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399369
Fatty Acids
Description
University Biochemistry Mind Map on Fatty Acids, created by Sophie Mae Neash on 28/11/2013.
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biochemistry
biochemistry
university
Mind Map by
Sophie Mae Neash
, updated more than 1 year ago
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Created by
Sophie Mae Neash
almost 11 years ago
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Resource summary
Fatty Acids
Fatty Acid Biosynthesis
Occurs in the cytoplasm
Occurs in the liver, kidney, brain, lungs, mammary and adipose tissue
Acetyl coA myst first be converted into malonyl CoA by acetyl CoA carboxylase.
Annotations:
Acetyl CoA carboxylase is allosterically activated by citrate and isocitrate and inhibited by palmitoyl CoA negative feedback.
Insulin stimulates acetyl CoA carboxylase activity. Glucagon and adrenalin inhibit it by increasing intracellular levels of cAMP.
Formation of malonyl CoA involves covalent binding of CO2 to biotin using ATP hydrolysis.
Using the same enzyme, CO2 is then tranferred to acetyl CoA, producing malonyl-CoA
Remaining reactions take place on a multifunctional protein called fatty acid synthetase (FAS)
Initial condensation involves an acetyl group and a malonyl group.
Acetyl group and malonyl group must be transferred from their CoA derivatives to a condensing enzyme and ACP.
Annotations:
Catalysed by acetyl transacetylase (ATP) and malonyl transacetylase (MT)
Four reactions - condensation, reduction, dehydration and then another reduction.
Lipolysis
TAG is formed from acyl CoA and glycerol-3-phosphate in the adipose tissue.
Glucose entry into the adipocytes is facilitated by GLU4 transporter
Annotations:
GLUT 4 - Translocated from the Golgi complex to the plasma membrane in the presence of insulin.
When glucose levels are high, a large proportion is converted to acetyl CoA and then to LCFA or goes into the TCA cycle.
As glucose runs out, it is directed to the formation of glycerol 3-phosphate and TAG.
Insulin also activates lipoprotein lipase (LPL) resulting in the hydrolysis of TAG contained in the chylomicrons.
Provides FA for esterfication with G-3-P inside adipose tissue.
Regulation
Adrenalin act rapidly in promoting lipolysis by stimulating membrane bound adenyl cyclase, thus increasing levels of cAMP
Increasing levels of cAMP are responsible for converting inactive HSL into its active phosphorylated form thus promoting lipolysis
Annotations:
cAMP stimulates cAMP-dependent protein kinase (PKa)
Intracellular cAMP levels are reduced through the activity of cAMP dependent phosphodiesterase which is activated by insulin.
Glucocorticoids promote lipolysis through a cAMP-independent pathway.
They promote gene transcription and so increase HSL biosynthesis.
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