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32 Cards in this Set

  • Front
  • Back
Which complex's contain cytochromes, and what oxidation/reduction cofactor do these contain...
...a haeme group
(complex 3 and 4)
Adrenaline stimulates Glycogen metabolism...
...in both muscle and liver
Glucagon just in liver
Phosphorylase kinase activated by
Calcium ions (bind calmodulin)
and...
PKA phosphorylates it - via cAMP cascade
Glycogen synthase is activated by....
dephosphorylation (by PP1 liberated from ....)
Alanine and glutanine major substrates for Gluconeogenesis?
Yep!
Fatty acid oxidation reaction steps (draw it out!)
dehydrogenase (oxidation by FAD)
Hydration
Oxidation - NAD this time
Thiolysis
Patient with liver disease problems?
Jaundice
problems with blood clotting
Severe hypoglycaemia
plasma albumin low
blood ammonia up
Glucogenic and Ketogenic amino acid
Isoleucine
product of transamination reactions of many amino acids
glutamic acid
Body iron store controlled by?
Transported in plasma bound to?
Uptake into cells by?
Intestinal mucosa
transferrin
receptor mediated endocytosis
Glucagon's effect on Glycogen metabolism
Liver affected
Gs (inherant GTPase activity ensures not all glycogen broken down!) to PKA - Phosporylates;
Phosphorylase kinase - activates (which then phosphorylates Glycogen phosphorylase - to a form )
Glycogen synthase a to b form - inactive
Phosphorylates PP1 - inactivates
(also phosphorylates part of Glyc phosphorylase to make susceptible to breakdown by PP1)
Glucose's role in causing Glycogen synthesis switch on
High glucose inhibits Glyc Phosphorylase a, by shifting eqm to T state - has bound PP1, which dephosphorylates to b form, and is thereby released.
PP1 then goes on to dephosphorylate Glycogen synthase - synthesis turned on!
Adrenalines action on liver to increase glycogen metabolism
on alpha receptors - IP3 cascade - increased calcium - activates PK
Difference between M and L isoform of Glycogen phosphorylase
M b form can be allosterically activate by AMP, and inhibited by ATP and G6P (reflects intracellular energy charge)
L a form allosterically inactivated by glucose
Allosteric activator of b form of Glycogen synthase?
G 6 P - very high concs
Glycerol 3 phosphate shuttle?
Mainly in Skele muscle - to maintain high rate of Ox Phos
DHAP reduced to Glycerol3Phos by cytosolic Glycerol 3 phos dehydrogenase
Glycerol3phos oxidised back (giving NADH's electrons to FAD (part of ETC - goes on to release QH2))by inner mito memb bound Glycerol 3 phos dehydrogenase
Von gierke disease?
Swollen abdomen because Liver stuffed with glycogen
Due to G 6 Pase deficiency or lack of transporter into SER
Severe Hypoglycaemia between meals.
McArdle Disease
Lack of Muscle Phosphorylase
Cant do strenuous exercise - need use fats for exercise - evidence for isozymes
Type VIII glycogen metabolism disease
Absense of Phosphorylase kinase
Enlarged liver/abdomen
Hypoglycaemic between meals
Activators + inhibitors of PFK
+ve;
Fructose 2,6 BP AMP
-ve;
ATP, H+, citrate
Because committed step - controlled by energy charge, acid status and number of fat precursors
Why is Gluconeogenesis not exact reverse of glycolysis?
Irreversible steps of Gluconeogenesis (LARGE free energy change)
Gluconeogenesis energy cost? Where used
4 ATP 2 GTP
2 ATP = 2Pyruvate to 2 Oxaloacetate
2 from 3Phosphoglycerate to 1,3Bisphosphoglycerate
Pyruvate carboxylase cofactor?
Biotin with CO2 bound
Why glucose over other monosaccharides?
Low tendency to non-enzymatically glycosylate proteins and therefore deactivate them.
Due to high stability in ring structure
Galactose metabolism
Phosphorylated by ATP,
UDP-glucose added - so to UDP galactose and Glucose 1 phosphate (which can go into Glycolysis pathway)
UDP galactose to UDP glucose by enyzme, keep cycling!
Example of alternative splicing?
L and M isoform of bifunctional enzyme of Glycolysis - PFK2 and F-2,6-BPase
Galactosaemia
Cant catalyse (enzyme lack);
Galactose 1 phos + UDP glucose to UDP Galactose + Glucose 1 phosphate
Pyruvate dehydrogenase
Very important regulatory step of pyruvate metabolism.
Enzyme has 3 activities;
Pyruvate dehydrogenase (TPP)
Dihydrolipoamide acetyltransferase (Lipoic acid)
Dihydrolipoamide Dehydrogenase (FAD - regenerated by NAD)
Importance of Pentose Phosphate pathway
Need to create NADPH for synthesis, and for glutathione reduction - this important to detoxify H2O2 (strong oxidiser) - otherwise in RBCs it oxidises Hb and prevents O2 carrying capacity.
CE G6PD deficiency - haemolytic anaemia following fava beans/ox. drugs - Hb oxidatively damaged and then these cells containing it are destroyed by spleen.
MCAD deficiency
Fasting Hypoglycaemia
No ketosis on fasting
Seizure coma death
Give alternative energy source
LCAD deficiency
Similar to carnitine deficiency;
skeletal muscle weakness
fatty infiltration of organs
Insulins effects on fat metabolism
Insulin (vs glucagon) stimulates AcCoA carboxlase, via enzyme phosphorylation state (?)
-FA synthesis committed step
ALSO Insulin increases PP pathway to provide NADPH