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Metabolic homeostas.
Uni of Notts, Genes, Molecules and Cells, first year
| Term | Definition |
|---|---|
| Metabolic homeostasis | The balance struck between fuel availability (nutritional intake & de novo synthesis) & tissue needs (oxidative rates & rates of metabolism from storage) |
| 4 types of metabolic pathway | Fuel oxidative pathways Fuel storage & mobilisation Biosynthetic pathways Detoxification & waste disposal |
| Roles of metabolic homeostasis | Synthesis of chemicals not obtainable through diet, balancing energy intake & expenditure, maintaining stable internal for metabolism, & protection from environmental toxins & changes |
| Metabolic homeostasis in complex eukaryotes | There are many different homeostatic systems across various cells, tissues, & organs in eukaryotes that are semi-independently maintained by different enzymes for different specialisations |
| How metabolic homeostasis is maintained | Blood, hormones, & central nervous system |
| How insulin is produced | Primary polypeptide prohormone proinsulin is released when blood glucose >80mg/dL & is activated by cleaving the C chain. After it has completed it's role it's degraded by either liver, kidney, or skeletal muscle |
| Insulin secretion | When the TCA cycle has produced enough ATP, KATP (ATP sensitive K+ channels) close so an action potential is generated causing an influx of Ca2+ & the exocytosis of insulin vesicles |
| Glucagon secretion | KATP channels are kept open, no inhibition from insulin & somatostatin, T-type (low V) Ca2+ & Na+ channels open to allow an influx that may lead to intermittent depolarisation & exocytosis |
| Mode of action of glucagon | Activates protein kinase-A & adenyl cyclase in liver, skeletal muscle, & adipose tissue by 2nd messenger model to up or downregulate enzymes affecting transcription of metabolic genes |
| Absorptive (well fed) state | 2-4h after meal insulin to glucagon ratio raises dramatically, glycolytic enzymes are more active, storage molecule production upregulated, increased glucose phosphorylation, amino acids are moved to other tissues |
| Pentose Phosphate Pathway (PPP) | Cytosolic metabolic pathway which interfaces with glycolysis to produce NADPH for biosynthesis & ribulose-5-phosphate for nucleotide, nucleic acid, or glycolytic purposes |
| Fasting state | Lack of dietary glucose intake causes spikes in adrenaline & glucagon to induce a catabolic state. Tissues exchange components: fatty acids from adipose or ketone bodies from the liver to maintain plasma glucose levels |
| Enzymes during fasting state: Allosteric regulation & covalent modification | AMP & citrate bind allosterically to slow glycolysis & speed gluconeogenesis, key enzymes are phosphorylated & dephosphorylated especially absorptive enzymes are phosphorylated to reduce their function |
| Enzymes during fasting state: Induction-repressed synthesis & hormone dependence | Gene expression changes due to fasting so more catabolic enzymes are synthesised & less anabolic. Glucagon activates adenyl cyclase to produce cAMP for a cascade, this activates glycogen phosphorylases & hormone sensitive lipases |
| How fatty acid oxidation is favoured in the liver during fasting | Malonyl CoA activates CPT-1 (carnitine) so B-oxidation occurs. NADH inhibits TCA cycle, acetyl CoA inhibits pyruvate dehydrogenase so gluconeogenesis is favoured, & ketone body synthesis is increased due to high acetate conc. |
| Extreme catabolic states | Injury causes extreme catabolism by raising ATP demand in the tissues for repair, immune function, inflammatory response, increased cortisol & catecholamines, & protein synthesis demand |
Created by:
Beech47
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