Unit 6 - Metabolic Integration Flashcards Preview

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Flashcards in Unit 6 - Metabolic Integration Deck (13):

what is the importance of the TCA? what are exceptions?

we can't make glucose from FA
-OAA can be converted to glucose, but there is no NET conversion of ACoA to glucose
-exceptions: 3 C of glycerol backbone makes glucose in prolonged fasting (via lipolysis), and odd-chain FA make PCoA that becomes glucose


what is the major carbon source for anaplerotic (re-building stock) reactions?

pyruvate (from glucose, glucogenic AA, or cytosolic OAA via malate dehydrogenase and malic enzyme, but not significantly from fat)


what are the 5 major anaplerotic pathways?

1. pyruvate carboxylase (make OAA)
2. glu:a-KG transaminase and glu dehydrogenase (make a-KG)
3. PCoA carboxylase and mmCoA epimerase + mmCoA mutase (make SCoA)
4. AA --> fumarate
5. asp:OAA transaminase (make OAA)


are catabolic and anabolic enzymes phosphorylated or dephosphorylated when active? what are examples?

catabolic: active when phosphorylated (AMP high, ATP low; release glucose)
-ex: phosphorylase kinase, glycogen phosphorylase, HSL

anabolic: inactive when phosphorylated (ATP high, AMP low; store glucose)
-ex: ACoA carboxylase, glycogen syntahse, HMG-CoA reductase


is epinephrine anabolic or catabolic?

catabolic; signals that E is needed right away
-stimulates breakdown, and inhibits synthesis of glycogen, fat, PRO


what is an example of futile cycle (waste ATP)? why does this happen?

adipocytes during fasting conditions
-30-40% of NEFA made during lipolysis is re-esterified, instead of being released into circulation
-due to availability of glycerol-3-phosphate under fasting conditions
-acts as a brake on lipolysis, preventing too-rapid release of NEFA
-generates heat and contributes to hormonally controlled thermogenesis to regulate body mass


what happens in the fed state to:
1. ACoA carboxylase
2. HMG-CoA reductase
3. HSL
4. CREB (in fat cells)

1. active, so more FA synthesis
2. more active, so more cholesterol synthesis
3. inactive, so less lipolysis, with unphosphorylated perilipin blocking access to fat droplets
4. inactive, so decreased production of PEPCK (less gluconeogenesis)


what happens in the fasted state to:
1. ACoA carboxylase
2. HMG-CoA reductase
3. HSL
4. CREB (in fat cells)

1. inactive, less FA synthesis
2. less active, so less cholesterol synthesis
3. active, so more lipolysis, with phosphorylated perilipin no longer blocking access to fat droplets
4. active, so production of PEPCK for gluconeogenesis, TG resynthesis, and decreased NEFA


-KB production
-metabolic adjustments

-low insulin/glucagon ratio, but always some insulin
-moderately high rate of lipolysis in fat cells
-moderate KB production by liver
-gradual/manageable adjustments (shift in use of KB as fuel, and excess is excreted by kidneys)
-no ketoacidosis (blood pH kept stable)


diabetes mellitus I
-KB production
-metabolic adjustments

-NO circulating insulin
-uninhibited, max (runaway) lipolysis in fat cells
-max production of KB by liver, and production overwhelms removal
--metabolism in extrahepatic tissues, kidney excretion, and exhalation of acetone
-metabolic ketoacidosis


how do epinephrine and glucocorticoid actions compare and contrast?

both generally encourage breakdown (counterregulatory hormones)
-E: stimulates glycogen breakdown, gluconeogenesis, and lipolysis
-G: stimulate lipolysis, AA release, and gluconeogenesis, BUT also stimulates glycogen synthesis


what is the Warburg effect?

aerobic glycolysis in cancer cells
-most ATP from glycolysis with release of lactate (pyruvate is used to make lactate, instead of TCA)
-cells take up lots of gln, which is converted to glu in mitochondria


what does inactivation of p53 do?

tumor suppressor gene
-promotes switch toward aerobic glycolysis, and away from use of TCA