9 28 Metabolism and Glucosogen Insilin-Table 1 Flashcards Preview

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Flashcards in 9 28 Metabolism and Glucosogen Insilin-Table 1 Deck (53):

what if the blood glucose levels drop?

then hypoglycemia and you get a epinepherin response to get jittery and sweaty etc. then goes to nervous system shut-down and coma.


what if too much glucose in the blood

Eye, Kidney, Nerve, and heart disease damage (diabetes)


what happens to insulin after a meal with sugar?

the level of it spikes


what is insulin and its functions?

Comes from the Beta cells it signals growth, glucose uptake; signals anabolic pathways (most potent anabolic hormone); glycogen synthesis; Inhibits release of fatty acids. [[Just eaten build and store potent anabolic hormone!]]


what would be expected to happen to someone who makes no insulin?

low muscle mass, low protien synthesis; spiking blood glucose levels;


what if you have insulinoma?

over expression of blood insulin -- Hypoglycemia: seizures; irritable; sweaty; jittery; weight gain;


what pathways in the liver would be inhibitted by insulinoma?

gluconeogenisis is inhibited, glycogen breakdown inhibited


the endocrine cells in the pancreus:

the pancreatic islet cells. Beta-cells: Insulin; Alpha-cells: Glucagon


When (compared to glucose in the blood) is insulin released?

when blood glucose reaches 80mg/dL and insilin is released within munuties.


how does glucose lead to insulin release?

glucose comes in through Glut 2: glycolysis: TCA etc.: ATP conc. up: ATP stops the K+ channels and won't let K+ out: Increase cell potential (depolariztion): allow Ca2+ channels to open: Ca2+ binds to Insullin vesicles and cause them to bind to the plamsa membrane and be released.


what is glucagon and what does it do

comes form the alpha cells in the islets: insulin counter regulatory that increases blood glucose. Signal in the liver to release glucose into the blood.


what is the primary target of glucagon?



how does muscle and most cells in the body reacte to glucagon

they don't they don't have receptors


how is the liver targeted by the pancreatic hormones?

the portal vien right to the liver means the liver sees 4X the level of hormone.


how does insulin act on the alpha cells

appears to have a paracrine effect and inhibit the release of glucagon


how does the flux of glucose affect glucagon

drop in glucose means a rise in glucogon


What type of signalling pathway is glucagon?

G-protien coupled receptor that leads to transcription regulators and other effector protien changes


What type of signalling pathway is Insulin?

Receptor Tyrosine kinase that leads to effector proteins and transcription regulators.


what is glycogen ultimately?

A source of glucose storage


What are the main parancymal tissue cells of the liver?



what is the purpose of glycogen in hypatocytes

to store energy for release into the blood stream for use in other organs


why would we want to store a highly branched glycogen instead of startch?

because we can add and take off glucose from all of the many branch points in glucose!


how do we make glycogen?

we make UDP-glucose; add this to the branch points of glycogen by glycogen synthase; then when the branch is long enough a transferase moves the brach over to a new spot on the chain of glucogen


how do we break down glycogen?

phosphorylase trims off the glucose and then debranching enzyme takes the little branches and adds them to the longer branches to allow phosphorylase to continue to pluck off glucose.


what is a phosphorylase vs. phosphatase vs. kinase

phosphorylase activates phosphate to do the cleavage of glucose; phosphatase activates water to break off a phosphor group; kinase uses ATP to add phosphor group


what effect does insulin signaling have on hepatic glycogen?

synthesize more of it!


what effect does insulin signaling have on muscle glycogen

synthesize more of it!


what effect does glucagon signaling have on hepatic glygcogen?

break it down!


what effect does glucagon signalling have on muscle glycogen

no effect!!! (there are no receptors)


what effect does epineprine signaling have on hepatic glycogen?

stimulate breakdown so you get more energy


waht effect does epinerprine signaling have on muscle glycogen?

stimulate breakdown so you get more energy!


what is special about glucose 6-phosphatase

it allows the removal of phosphase off of glucose 6 phosphatase to get just glucose that can go out the GLUT 2 transporter to the blood stream!


what does a phosphatase do?

it removes phosphase


what does a dehydrogenase do?

