Glycolysis Flashcards
Glucose Store
Glycogen
Why glucose levels are kept consistent in blood
Some tissues can only use glucose in metabolism (eg brain and RBCs), hypoglycemia =confusion, coma and death, hyperglycemia = confusion , cornea damage and death and ATP
GLUT1 Transformer
Facilitated diffusion of glucose into brain and erythrocytes
GLUT 2 Transformer
Facilitated diffusion of glucose into hepatocytes
GLUT 3 Transformer
Facilitated diffusion of glucose into neurons
GLUT 4 Transformer
Facilitated diffusion of glucose into adipose tissue and skeletal muscles
SGLT Transformers
Glucose secondary active transport
How is glucose trapped in cells
Phosphorylated by hexokinase (most cells)/glucokinase (parenchynl cells and pancreatic islet cells) transforming into glucose-6-phosphate. Phosphate can’t move through pumps or across membrane
Hexokinase Outline
Low Km (high glucose affinity) and low Vmax (enzyme works slowly). Allows for glucose to enter essential tissue eg brain under fasting conditions. Low enzyme capacity. Regulated astosterically by glucose-6-phosphate
Glucokinase Outline
High Km (low glucose affinity). Only takes up glucose while it’s high, minimises uptake by liver. Low Vmax = high capacity. Helps monitor blood glucose, motivates liver to absorb glucose. Regulated by glucose conc
Glycolysis End Product
2 x Pyruvate (2 x 3 C chains)
What conditions are necessary for pyruvate to move into TCA cycle
Oxygen. Aerobic conditions
What does Glucose-6-phosphate convert to
Fructose 6 phosphate (still 6 C chain)
Fructose-6-kinase conversion
enzyme phosphofructokinase adds phosphate and converts to fructose-1,6-bis-phosphate. Energy from ATP
Fructose-1,6-bis-phosphate conversion
dihydroxy-acetone-P splits molecule into 2 smaller glyceraldehyde-3P (3 C chain). Means 2 cycles of glycolysis per 1 glucose molecule
Cell energy regulation in glycolysis
Invest 2 ATP at beginning. Obtain 4 ATP and 2 NADH later in glycolysis
Phosphofructokinase 1
Glycolysis, limiting enzyme (activity is tightly regulated). Inhibited by ATP (when cell has enough energy) and activated by fructose-1,6-bisphosphate (high substrate conc, created by high insulin and low glucagon).
Effects of fructose-1,6-biphosphate
inhibits phosphofructosekinase 1 and inhibits glucogenesis. Controls blood glucose cons
Effect of lactic acid accumulation
circulatory collapse or hemorrhage
Lactate to pyruvate conversion
reversible
Direct ATP Production
Substrate phosphorylation by kinase enzymes
Indirect ATP Production
Oxidative phosphorylation. Redox reactions of electron carriers
Pyruvate fates
dehydrogenase complex (Acetyl Co A in TCA cycle and precursor fatty acid synthesis), Carboxylase (oxoacetate in TCA or glucogenesis) and Decarboxylase (ethanol)
Fate of oxalates
Fat synthesis
Pyurvate Dehydrogenase enzymes
pyruvate decarboxylase, dehydrolipoyl transacetylase and dihydrolipoyl dehydrogenase. All irreversible reactions. high ATP inhibits
Pyruvate Dehydrogenase Co enzymes
NAD+, Co A, FAD, TPP, Lipoic acid
Pyruvate Dehydrogenase Deficiency
Mitochondrial disorder (maternal line). Congetial lactic acidosis. developmental defects, muscular spasming, early death. No effective treatment
Arsenic poisoning
Inhibits liopoic acid cofactor. Inhibit pyruvate dehydrogenase. Symptomas neurological disturbances and death
