BIOC 3560 FA metabolisn.docx

Acts on liver and adipose tissue o adipose release

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Acts on liver and adipose tissue o Adipose – release FAs from TAGs o Liver – promotes gluconeogenesis, glucose is stored as glycogen or is exported Net effect: restore blood glucose levels and increase glycogen stores Diabetes – a disease of metabolic disregulation Diabetes is characterized by absence of, or improper response to, insulin Without an insulin response, metabolism is dictated by glucagon As a result, even when glucose is abundant, it is not stored or used as a fuel The organism thinks it is fasting, when it actually has excess glucose Nearly 7% of the Canadian population has diagnosed diabetes Metabolic effects of diabetes – glucose In the liver, the concentration of fructose-2,6-biphosphate is kept low by an active FBPase-2 phosphatase o Decrease glycolysis o Increase gluconeogenesis in the liver GLUT4 glucose transporters are not moved to the membrane (muscle and adipose) So sugar is not appropriately used or stored Excessive blood sugar is secreted in the urine Metabolic effects of diabetes – FAs Glucagon causes phosphorylation of acetyl-CoA carboxylase, inactivating it Acetyl-CoA accumulates in the cytosol, but it is not converted into malonyl-CoA So TAGS are not made and stored Acyl-carnitine transport is highly active because malonyl-CoA concentration is low FA β-oxidation increases, but oxidation is incomplete as high levels of NADH/NAD+ inhibits TCA Excess acetyl-CoA turned into excess ketone bodies This can result in ketosis (excess ketone bodies) and acidosis (ketone bodies are acidic, lowering blood pH) Example of regulation – Glycogen synthase kinase 3 GSK3 cannot act unless casein kinase II phosphorylates/primes GS first
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GSK3 helps turn active glycogen synthase a to inactive glycogen synthase b GSK3 is inhibited by insulin PP1 does the reverse process and it is activated by insulin, G6P, glucose, and inhibited by glucagon and Epi GSK3 can only phosphorylate a Ser if the residue $ c-terminal to it is a phosphoserine The priming site phosphorylated by CK2 has positively charged amino acids GSK3 is auto-inhibited by a substrate-like sequence at its N-terminus When phosphorylated by PKB, this sequence binds in the catalytic site, where it blocks other real substrates Because the amino acid 4 upstream (0 site) is Pro, not Ser/Thr, the enzyme cannot further phosphorylate this sequence Instead this pseudosubstrate just binds in the catalytic site, blocking real substrates
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