Oxidize a substrate to give NADH or FADH


what does a kinase do

add a phosphate


what does a cylcase do?

forms a cyclic compound


what do the blue arrows on the metabolic pathway?

occurs only in or primarily in hepatocytes


how do we maintain blood glucose level?

at about 3 to 4 hours after eating we have a rise in hepatic glycogen, then at about a day that response goes off, and then hepatic gluconeogenesis takes over and goes on until die!


what is glucagon's effect on liver glycogen synthesis and breakdown

glucagon's G-protien receptor binds and tells us we need more glucose in blood with the goal of activating glycogen phosphorylase and getting glucose out of the cell! therefore we will decrease glycogen synthase activity! this is throuhg: The G-protien receptor doing: 1. Increasing cAMP which increases the activity of Protein kinase A which does two things: 1. phosphorylate glycogen synthase to stop the production of glycogen and 2. phosphorilates phosphorylase kinase, which then phosphorlates glycogen phosphorlase and allows the release of glucose.


what is insulin's effect on liver glycogen synthesis and breakdown?

Insulin binds to the tyrosine kinase receptor that acts on AKT that acts on PP1 that then does two things: 1. removes the phosphor on glycogen synthesis to activate it (phosphorlase activity); and then it removes phosphor off phosphorylase kinase, and the phosphorlase off of glycogen phosphate to turn off the release of glucose to the blood stream. (basically the opposite of what glucogon does!


when glucose is low and insulin is low and glucagon is high:

glycogen goes to glucose in the liver and this goes to the RBC and then to the brain etc.!


The stores of glycogen in the liver are limited, so how do we get more glycogena to supply the liver to supply body with glucose after the short term response to glucagon wears off?

TG (little piece of glycerol) from adipose goes to the liver; or Protein from muscles and the lactate from RBC are converted to pyruvate and that goes to the liver.


how do protiens end up giving us glucose

many go through oxyloacitate then up the glycolysis chain backwards to glucose. (some go through pyruvate as well)


what is the one place where insulin inhibits an anabolic pathway

it inhibits gluconeogenisis


why can't we use the fatty acid carbons to make oxyloacitate to make glucose?

becuase the carbons from the fatty acids are used to just produce CO2 in the TCA cycle and you don't get any net carbons out of the fatty acids to produce more oxyloacitate


which steps in gluconeogenisis are not just the reverse of glycolysis?

the irreversible steps: The first step of glycolysis that adds Phos. to glycolysis; the third step that makes bis-p from single phosph. fructose, and the last step: pyruvate kinase.


how do we get around the non-reversible steps in glycolysis for gluconeogenisis?

4 enzymes specific to gluconeogenesis: 1. pyruvate carboxylase 2. phosphoenolpyruvate carboxykinase (PEPCK) 3. fructose1,6 bisphoshpatase 4. glucose 6-phoshpatase


gluconeogenisis is along time-line process so how is it regulated?

transcriptionally regulates the expression of the 4 enzymes that are needed for gluconeogenisis


what if you have been fasting for a while how do you get to gluconeogenisis?

Glugagon binding to the G-protien receptor and increasing cAMP and protien kinase A can activate a transcritption factor CREB that will aid in making PEPCK.\


what if you eat a meal now what happens to gluconeogenisis

Insulin binding to TKR activates Akt that activates PP1 that will de-phoshporilate CREB and turn off the transcription of PEPCK. It will also posphorilate the other transcription promoters for gluconeogenesis.


where do hepatocytes get the energy for gluconeogenisis?

from oxydating fats!


what are the short and long term responses to fasting?

glucagon signals glucose release form glycogenolysis short term and from gluconeogenesis long term. this is of course to prevent hypoglycemia.


what level of glucose in the blood is normal?

70-100 mg/dl