Lecture 2: Glycogen breakdown

what are the 3 main fuel molecules?

1) carbohydrates 2) proteins 3) fats

what are the 3 ways signaling pathways can be shut down?

1) receptor interaction is reversible 2) GDP has the beta and gamme subunits on them instead of on the GTP 3) cAMP is converted to AMP which stops the activation of protein kinase A

what are the 3 types of amino acids that can be phosphorylated?

1) tyrosine 2) serine 3) threonine

if a person had a defective debranching enzyme in the liver, how much of the glycogen particle would remain during glucagon signaling? A. very little, phosphorylase removes most of the glucose residues B. most of it, phosphorylase can only remove glucose residues up to a certain distance within a branch

B. most of it, phosphorylase can only remove glucose residues up to a certain distance within a branch the debranching enzyme wouldn't be cutting off any more glucose molecules. glycogen stores cannot be mobilized and glycogen chains can grow more than be broken down. clinical result: enlarged liver and skeletal muscle weakness

glucose 6-phosphotase is not expressed in muscle cells. in muscle cells how many net ATP will be generated in glycolysis by breaking down glycogen by phospohorolysis? a. 1 b. 2 c. 3 d. 4

C. 3 b/c muscle cells dont have to carry out this rxn of hexokinase since its irreversible so it results in 1 extra ATP glucose net gain is 2 ATP

During times of fasting, which type of 'fuel molecule' do liver cells use to generate energy for its own use? Acetyl-CoA Fatty acids Glucose Ketones

Fatty acids cant be ketones b/c that involves muscle cells fatty acids enter the liver and oxidizes Acetyl CoA, creating reducing power (NADH/FADH2) which goes through the electron transport chain generates ATP

Which of the following hormones will stimulate glycogen breakdown? Insulin Glucagon

Glucagon

glucagon signaling activates

PKA

Which of the following types of regulation is considered the major way liver cells activate glycogen phosphorylase? Gene expression Compartmentalization Allosteric regulators Post translational modification

Post translational modification modifies enzymes to activate them

when cAMP binds to its binding domains, what does it cause?

a conformational change and activates C

fatty acids are transported to other tissues to provide energy via what?

beta-oxidation and aerobic respiration

What is glycogenolysis?

breakdown of glycogen to glucose -occurs in muscles and liver

what enzyme activated protein kinase A?

cyclic AMP (cAMP)

where does a person get the majority of their energy when they sleep (nocturnal fasting?) a. triacylglycerols (fatty acids) b. glycogen (glucose) c. protein d. A and B e. A and C

d. A and B

what does glucagon bind to?

fat and liver cells *** NOT MUSCLE CELLS!! b/c there are no receptors for glucagon on muscle cells

what is the function of glycogen phosphorylase? is it upregulated or downregulated?

function: cleaves 1,4 glycosidic bond by attaching phosphates onto them -makes glucose 1-phosphate upregulated b/c increased in cellular response to molecules

Glycogen is directly converted to monosaccharide units by: glycogen phosphorylase protein kinase A glucose-6-phosphatase GPCR

glycogen phosphorylase

active lipase catalyzes

hydrolysis of triacylglycerols to free fatty acids

why does no amplification occur at cAMP?

it is NOT an enzyme, it is a small molecules that is a second messenger instead!

Is glycogen a monomer or polymer?

it is a homopolymer

what is the function of protein kinase A? is it upregulated or downregulated?

it is activated by cAMP -key part of glycogen breakdown signal transduction pathway upregulated

the major produce of glycogen breakdown is glucose-6-phosphate. What is the subsequent fate of glucose 6-phosphate moelcules in the MUSCLE?

it is stuck as glucose 6 phosphate -epinephrine activates glycogen breakdown in the muscle NOT glucagon -it may undergo glycolysis you are using 1 less ATP since first step is irreversible

the major produce of glycogen breakdown is glucose-6-phosphate. What is the subsequent fate of glucose 6-phosphate moelcules in the LIVER?

it will be used to increase blood glucose levels -G6P will be converted to free glucose molcule in the E.R. and then will exit into the liver which it will then go through the GLUT 2 transporter and into the blood vessel which will increase blood glucose levels

what leads to the activation of the G proteins?

ligand binding to 7TM (glucagon receptor)

PKA activates

lipase via phosphorylation

several hours after digesting a meal blood glucose levels fall below the normal range. which organ will replenish glucose to normal levels in the blood and what hormone will signal the release of glucose?

liver- look at glycogenolysis glucagon

if the enzyme phosphorylase kinase has a mutation that made it constitutively active (always on) how would glycogen mobilization (breakdown and synthesis) be affected in the liver during times of low blood glucose, normal blood glucose, and high blood glucose

low blood glucose (hypoglycemia): not affected as glucagon signals to breakdown and release of glucose high blood glucose (hyperglycemia): glucose will bind to phosphorylase and decrease its activity normal blood glucose: continuously catalyze the phosphorylation of phosphorylase making it active

what is the primary/largest storage for glycogen?

muscle and liver

what allows phosphorylation to convert phosphorylase to the active form?

phosphoserine residues cause conformational change which allows access to the catalytic site phosphorylase b----> phosphorylase a (active form) 2ATP---> 2ADP

fatty acids contain more energy per gram than carbohydrates. why is it necessary to store some some glucose as glycogen when it is more efficient to store excess energy as fat?

rapid release of glucose can provide energy in the absence of O2 (supply energy under anaerobic conditions) which is energy that is needed right away -short term (12-24 hours)---> glycogen -long term (fasting state) ---> converted to fat

how does the binding of a single hormone on a single receptor release thousands of glucose 6-phosphate molecules from glycogen?

the same enzyme can be used multiple times and by amplifying the signal that you initially have

When does glycogenolysis occur?

when blood glucose levels are low (fasting state)