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24 Cards in this Set

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Partitioning of glycolysis and glyconeogenesis is
during exercise
Glycogen metabolism
oops
glyconeogenesis
how non-carbonhydrate goes back to glucose, pyruvate back to glucose. Primarily in liver and important during extendded exercise ,fasting and not a simple reversal of glycosis
3 irreversiable replaced by 4 step

Fructose 1,6 Bisphosphatase
F‐1,6‐BP →F‐6P + Pi
Inhibited by AMP, F‐2,6‐BP
Activated by citrate
Also Consider
Consider:
F‐6P + ATP →F‐1,6‐BP + ADP
F‐1,6‐BP →F‐6P
Net: ATP →ADP + Pi
Feudal cycle is not good. Hence Important that F1,6BPase and PFK not operate simultaneously
So, we need regulation
If AMP is high , then ATP is low which mean that
promote gluconeogenesis
Partition of glycolysis and gluconeogenesis
during exercise, pyruvate made faster in muscle than citric acid cylcle and can oxidized it -> lactate production.
Lactate in blood taken up by liver -> glucose. Lactate in Cory cycle
Well, Cardiac muscle has tons of mitochondria (mito) that could convert lactate
so the blood stream must keep moving ( running to the bus in the morning )
UDP and UTP glucose
glucose is store as glycogen

Glucose 1 phosphate -> UDP-glucose
This reaction to convert glycogen to Glucose -1 phostphate catalyzed by
glycogen phosphorylase.
Glucose 1 P to G 6 P
is catalyzed by phosphoglucomutase
Blood glucose levels regulated by two hormones, glucagon and insulin
Insulin released from pancreas when blood glucose is high, stimulates synthesis of glycogen from glucose.
Glucagon released from pancreas when blood glucose is low, stimulates the breakdown of glycogen to glucose
Another important hormon (adrenalin) . Muscular activity or its anticipation stimulates release of epinephrine(adrenalin) from adrenal medulla
same as how glucagon works in liver.
Glucagon binding to receptor on liver cell, or epinephinebinding on muscle cell activates
adenylatecyclase: ATP → cAMP+ PPi
cAMP is the second messager
will activate protein kinase slnuatheus
Activated PKA phoshorylatesGlycogen phosphorylasekinase(GPK)
converts it to activeform
Note
Synthesis/breakdown of glycogen hormonally regulated via protein phosphorylation
Activated GPK phosphorylatesGlycogen phosphorylase→
converts it to activeform → breakdown of glycogen to G1P
Glucagon is high
in the morning to maintain the blood level glucose.
Activated PKA phosphorylatesGlycogen synthase(GS) → converts it to inactiveform
Activated PKA phosphorylatesand activates inhibitor of phosphoproteinphosphatase(IP), turns off PP
Hormonal activation → stimulation of glycogen breakdown to G1P, G6P
After removal of hormonal stimulus, cAMPlevel drops: cAMPphosphodiesterase
When cAMPdrops, PKA no longer active
Leads to inactivation of IP, activation of Phosphoproteinphosphatase
Removal of phosphates from GP and GPK → conversion back to inactive forms
Removal of phosphate from GS → conversion back to active form
Removal of hormone → conversion of G1P, G6P to glycogen
Oxidative states of metabolism
Kreb's cycle
The tricarboxylic acid (TCA) cycle (Krebs cycle)
Common pathway for fuel molecule (carb’s, fats, aa’s) oxidation
Carb’s →pyruvate →acetyl CoA
Allows recovery of much greater portion of free energy than glycolysis
Occurs in mitochondria