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WEEK 9:
Fatty acid metabolism 1- breakdown of fatty acids and synthesis of ketone bodes:
| Question | Answer |
|---|---|
| storage of lipids | triacylglycerol, mostly in adipose tissue |
| structure of lipids | phospholipids in cell membranes |
| groups in a fatty acid | hydrophobic hydrocarbon chain and hydrophilic carboxyl group (amphipathic) |
| saturated meaning | no double bonds in the alkyl chain |
| unsaturated meaning | one or more double bonds in the alkyl chain |
| double bonds can be | cis or trans |
| trans fatty acids | rare in natural products |
| cis fatty acids | are the only bent ones |
| trans fatty acids are formed in | processed foods by hydrogenation of vegetable oils and are widely used in snacks and biscuits and are associated with greater risk of coronary heart disease |
| why do many omega fatty acids have to come from diet | because desaturase (in humans) cannot insert double bonds beyond C-9 |
| lionleate C-9 C-12 omega fatty acid is found in | nuts, vegetable oils, and avoocado which is required for synthesis of arachidonate prostaglandins) |
| linolenate (C-9 C12 C15) omega 3 fatty acid is found in | fish oils for retinal cell membranes/ brain development and it reduces risk of CVD |
| what happens to fatty acids stored in adipose tissue | esterified (linked) to glycerol (ester bon between fatty acid and carboxyl and glycerol hydroxyl group) |
| triacylglycerols made of | three fatty acids esterified to glycerol (are highly reduced so have high calorific value, are virtually anhydrous and forms droplets within cells) |
| when fatty acids are metabolised by liver and muscle they are broken into | 2 carbon acetate units by beta oxidation in mitochondria and this acetate enters TCA cycle for ATP production |
| what activates hormone sensitive lipases | stress (adrenaline) and glucagon (fasting) |
| function of hormone sensitive lipases | hydrolyse TAGs in adipose tissue to free fatty acids and glycerol |
| free fatty acids (FFAs) enter | circulation bound to plasma albumin |
| when are fatty acids released | at target tissues crossing into cytosol of cells |
| what type of oxidation does fatty acids undergo | beta oxidation |
| what happens to glycerol | transported to liver, phosphorylated to glycerol 3-phosphate and converted to dihydroxyacetone phosphate DHAP) which is used in glycolysis/ gluconeogenesis |
| what happens to fatty acids | taken up by tissues (freely cross membrane) and are converted to acetate units (acetylCoA) by oxidation |
| explain beta oxidation of fatty acids | long chain fatty acids activated in cytosol to form thiol esters with CoA (using ATP) -> imported into mitochondria for B-oxidation to generate NADH, FADH2 and acetyl CoA |
| CoA fatty acid esters cannot cross the | IMM |
| how can CoA fatty acid esters to cross the IMM | reversibly link to carrier (Carnitine) to enter the mitochondrial matrix |
| where does carnitine come from | obtained from meat in diet and synthesised in liver and kidney, and supplied to muscles by kidney via blood |
| carnitine deficiency | from liver disease, malnutrition, trauma, pregnancy or congenital deficiency which can lead to build up of toxic LCFAs leading to neurological damage |
| LC-fatty acyl group transferred to | carnitine which is then transported into mitochondrial matrix and then transferred to CoA then carnitine is re exported as same transporter to repeat process |
| LCFAs are subjected to repeated rounds of (4) OHOT | oxidation (generates double bound on C2 trans and FADH2) hydration (generates OH on C3 (B carbon) oxidation (generates carbonyl on C3 and NADH) thiolytic cleavage (generates acetyl CoA and shortened fatty acyl-CoA (minus 2C) |
| B oxidation is regulated by | supply of substate- depends on rate of lipolysis in adipocyr and regulated by hormones eg glucagon and adrenaline |
| malonyl CoA | staring point for fatty acid synthesis which inhibits carnitine palmitoyltransferase I (CPTI) enzyme - which is repsonsible for the uptake of LCFA into mitochondria |
| malonyl CoA inhibits fatty acid oxidation how (break down) | blocks transport of fatty acids into mitochondria (via CPTI) preventing beta oxidation |
| ketone bodies | 'alternative fuel' synthesised from acetyl CoA in liver mitochondria and is made when levels of acetyl CoA are high from B-oxidation eg starvation, uncontrolled diabetes |
| when are ketone bodies used as a fuel | during starvation, uncontrolled diabetes, acting as an important fuel source for the brain during extended fasts |
| elevated level of ketone bodies leads to | ketosis- where babies can become ketotic quickly due to small glycogen stores |
| examples of ketone bodies formed | acetoacetate and 3-hydroxybutyrate (acetone also formed but excreted in breath which can be indicative of ketotic individual) |
| acetoacetate is reduced to | 3-hydroxybutyrate when NADH conc high (NADH conc increased in liver when B-oxidation active- starvation) |
| 3-hydroxybutyrate is oxidised in | tissues to become acetoacetate with NADH produced which yields ATP |
| acetoacetate converted to | acetyl CoA which enters TCA cycle |
| acetoacetate has how many carbons | 4 carbons (2 acetate groups) |
| why does the brain using ketone bodies | because the brain cannot directly use FFA bound to albumin |
| high ketone body use does what | reduces protein breakdown eg muscle loss in starvation |
| normal ketone body concentration of plasma | 0.1mM |
| when ketone body concentration reaches 7mM, utilisation by tissues is | saturated (ketones excreted in urine - ketonuria) |
| in uncontrolled diabetes, plasma ketones can rise to | 20mM |
| acidic ketone bodies result in | drop in blood pH (ketoacidaemia) which is life threatening |
| how are ketone levels tested | using urine or blood test kit eg Ketostix, KetoRx sticks |
Created by:
kablooey
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