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TAMU BICH 411 - Gluconeogenesis
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BICH 411 1st Edition Lecture 14Outline of Previous LectureI. Gluconeogenesis OverviewII. InhibitorsIII. RegulationOutline of Current Lecture I. GlycogenolysisII. Glycogen synthesisIII. EfficiencyIV. Issues with diabetesV. Glycogen MetabolismVI. InsulinVII. Hormone regulationVIII. Example ProblemsCurrent Lecture**be sure to know all about gluconeogenesis regulation for the test!**know figure 22.8 for quiz (what regulates where, etc)-at the end of gluconeogenesis, glucose becomes glycogen (branched polymers). This involves glycogenolysis. -glycogen comes from anything consumed that’s starch – broken down by alpha-amylase (endoglycosidase, breaks alpha 1-4 bonds internally). Stops 4 units before branch.-debranching enzyme cleaves four remaining units (limit dextrin). Transfer the three outer glucose groups, cleaves the remaining glucose. -Glycogenolysis releases a glucose-1-phosphate, rearranges glycogen, and converts glucose-1-phosphate to glucose-6-phosphate. -Dietary starch (100% digested) and tissue glycogen are different!-Tissue glycogen (stored in the liver and muscle) is where the energy comes from when broken down. Glycogen phosphorylase cleaves glucose from non-reducing ends (remember that alpha-amylase cleaves internal bonds! These have cleave differently!) The produce (sugar-phosphate) is a good glycolysis substrate. **The fate of glucose-6-phosphate depends on what is needed. It can enter glycolysis (like if you’re running), become glucose (if you’re hungry or starving), or enter the pentose phosphate pathway (electrons for biosynthesis or ribose for making nucleic acids). These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.Glycogen synthesis -derivitizing glucose activates it-UDP-glucose pyruphosphorylase causes phosphoanhydride exchange – the reaction involves spontaneous hydrolysis. End result is UDP-glucose (activated form of glucose) for synthesis of glycogen.-glycogenin (protein) initiates glycogen formation. Glucose added to –OH on Tyrosine. Sugar units added (glycogen synthase) via alpha 1-4 bonds. UDP-glucose loses glycosyl units to C-4 hydroxyl of glycogen strand. **an oxonium intermediate is involved** The branching enzyme is responsible for forming the branches.Net reaction:Glucose-6-Phosphate + ATP + Glycogenn + H2O  Glycogenn+1 + ADP + 2 Pi (Enzymes involved: phosphoglucomutase, UDP-glucose pyrophosphorylase, Inorganic pyrophosphatase, glycogen synthase, nucleotide diphosphokinase)Efficiency90% glycogen cleaved to glucose-1-Phosphate 10% of glycogen hydrolyzed to glucose and then turned into glucose-6-phosphate.Overall efficiency is 97%Issues with diabetes-ligation disease in diabetes:-glucose can form Schiff base linkages which undergo Amadori rearrangements to formGlycation end products (AGEs) – irreversible!-causes many problems in diabetics-measure glycated hemoglobin for diagnosticsRAGE (receptor for advanced glycation end-products)-protein in immune systems – can trigger intracellular responses in diabeticsGlycogen Metabolism-glycogen metabolism is highly regulated -involves glycogen phosphorylase (GP) and glycogen synthase (GS) – reciprocal regulation – both regulations involve phosphorylation!-GP is activated by AMP (turns on), inhibited by ATP, glucose-6-Phosphate, and caffeine (turn off)-GS is stimulated by glucose-6-phosphate-regulated by covalent modification-GS-I = dephosphorylated form (insensitive to glucose-6-P)-GS-D = phosphorylated form-dephosphorylation by phosphatase (like PP1) activates GS and inactivates GPInsulin-binding of insulin triggers protein kinase cascades, GS stimulated-has several effects (job is to lower blood sugar – wants to dump glucose out of blood to glycogen, ATP, amino acids, etc)-glucose uptake activates glycogen synthaseHormone regulation-glycogen metabolism regulated by hormones like insulin, glucagon, epinephrine, and glucocorticoids-insulin stimulates glycogen synthesis (gets rid of glucose)-glucagon and epinephrine cause glycogen breakdown (want to increase glucose)**Figure 22.20 is helpful to know for the quiz**-glucagon acts in liver and fat tissue, activates glycogen breakdown and gluconeogenesis-epinephrine acts in liver and muscles, activates glycolysis -Glucocorticoids act on liver, skeletal muscle, and fatty tissue-Cortisol is catabolic – acts on skeletal muscle (protein breakdown) and liver (gluconeogenesis)Example Problems-if fructose-1,6-bisphosphate is high, what is effect on glycolysis and gluconeogenesis? It increases glycolysis. -What is effect of increased blood glucose concentration? Gluconeogenesis turns off, glycolysis turns off. Glycogen synthesis increases.-What is effect of high insulin concentration? Glycolysis turns on, gluconeogenesis turns off, turnon glycogen synthesis, turn off glycogenolysis.-What is the effect of high glucagon levels in blood? It means high blood glucose so turns on glycogenolysis (GP on, GS off), turns on gluconeogenesis. -What is the effect of low ATP? Glycolysis turns on. ATP inhibits glycolysis a lot so if there’s little ATP, glycolysis will proceed. Also, low ATP means low energy in cell so need glycolysis to make energy.-What is the effect of high AMP concentration? Glycolysis stimulated. Turns off gluconeogenesis.-What is the effect of decrease in fructose-6-phosphate? There is no direct


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