Biochem Lec 22-23 Flashcards
what is aneorobic metabolism
occur during periods of limited oxygen and electron transport chain is inhibited
so all energy production in oxidative phosphorylation is inhibited and NADH inhibits PDC and CAC causing them to slow down so glycolysis is teh only means of genertaing ATP
lactate dehydrogenase is the enzyme that uses redox reaction to convert NADH bacj to NAD+ so glycolysis from step 6 can continue
what effect does low oxygen concentration have on body and biochemicla pathways
low ATP due to oxygen phosphorylation in mitochondria so pyruvate is convcerted to lactate and aneorobic glycolysis make 2ATP
how does metabolism change under starvation
that means during fasting state so glucogan and epinephrine signalling while there us no fat and glycogen synthesis
it also stimulate Acetyl CoA carboxylase to make malonyl CoA since the respond is to make ATP
why is glucose homeostasis important
it is teh primary energy source for brain and RBC so it is important fuel to function
describe Cori cycle
it is the way that lactate from aneorobic metabolism is converted back to pyruvate in liver to make glucose
what is gluconeogenesis
it is an anabolic pathway which means it needs energy source but it is also teh way liver can make glucose
very important since brain cannot use fats for energy so need that glucose to generate ATP
the substances involved in gluconeogenesis are lactate, glycerol, and certain amino acids that can be turned into glucose and these carbon containing molecules are readily available in large quantities from blodostream
desrcibe steps of gluconeogenesis
it isn’t reverse of glycolysis since glycolysis is exergonic and require lot of energy for the 10 steps to go in reverse
so gluconeogenesis is anabolic pathway that uses high energy intermediates and 4 different enzymes to pypass the three regulated steps of glycolysis with teh negative delta G which are also irreversible
what are the gluconeogenesis enzymes that will oversee the three regulated steps of glycolysis
glucose 6 phosphatase for step 1 of glycolysis
fructose 1,6 bisphosphate for step 3 of glycolysis
2 enzymes for last step of glycolysis which are pyruvate carboxylase and PEP carboxykinase
describe the function of pyruvate carboxylase and PEP carboxykinase on the last step of glycolysis
pyruvate carboxylase is gonna add CO2 from bicarbonate but requires ATP and makes oxaloacetate
then PEP carboxykinase takes that oxaloacetate and decarboxynate teh moelcule to be able to add phosphate to it from GTP
so both enzymes need energy
describe the function of fructose-1,6-bisphosphatase on step 3 of glycolysis
will form fructose-6-phsophate
takes the PEP product from PEP carboxykinase catalyzed reaction and have it undergo through reverse sequences of enzymes in glycolysis and from the fructose 1,6 bisphosphate and then fructose 1,6 bisphosphatase reverse the reaction by taking a phosphate group and making the fructose 6 phosphate
fructose 6 phosphate is also isomerized to Glc 6 phosphate
how does glucose form after doing the reverse of step 10 and step 3 and are in step 1 of glycolysis
the glucose 6 phosphate that was isomerized from step 3 reverse reaction gets hydrolyzed off the phosphate and produce glucose by glucose 6 phosphatase and now teh free glucose can go through the body
some enzymes might act on glucose 6 phosphate from glycogen breakdown like glycogen phosphorylase and phosphoglutomutase
what is the glucose production from 2 pyruvate
2 pyruvate+4ATP+2GTP+2NADH+6H2O+2H—> Glucose +4ADP+2GDP+2NAD+6Pi
so gluconeogenesis is using 11 enzymes to make single glucose molecule but is overall favourable when energy is available
how is glycerol made to glucose
the fatty acids cannot be used to generate the glucose because production of pyruvate from acetyl CoA is unfavourable so the glycerol that is released during fat mobilization in fat cells can be used and is released in large amounts into blood
glycerol is a 3C moelcule and 2 glycerol molecules will be used to make 6C glucose that enters pathway as dihydroxyacetone (DHAP)
2 ATP are needed to drive this aneorobic pathway but 2 NADHs are also produced and 2 H20 help remove phosphates to make 1 glucose molecule
how does liver know whether it is glycolysis or gluconeogenesis on
if glycolysis is on that means energy is needed and AMP is high and so is fructose 1,6 bisphjosphate but ATP is low so that will make pyruvate
if GNG is on, that means there is high acetyl CoA and low ADP but there is a lot of energy so pyruvate gets turned to oxaloacetate
what are two amino acids used to make glucose
alanine, aspartate, glutamate
alanine gets converted to pyruvate which is used for GNG
asp is made into oxaloacetate which is used in GNG
glu is converted to alpha ketoglutarate which is made into oxaloacetate and that is used for GNG as well
what is teh allosteric regulation at PFK1 and FBP1
fructose 6 phosphate gets an adidtional phosphate group in glycolysis by PFK1 while fructose 1,6 bisphosphate gets phosphate group taken by FBP1 and become fructose 6 phosphate in GNG
what is the allosteric regulator of PFK1 and FBP1
that would be fructose 2,6 bisphosphate which when present will activate PFK1 and cause glycolysis and inhibit FBP1
it is made by PFK2/FBPase-2 and this tandem enzyme controls formation and hydrolysis of fructose 2,6 bisphosphate as it is single polypeptide with 2 active sites that can be reciprocally regulated via phosphorylation
how does reciprocal regulation work for GNG
in the glycolysis, glucagon is off and insulin is on which activates phosphotase and dephosphorylate the PFK2/FBPase-2 which turns on the kinase and cause phosphorylation of fructose 6 phisphate into fructose 1,6 bisphosphate
when glucagon is on and insulin is off, that activates kinase A which phosphorylate teh complex enzyme PFK2/FBP-ase 2 and that turns on the phosphate of that complex and the enzmye dephosphorylate the fructose 2,6 bisphosphate into fructose 6 phosphate
