehyde is oxidized to a carboxylic acid.
3. An inorganic phosphate group is attached.
4. NAD+ ------> NADH -- It is a redox reaction, coupled to
reduction of NAD+ to NADH.
5. The product is a an "acyl phosphate" -- a type of
anhydride. It has very high phosphorylation potential.
2. 1,3-bisphosphoglycerate + ADP ------> 3Phosphoglycerate + ATP
1. Reaction is "coupled" with #6. Bisphosphoglycerate is the
common intermediate.
2. Produces *two* ATP per original glucose. This is the
BREAK-EVEN POINT. We have recovered our original
investment.
3. Very exergonic (DeltaG is even more negative than that
required for ADP ------> ATP). The product is quite stable.
4. Remember that 1,3-bisphosphoglycerate is a powerful
phosphorylating agent.
5. Catalyzed by phosphoglycerate kinase.
6. This is referred to as substrate-level phosphorylation,
via a coupled reaction with #6, as opposed to oxidative
phosphorylation, via electron transport gradients.
1. Or, it is just a direct transfer of phosphate from one
compound to another.
3. 3-Phosphoglycerate ------> 2-Phosphoglycerate. Simple
isomerization.
1. Catalyzed by phosphoglycerate mutase.
REDUCTION
DESCRIPTION
Quinone ------>
Hydroquinone
Coenzyme-Q contains
the quinone group. THIS IS
THE MIDDLE STEP, WHERE
FADH2 IS ADDED IF
PRESENT
Hydroquinone ------>
Quinone
energy and give it off as heat rather than make ATP), except it
has terrible side effects -- severe cataracts.
3. Thyroxine = the body's natural uncoupling agent. Thyroxine is
released in response to cold temperature to raise body
temperature by acting as an uncoupler in the electrontransport chain.
PYRUVATE DEHYDROGENASE + THE TRICARBOXYLIC ACID CYCLE
ATP Value
Enzymatic Reaction
2 NADH
6 ATP
Glyceraldehyde-3-Phosphate
Dehydrogenase (glycolysis)
2 ATP
2 ATP
1 NADH
3 ATP
1 NADH
3 ATP
1 NADH
3 ATP
1 FADH2
2 ATP
1 GTP
1 ATP
TOTAL:
ACETYL-COA:
1. Acetyl-CoA cannot lead to sugar.
2. Sources of Acetyl-CoA
1. Glucose (via pyruvate)
2. Fats (via beta-Oxidation)
3. Proteins
3. Fates of Acetyl-CoA
1. TCA Cycle
2. Fatty Acid / Sterol Synthesis
3. Ketone Bodies
STEPS OF THE TRICARBOXYLIC ACID CYCLE
1. STEP I: Acetyl-CoA + Oxaloacetate ------>
Citrate + CoEnzyme-A -- THE COMMITTED STEP
1. (2C + 4C ------> 6C)
2. Condensation reaction.
3. ENZYME: Citrate Synthase.
4. INTERMEDIATE: Citroyl-CoA, which does not detach from
enzyme. Then, CoA comes off to yield Citrate + CoA.
5. CoA has the thioester linkage with high free-energy of
hydrolysis. This makes the forward reaction favored and
drives essentially the whole process.
6. CoA is then recycled back to the Oxidative
Decarboxylation system.
7. Equilibrium in this reaction very much favors citrate.
1. It takes the first glucose from activated UDPGlucose, releasing UDP (just like the synthase).
2. Glycogenin then dissociates from the growing
glycogen molecule after a few residues have been
put on.
REGULATION OF GLYCOGENESIS: Phosphorylation turns off the system.
1. TWO FORMS OF THE GLYCOGEN SYNTHASE ENZYME: ACTIVE
AND INACTIVE.
1. GLYCOGEN-SYNTHASE A: ACTIVE FORM. It
is dephosphorylated.
2. GLYCOGEN-SYNTHASE B: INACTIVE FORM. It
is phosphorylated.
1. Glucose-6-Phosphate stimulates Glycogensynthase-B to some extent. A surplus of G-6-P
indicates that glycogenesis should take place.
2. INHIBITORY EFFECTS /
PHOSPHORYLATION: Epinephrine and/or Glucagon are
secreted at times of low blood sugar or when we need cellular
energy. They cause a phosphorylation cascade.
1. cAMP, DAG, and Ca+2 (i.e. beta-adrenergic secondary
messengers) all shut off glycogen synthase by promoting
the phosphorylated form of the enzyme. There are two
mechanisms:
1. Direct phosphorylation of glycogen synthase itself,
thereby inactivating it.
2. Phosphorylation of Inhibitor-1 a ------>
phosphorylate (inhibit) the phosphatase ------>
glycogen synthase remains phosphorylated and
hence inactive.
3. STIMULATORY EFFECTS /
DEPHOSPHORYLATION: Glucose stimulates the production of
glycogen.
1. Glucose inhibits Glycogen Phosphorylase-A and the
phosphoprotein phosphatase, as noted above.
1. Phosphorylase-A inactivates Glycogen
Synthase. It is therefore necessary to inactivate
the phosphorylase before we can make glycogen.
2. Glucose therefore stimulates glycogen
synthesis by inhibiting glycogenolysis.
2. Glucose also stimulates Phosphoprotein
Phosphatase.
1. Phosphoprotein Phosphatase itself promotes
glycogen synthesis. It promotes the
dephosphorylated (active) form of Glycogen
Synthase.
INSULIN:
1. It acts by an autophosphorylating tyrosine-kinase receptor
protein.
2. It is generally anabolic: it promotes glycogen synthesis and
inhibits glycogenolysis.
3. It is secreted when glucose levels in the blood are high, and it
promotes uptake of glucose by most cells.
4. It does not affect glucose-uptake by liver cells, because the
liver can uptake as much glucose as it wants by facilitated
transport. Liver absorption of glucose is independent of insulin
levels.
OVERALL ENERGETICS OF GLYCOGEN:
OVERALL PURPOSE:
1. It produces 2NADPH, which is used instead of NADH in most
biosynthetic pathways. This is the primary (perhaps only?)
source of NADPH in metabolism.
REGULATION OF GLUCONEOGENESIS:
1. Positive Effectors: Generally things that indicate a surplus of
energy.
1. ATP
2. Acetyl-CoA
3. Citrate
2. Negative Effectors: Generally things that indicate a lack of
energy, as well as glycolytic intermediates.
1. AMP
2. Fructose-1,6-biphosphate or Fructose-2,6-biphosphate
3. Inorganic phosphate
NTERCONVERSION OF SUGARS / OLIGOSACCHARIDES / GLYCOPROTEINS