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Intro to Metabolism
Biochem and medical genetics
| Question | Answer |
|---|---|
| What is metabolism | Metabolism = from the greek metaballein, meaning to change Purely a means of getting from A to B by the most efficient route How we make energy to power reactions e.g. by converting glucose to ATP |
| Catabolism | Breaking things down Synthesis of energy - glycolysis and beta oxidation Breakdown of glycogen - glycogenolysis Breakdown of ketone bodies - ketolysis |
| Anabolism | Building things up Synthesis of storage molecules - glycogenesis and lipogenesis Synthesis of glucose - gluconeogenesis Synthesis of ketone bodies - ketogenesis |
| General principles | Input - source of energy and substrates Output - physical work and chemical work Substrates are reduced compounds of carbon e.g. fatty acids, carbohydrates and amino acids Energy released by oxidation |
| In vitro combustion | 1 step Incomplete conversion to CO2 and H2O Energy lost as heat and light E.g. glucose burnt in a flame |
| Biological oxidation | Controlled Multi-step process Can have partial or complete oxidation Some energy trapped in chemically useful form as ATP |
| Free energy | Gibbs free energy Must be negative for a process to be spontaneous If a reaction is non-spontaneous it is coupled to ATP hydrolysis to force it to occur Needed for mechanical work, active transport and synthesis of biomolecules |
| Fuels | Glucose Fatty acids Amino acids |
| Typical daily macronutrient intake | Carbohydrates (300g) - polysaccharides (66%), disaccharides (31%) and monosaccharides (3%) Fat (100g) - Triacylglycerols (94%), phospholipids (5%) and cholesterol (1%) Protein (100g) - 100% |
| Storage of fuels | Glucose - 15g in blood, 70g in liver and 200g in muscle Fatty acids - 11kg triacyl glycerides in adipose tissue Amino acids - protein throughout the body - not a true storage form |
| Energy from each store | Glucose - 17 kJ per gram - 2500 kJ in body Fatty acids - 38 kJ per gram - 420000 kJ in body Protein - 17 kJ per gram - 100000 kJ in body |
| ATP | Common energy currency Free energy donor Most tissues contain 6mM ATP Whole body contains 75g ATP - body uses 75 kg a day Rapid conversion between ATP and ADP ADP - signal for energy requirements |
| Sources of energy | 5% from substrate level phosphorylation - oxygen independent 95% from oxidative phosphorylation - oxygen dependent High constant ATP demand - high abundant of mitochondria - high O2 consumption RBCs do not have mitochondria - rely on substrate level |
| 3 stages of energy extraction | Large macromolecules broken down into smaller ones e.g. glucose and amino acids Small molecules degraded to common units e.g. acetyl - CoA TCA/Oxphos - complete oxidation to ATP |
| Different compartments involved in metabolism | Blood Cell membrane Cytoplasm Mitochondria |
| Formation of Acetyl CoA | Glycolysis - Glucose to pyruvate to Acetyl CoA Fatty acid oxidation - beta oxidation Acetyl CoA then used in Krebs cycle for oxidative phosphorylation |
| Formation of storage molecules | Glycogenesis - glucose to glycogen De novo lipogenesis - acetyl CoA to triglycerides |
| Other reactions | Glycogenesis and gluconeogenesis - formation of glucose Ketolysis - ketone bodies to acetyl CoA Ketogenesis - acetyl CoA to ketone bodies Amino acid oxidation - amino acids into krebs cycle |
| Positives of compartmentalisation | Clustering of related functions serving a common purpose or favoured by common environment Isolation - controlled access allows regulation Removal of potentially harmful processes from general cell environment |
| Negatives of compartmentalisation | Isolation means transport mechanisms required for substrates and products as well as intrinsic components of the compartment Genes need to adapt for targeting of proteins to specific compartments |
| Point of metabolism | All chemical reactions involved in maintaining the living state of cells and the organism Making energy Storing fuels for later use Liberating stored fuels for current use Making biomolecules Not constant in time and tissues |
| What determines metabolism | Physiological condition - anabolic vs catabolic, fed vs fasted vs starvation. relaxed vs fight or flight, rest vs exercise Tissue type - different tissues use different metabolism |
| What tells metabolism to change | Hormones Energy levels Metabolites themselves Oxygen availability |
| Substrate selection | Fatty acids - heart, skeletal muscle, liver, renal cortex Glucose - brain, red blood cells, renal medulla, skeletal muscle Amino acids - liver, gut, renal cortex, muscle |
| Allosteric control of metabolic flux | Binding of effector to site away from enzyme active site Usually intracellular effector - milliseconds E.g. phosphofructokinase in glycolysis is allosterically inhibited by high ATP |
| Covalent control of metabolic flux | Addition or removal of molecule attached to the enzyme via a chemical bond that shares electrons Usually a response to extracellular effector - seconds to minutes e.g. Pyruvate dehydrogenase is inhibited by phosphorylation |
| Translocation control of metabolic flux | Movement of one cell compartment to another - seconds to minutes e.g. glucose transporter moves from the cytosol to the cell membrane where it becomes active |
| Long term control of metabolic flux | Transcription/translation Enzyme induction or suppression Multiple enzymes targeted together e.g. transcriptional upregulation of genes involved in fatty acid metabolism on a high fat diet Upregulation of mitochondrial genes with exercise |
| Metabolic control between tissues | Most tissues don't metabolically exist in isolation - substrates transported from elsewhere and products removed to be treated elsewhere Regulated by delivery of substrates and uptake across the plasma membrane |
| Cori cycle | Lactate produced by anaerobically respiring muscle, red blood cells, renal medulla Exported to liver Liver resynthesized glucose via gluconeogenesis to avoid wastage of fuel |
| Inborn errors of metabolism | Genetic mutations present from birth A metabolic enzyme or protein does not work E.g. phenylketonuria and MCAD deficiency - all neonates screened |
| Warburg effect in cancer | Cancer cells respire anaerobically despite plenty of oxygen and mitochondria Allows survival with no vasculature We can screen for tumours by looking for areas with high lactate concentration e.g. by labelling and using MRI |
| Energy starvation in heart disease | Failing hearts have less ATP Phosphate peaks in the heart on MRS P13 decrease This is a good predictor of mortality |
| Nutrient excess in obesity and type 2 diabetes | Excess lipid deposition in the liver causes fatty liver disease Liver deals with fat - lipid droplets form in the liver e.g. in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis |
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