this process allows either glycolysis or GNG to be on and not both
what is an overview of the 4 processes that can occur in liver
in order of preferred as in view of the liver:
1- glycolysis as it makes ATP
2- glycogen synthesis as it takes that glucose and converts it to glucose 6 phosphate that gets changed to UDP-glucose that is stored in glycogen by glycogen synthase
3- glycogen breakdown as that is when energy is needed and glycogen gets converted back to glucose 1 phoshphate and become glucose
4- gluconeogenesis is when there is energy available and turns off glycolysis as the GPCR receptor inhibits the pyruvate kinase and tandem enzyme is phosphorylated
what is major difference between type I and type II diabetes
type I is genetic and autoimmune damaging beta cells so no insulin secretion while type II is the one where cells become insensitive to glucose so don’t secret insulin no matter how high concentration get
connection between hyperglycemia and glycation
glycation is when spontaneous reaction happen to modify the hemoglobin an dhyperglycemia is high blood glucose
the thing about glucose is that it is highly reactive and can react with N-terminal valine residues of beta chain in hemoglobin
the form of hemoglobin A1C is a merker for high blood glucose since RBC are turned over every 120 days
other moelcules in body can be glycated and that result in their modification which may affect their function
what are some hormonal regulation for people with diabetes
for peopel with diabetes I, they need to balance insulin injections with carbohydrates intake and exercise
insulin injection are important for glucose uptake and can also inhibit the glucagon secretion
in people with diabetes II, the insulin insensitivity lead to poor cellular glucose uptake and hyperglycemia as glucagon signalling can turn on GNG which will worsen the hyperglycemia
when blood glucose gets too low in presence of insluin, glycogenolysis and gluconeogenesis cannot help maintain glucose level
what are the reasons that could cuase hypoglycemia in person with type I diabetes
too much insulin, no dietary carbohydrates, liver function, eyc
when does ketogenesis occur nad how does it relate to acetyl CoA
it is the catabolism of amino acids to produce glucose or acetyl CoA in liver
occur when acetyl CoA rises so ketone bodies are used as alternate source to glucose
what is difference between glucogenic and ketogenic amino acid
glucogenic are ones like ala, arg, asp, and Glu which can be made from CAC if needed or make the molecules of CAC
ketogenic amino acids are ones like Ile, leu, thr, and trp, and these need to be modified to become ketone body
describe metanolism of amino acids
to enter metabolic pathway, they alpha amino group is first removed and metabolized in urea cycle for excertion as ammonia and the carbon backboen is used to make ATP, glucoe, or ketone bodies
nonessential amino acids are made from intermdeiate metabolites
the excess maino acids are degraded in liver
glucogenic amino acids will be used to make glucose while ketogenic are used to make acetyl CoA< and Ketone bodies
what are teh three types of ketone bodies made in liver
B-hydroxybutyrate, acetoacetate, and acetone
but acetone get exhaled as waste product while b-hydroxybutyrate and acetoacetate as the ones that release protons which contribute to teh acidosis
describe ketone body synthesis
the three acetyl CoA are brough together to generate the 3 different ketone bodies and there is no ATP involved as there is high concentration of Acetyl CoA wherever
how are ketone bodies used as fuel by brain or other tissues
when the ketone bodies leav ethe liver and enter bloodstream, they cna cross BBB so tissues liek brain, muscle, and heart cna take it and convert it back into acetyl COA and generate energy but need to have oxaloacetate to get taht energy from Acetyl CoA and that pyruvate that will help with that come from GNG
what is ketoacidosis
occur when ketone levels rise in body due to depeleted liver glycogen stores and increased acetyl CoA so the blood biffering system initially compensate along with proton absorption by bone an tissues
so acidosis occur when bicarbonate is depleted and blodo pH is below 7.35
discuss the overall of liver metabolism
liver is main supplier of glucose for rest of body releasing glucose from glycogen breakdown and producing it in gluconeogenesis
cholestrol and fatty acids also take place in liver and releasing them as lipoproteins complexes in bloodstream
fatty acids can’t be used by brain for energy but liver provides ketone bodies that cna be converted back to acetyl CoA
acvetyl CoA from fat breakdown and ketogenic amino acids can be used to make ketoine bodies, while glucogenic amino acids can be used to make glucose
liver helps supply important fuel moelcules for rest of body
what happens when there is ketoacidosis and no insulin
without insulin, that means glucose transporters aren’t getting to cell surface to help with glucose import
glucose isn’t talen up to be broken down and make energy so fat catbolism is the oen to help
CAC in liver slows down because teh intermediates don’t aren’t replenished due to absence of pyruvate/OAA causing excess acetyl CoA being converted to ketone bodies
producing ketone bodies is associated with drop in blood pH and causing ketoacidosis
deep respiration removes CO2 from blood which causes loss if bicarbonate and lack of buffering capability
acidosis is dangerous as it affects protein structure and can lead to unconsciousness, coma, death
what is affect of insulin administration
reduces hyperglycemia and ATP levcels rises
poly dipsia and polyuria are eliminated due to drop in blood glucose and ketone body formation
blood tonicity normalizes along with water balance
glycolysis is stimulated while gluconeogenesis is inhibited
fat breakdown is laso inhibited as fat and glycogen synthesis rise
sympotoms of type I diabetes
thinner, using toilet more tahn frequentl, thirsty, and tires
