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Gluconeogenesis

Uni of Notts, Signalling & Metabolic Regulation, Year 2, Topic 10

TermDefinition
Gluconeogenesis & energy requirements Production of glucose from non-carbohydrate precursors. Requires high ATP & low glucose
Primary cellular & tissue sites of gluconeogenesis Cytosol of liver, kidneys, & small intestine (they produce G3Pase)
Where gluconeogenesis differs from glycolysis (3 steps) Same as glycolysis except reversed & with 3 bypasses: pyruvate to PEP, F1,6BP to F6P, & G6P to glucose
Mitochondrial pyruvate carboxylation (+similar process with amino acids) Pyruvate is carboxylated to oxaloacetate via pyruvate carboxylase using ATP. Some amino acids can also be converted to oxaloacetate
Malate shuttle mechanism & function Reduces mitochondrial oxaloacetate to malate using NADPH, exporting using the malate shuttle, then regenerating it in the cytosol
PEPCK catalytic action Hydrolyzes GTP to phosphorylate & decarboxylate oxaloacetate into phosphoenolpyruvate
Gluconeogenesis using pyruvate total pathway chemical stoichiometry Consumes 2 pyruvate, 4 ATP, 2 GTP, 2 NADH, & 8 H2O per generated glucose
Reciprocal metabolic coordination Coordinated with glycolysis to prevent futile energy waste
Fructose-1,6-BPase regulation profiles Inhibited by F-2,6-BP & AMP; upregulated by excess citrate
Pyruvate carboxylase & PEPCK regulators Upregulated by acetyl-CoA; downregulated by ADP. PEPCK is downregulated by ADP & isn't upregulated
Glucagon & insulin impacts on enzyme transcription Glucagon increases PEPCK expression; insulin inhibits it & promotes glycolytic enzyme synthesis
Lactate clearance during exercise Muscle lactate enters blood cotransported with H+, causing toxic acidosis; liver metabolizes it to pyruvate & glucose
Alanine utilization during short-term fasting (i.e., between meals) Alanine aminotransferase aminates alpha-ketoglutarate to glutamate, transforming the carbon skeleton into pyruvate
Transition timeline of glucose sources after a meal (100g glucose) Max glycolysis after 8 hours. Equal glycogenolysis & gluconeogenesis around 16 hours when all glucose is used up. From here glycogenolysis slowly tapers off while gluconeogenesis plateaus
Glycerol contribution to gluconeogenesis Adipose degradation releases glycerol, which is converted to triose phosphate
Why free fatty acids aren't good for gluconeogenesis (+the exception) Free fatty acids cannot produce glucose precursors since acetyl-CoA is lost as CO2 in the TCA cycle. Odd numbered fatty acids make a molecule or propionate which can be used
Ethanol-induced pathway inhibition Alcohol metabolism elevates hepatic cytosolic NADH, diverting gluconeogenic intermediates into alternate reactions e.g., pyruvate - lactate, oxaloacetate - malate which reduces available intermediates
Diabetic default state activation Impaired insulin signaling prevents membrane GLUT recruitment, signaling constant glucose scarcity & default gluconeogenesis activation
Trauma-induced insulin resistance pathways Physical trauma prompts glucose insensitivity via pathways distinct from typical diabetes (extreme chronic HPA axis dysregulation)
Anaplerotic (intermediate forming) role of pyruvate carboxylase Mitochondrial pyruvate carboxylase reaction replenishes oxaloacetate intermediates to sustain the TCA cycle during periods of heavy amino acid & neurotransmitter synthesis across most tissues
Radiolabelled acetate experiments Can be infused intravenously into the patient to analyse proportion of molecules made from this. This can be compared between healthy & diseased phenotypes
How gluconeogenesis bypasses the DHAP⇌glyceraldehyde-3-phosphate step & what happens next Converts glyceraldehyde-3-P to DHAP then fuses 2 of them to F-1,6-BP using aldolase & uses FBPase to hydrolyse this to F6P which can be isomerised to G6P
Created by: Denny12
 

 



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