BIOC 3560 FA metabolisn.docx

Triacylglycerol can be made in adipose tissue or

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Triacylglycerol can be made in adipose tissue or liver it is simultaneously broken down (only in adipose) Approximately 75% of FAs released by lipolysis are reesterified to form triacyglycerols This futile cycle may help make the system more responsive to quickly changing needs Regulation and integration of metabolism Regulation of FA biosynthesis/degradation Roles of specific tissues in metabolism Hormonal responses to metabolic state Detailed example of regulation – GSK3 Regulation methods – levels of control Rapid – cellular regulation of enzymes (sec to min) o Eg. High concentration of ATP inhibits phosphofructokinase-1 Slow/moderate – hormonal regulation (min to h) o Eg. Glucagon, insulin trigger signalling cascades Gradual/adaptive – changes in gene expression (h to days) o Eg. high fat diet triggers β-oxidation enzyme synthesis
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Regulation of FA β-oxidation The transfer of FAs into the mitochondria is the committed step o Once in the mitochondria, FAs will be broken down by β-oxidation The most important regulatory mechanism is malonyl-CoA inhibition of carnitine acyltransferase I In the mitochondria: o High [NADH]/[NAD+] inhibits β-hydroxyacyl-CoA dehydrogenase o Acetyl-CoA inhibits acyl-CoA acetyltransferase (thiolase) Citrate lyase is activated by insulin; it converts citrate to acetyk-CoA Acetyle-CoA carboxylase catalyzes the committed step where acetyl-CoA is converted to malonyl-CoA Regulated by both metabolites (allosteric) and hormones (by phosphorylation) Regulation of acetyl-CoA carboxylase Acetyl-CoA carboxylase (ACC) is the key target of regulation in FA synthesis Regulated by metabolites: o Palmitoyl-CoA (ultimate product) inhibits ACC o Citrate (acetyl-CoA precursor) activates ACC Regulated by hormones: o Epi/glucagon causes phosphorylation of ACC, inhibiting it o Insulin promotes dephosphorylation of ACC, activating it by polymerizing it into active ACC filaments Reciprocal regulation of fatty metabolism High blood glucose will cause insulin to be released Insulin will activate phosphatase that will affect acetyl-CoA It will dephosphorylase ACC so that it is active Malonyl-CoA is an important product that inhibits carnitine acyl transferase I, which helps with fatty acid β-oxidation in the mitochondria Relief of inhibition is when there is no malonyl-CoA to inhibit carnitine acyl-transferase I, causing an increase in β-oxidation Fatty acid synthesis and degradation are regulated to only one occurs at a time Specialized roles of mammalian tissues Pancreas – secretes insulin and glucagon in response to changes in blood glucose concentration Brain – transports ions to maintain membrane potential; integrates inputs from body and surrounding; sends signals to other organs Cardiac muscle – uses ATP generated aerobically to pump blood Lymphatic system – carries lipids from intestine to liver
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  • Spring '10
  • dawson
  • FAS, Ketone bodies

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