BCM 475 Chapter Notes - Chapter 27: Glycogen Synthase, Acetyl-Coa, Mitochondrial Biogenesis
Document Summary
Step by step oh baby: binding | insulin to receptor, activation | dimerization & auto- crossphosphorylation. Each subunit of dimer phosphorylates its partner: generates binding sites | for irs (insulin-receptor substrates) Facilitates translocation of glut4-containing vesicles to cell membrane: glut4 transports glucose into muscle/fat cells. Phosphorylates/inhibits glycogen synthase kinase (gsk3: gsk3 inhibits glycogen synthase (inhibits glycogen synthesis) Tyrosine phosphatase ib: removes p groups from receptor. Normally phosphorylates oh groups of tyrosine (also pyridine) Dephosphorylates pip3 forms pip2 (with no second-messenger properties) Grossly abnormal fuel usage: glucose is overproduced by liver, underutilized by organs. Leading cause of blindness, kidney failure, amputation (body thinks its starving) Normal or higher level of insulin, but unresponsive to hormone. Excess fatty acids insulin resistance in muscle modify metabolism. Rate of b oxidation increases with increased [fat], but mitochondria cannot handle excess. Fatty acids accumulate reincorporation in tags, fats collect on cytoplasm. Increased levels of diacylglycerol and ceramide = diet-induced insulin resistance.
