Flashcards in Midterm 2 Deck (22):
Where does glycolysis take place?
- aerobic: cardiac muscle, brain, liver
- anaerobic: RBC, muscle
How is glycolysis regulated?
+ F, 2-6 P, AMP
- ATP, citrate, H
+ F, 1-6 P
- ATP, alanine
Energy Production of glycolysis
glucose -> glucose-6-P = -1 ATP
fructose -> fructose 1-6 PP = -1 ATP
1,3 bisphosphofructose (x2) -> 3PG = +1 ATP
PEP -> pyruvate (x2) = +1 ATP
net = +2 ATP
Where does glyconeogenesis take place?
- liver (kidney, especially in prolonged
How is glyconeogenesis regulated?
+ acetyl CoA
Fructose, 1-6 P
+ ATP, citrate
What is gluconeogenesis?
Gluconeogenesis is the synthesis of
glucose/ glycogen by non-carbohydrate
precursors (lactate, glycerol, amino acids
and in Ru propionate)
Energy Balance of GNG?
2 lactate + 7 ATP -> 1 glucose unit + 7 ADP
Amino acids of GNG?
Almost all amino acids are glucogenic (except leucine)
Alanine -> pyruvate
Glutamic acid -> alpha-keto glutarate
Aspartic acid -> oxaloacetate
Hormonal control of GNG?
-Glucagon: +GNG - Stimulates mobilisation of aa. in muscle. Stimulates uptake of aa in the liver. Raises cAMP levels in adipose cells.
-Glucocorticoids: + GNG - Favours synthesis of glucose by aa.
-Insulin: -GNG - Antagonist of glucagon.
Oxidation of pyruvate to AcCoA
1.What kind of reaction is it?
2.Where does it happen?
4.What does it require?
3.Pyruvate + HSCoA + NAD+ -> AcCoA + CO2 + NADH + H+
4.Requires the pyruvate dehydrogenase complex:
-Enzymes: pyruvate decarboxylase, dihydrolipyl transacetone, dihydrolipoic acid dehydrogenase
-Cofactors: thiamine (TPP), pantothenic acid (HSCoA), nicotinic acid (NAD+), riboflavin (FAD), lipoic acid
5.Pyruvate dehydrogenase complex is inhibited by ATP.
Citric acid cycle
1.Another word for it?
1.Tricarboxylic acid cycle
2.Mitochondrial matrix (not in RBCs)
3.3NADH + H + = 9 ATP
1FADH2 = 2 ATP
= 12ATP x 2 = 24 ATP
4.Citrate synthase: + ADP, NAD, - ATP, NADH, Isocitrate dehydrogenase: - ADP, NADH, Succinate dehydrogenase: + succinate, - oxaloacetate
THE RESPIRATORY CHAIN
1.What is it?
1.A series of e- carriers which are red. and ox. The released E can be used to form ATP via ox.ppr.
2. inner membrane of mitochondria
Steps of resp.chain
1.From the glycerol phosphate shuttle NADH+H+ is
ox. to NAD+ by substrate dehydrogenase
2.The 2 e- generated are used to red. the FMN -> FMNH2 by NADH dehydrogenase in the Fe-S complex 1 (4H+)
3.The e- are transferred to coQ. Oxidised = ubiquinone, reduced = coQ.
4.Between CoQ and oxygen are the cytochromes which are e- carrying proteins that contain a haem prosthetic
group. The iron atom in the haem alternates between a
red. Fe2+ and ox. Fe3+ state.
5-8: -CoQ —Fe3+ -> Fe2+ —>cytochrome B (Complex III)
-cytochrome B —Fe2+ -> Fe3+ —> cytochrome C
-cytochrome C —Fe3+ -> Fe2+ —cytochrome a + a3 (Cu2+
-cytochrome a + a3 is reoxidised by O2 and prod. H2O
3.What does it do?
4.Role of NADH + H+ and FADH2
5.What is the net result?
1.inner membrane of mitochondria
2.to generate ATP
3.Generates a proton gradient across the inner mitochondrial membr. Once established, the protons will flow through the ATPase complex back into the mitochondrial matrix. As they lose E, this E is utilised by the ATPase complex to phosphorylase and therefore generate ATP (11 molecules).
4.serve as H/e- donors and cofactors for the protein complexes in the electron transport chain.
5.an influx of protons into the inter membranous
Uncouplers of ox.ppr?
Protons pumped out are carried by the uncoupler back to the matrix preventing a pH/ electrical gradient.
-Thermogenin: in brown adipose tissue of newborns and hibernating mammals. Stimulates resp. and heat prod. (non-shivering thermogenesis).
-Dinitrophenol: a yellow toxin that affects cattle
1.Why do we have it?
2.What does it do?
3.What catalyses it?
1.Aa can´t be stored by the body, so a surplus is degraded and excreted as urea, while their carbon skeletons are converted into major metabolic
2.Ultimately all amino groups are collected by alpha-keto
glutarate yielding glutamate. Glutamate enters the
A. It is deaminated by L-glutamate dehydrogenase or
B. Its amino group is transferred to oxaloacetate to yield
1.What is it?
1.The alpha-amino groups from the aa. end up as the amine group of L-glutamate. Glutamate undergoes oxidative deamination by mitochondrial L-glutamate
2.+ ATP, GTP, - ADP, GDP
THE UREA CYCLE
1.only in the liver. Mitochondria until citrulline leaves to the cytosol
2.carbamoyl phosphate synthetase + N-acetyl glutamate
3.CO2 + NH3 + 3ATP + 2H2O -> urea + 2ADP + 2Pi
+ AMP + PP
2.What is it?
2.the breakdown of fats and other lipids by hydrolysis to release fa.
What is adenylate cyclase in the lipolysis, how is it activated and what does it cause?
Catalyses the synthesis of cAMP.
Activated when adrenaline, noradenaline, glucagon or ACTH bind to receptors on the cell membr. cAMP activates protein kinase A which activates after a cascade of reactions hormone-sensitive lipase.
1.cytoplasm and adipose tissue, liver, mammary gland