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Flashcards in integration of metabolism Deck (36)
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-storage fuel
-preffered fuel
-exported fuel

-glyvogen and TG
-glucose, FA, AA's
-glucoes, FA's and ketones


skeletal muscle at rest
-storage fuel
-preffered fuel
-exported fuel



skel muscle working
-storage fuel
-preffered fuel
-exported fuel

-doenst store in this state
-alanine and lactate


-storage fuel
-preffered fuel
-exported fuel

-FA, and glycerol


preffered fuel of the heart



preferred fuel of the brain

-ketone bodies in starvaation


which enzymes are out of equilibrium?

-those which are regulated


4 ways to regulate a step in metabolism

-allosteric inhibition or stim
-regulate the amount of enzyme present (regulate gene transcription or protein degradation, enzymes must be turned over rapidly)
-covalent modification (phosphorylation)
-compartmental separation


adaptive changes in regulation are done by

-regulation of the amount of enzyme
-inhibition or stimulation of gene transcription
-protein degradation or stabilization
-regulation is changed by changes in the diet


fructose 2,6 BP regulation
-what hormones effect it and how
-what molecules does it affect

-regulated by glucose and insulin via phosphorylation
-when F6P is phosphorylated into F2,6BP, this activates glycolysis and inhibits gluconeogenesis via PFK1 (glycolysis) and F1,6BPase (gluconeogenesis)


CPT 1 regulation
-what is it an example of
-what does it do?
-what regulates it?

-this is the protein that transports fatty-acyl CoA into the mitochondria for beta oxidation
-this is an example of regulation of metabolism by the compartmentalization of certain intermediates
-malonyl CoA, which is an intermediate of fat metabolism, inhibits this protein
-low energy (high AMP) triggers the inhibition of acetyl coa into malonyl coa via ACC2 and stimulates the conversion of malonyl coa into acetyl coa via MDC


-major metabolic pathway effects

-promotes fuel storage after a meal
-promotes growth
-stimulate glucose strage as glycogen (muscle and liver)
-stimulates fatty acid synthesis and storage
-stimulates amino acid uptake and protein synthesis


-major metabolic affects

-mobilizes fuel sources
-maintains blood glucose levels during fasting
-activates gluconeogenesis and glycogenolysis
-activates fatty acid release from adipose tissue


-major metabolic pathway affected

-mobilize fuels during acute stress
-stimulates glucose production from glycogen
-stimulates fatty acid release from adipose tissue



-provides for changing requirements over the long term
-stimulates amino acid mobilization from muscle protein
-stimulates gluconeogenesis
-stimulates fatty acid release from adipose


characteristics of the G prtoein coupled receptor, just the receptor

-7 membrane spanning domains
-all with different extracellular domains which confer the specificity of the receptor
-all with similar intracellular domains as this is what will interact with the G protein


the g protein that associate with the recetor

-these are all the same for all the different types of receptors as the downstream affect is the same


g protein cycle

-3 subunits, alpha, bet, and gama
-alpha is bound to GDP in the inactive state
-once the receptor receives a signal, the GDP it substituted for GTP via GEF
-depending on if Galpha is inhibitory or stimulatory it will either inhibit or stimulate adenylate cyclase
-GAP then facilitates the conversion of GTP back into GDP on the alpha subunit
-alpha subunit and GDP then reassoicate with the beta and gama subunits


examples of diseases of the inhibitory and stimulatory alpha subunits

-inhibitory: pertussis renders the inhibitory subunit inactive therefore increase cAMP
-stimulatory: cholers renders the alpha subunits constitutively active causing increased cAMP


what does caffeine do?

-inhibits cAMP phosphodiesterase
-which converts cAMP into 5'-AMP, therefore leaving cAMP around for longer


how does cAMP stimulate PKA

-PKA is composed of two regulatory (R) subunits and two catalytic subunits
-cAMP binds to the R subunits, allowing the catalytic subunits to dissociate from the complex and become active


what does PKA regulate as a whole

-both glycogen breakddown and synthesis (promoting breakdown and inhibiting synthesis
-this protein has a very wide affect
-phosphorylates both phosphorylase kinase (active when phosphorylated) and glycogen synthase (inactvie when phosphorylated


how does Hsp90 function

-this is a chaperon protein which binds a trnascription factor when hormone is not present, keeping the transcription factor in the cytoplasm
-when hormone diffuses into the cell, it dissociates Hsp90, allowing the transcription factor that it was bound to to translocate to the nucleus and begin transcription


causes of starvation

-self starvation


stage 1 of starvation
-origin of blood glucose
-tissues using glucose

-first four hours after a meal


stage 2 of starvation
-post absorptive stage
-origin of blood glucose
-tissues using glucose

-4 to 16 hours
-glycogen and hepatic gluconeogenesis
-all except the liver. muscle and fat tissue at decreased rate of using glucose
-fatty acids are provided by adipose tissue
-usually associated with an overnight fast


3rd phase of starvation

-gluconeogensis from amino acids
-lactate and glycerol provide blood glucose
-TAGs are mobilized to form fat for energy and glycerol for glucose production
-muscles decreaes the use of glucose and increase the use of fats


4th phase of starvation

-middle stage
-decrease in total glucose consumption
-decrease in gluconeogensis
-brain adapts to lower glucose levels and begins to use ketone bodies for energy
-this is when you run out of glycogen and gluconeogenesis completely takes over


5th phase of starvation

-glucose is still produced by gluconeogenesis and is used mainly by RBC's and the brain
-however, the signicant contributor in the brain is ketone bodies
-severe depletion of muscle mass and adipose tissue
-utilization of lactate is pretty constant as the cori cycle continues to supply the RBC's with glucose from the liver


the liver during starvation
-citric acid cycle intermediates
-fatty acids

-proteins yield glucogenic amino acids and the wast is converted to urea and excreted by the liver
-citric acid cycle intermediates are diverted to gluconeogenesis and the glucose produced is sent to the brain via the blood
-fatty acids from adipose tissue are oxidized as fuel to produce acetyl coa. the lack of oaa in the TCA cycle (since it has been used in gluconeogenesis) leads the acetyl coa to be used to make ketone bodies which are sent to the brain