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Fatty Acid Oxidation

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Question	Answer
Role of Hormones	Signal to metabolism a fed state, substrate deficiency or fight or flight Metabolism responds by taking substrate up into tissues, returning substrate to the blood and diverting substrate into energy producing pathways
Insulin	Secreted by beta cells in the fed state Stimulated by increased blood glucose, certain amino acids and fatty acids Signal of substrate excess Tells tissue to store fuel and breakdown glucose
Glucagon	Secreted by alpha cells in the fasted state Stimulated by low glucose Signal of substrate deficiency Only acts on liver Signal to liberate glucose into blood from liver
Adrenaline	Secreted by the adrenal gland Fight or flight response Tell tissues to divert substrates towards making ATP
What are lipids	Diverse group of molecules Stored as triglycerides Used for energy as non-esterified fatty acids Converted into sterols and phospholipids Hydrophobic - need specialised transport molecules
Function of lipids in energy production	Large stores More energy dense per molecule than glucose Rapidly mobilised and stored Ideal for tissues with high energy demand Cant be used by all tissues Requires more oxygen than glucose
Processes involving fats	Digestion of dietary fats De novo lipogenesis Use in oxidative tissue to make energy Storage in adipose tissue Used to make ketone bodies in the liver
Digestions	Large triglycerides are hydrophobic and cannot move into cells Broken down by bile salts into smaller droplets Attacked by pancreatic lipases which break down TAG to generate NEFA and glycerol Makes mixed micelles which can be absorbed
Packaging into chylomicrons	Inside intestinal cells, mixed micelles are reformed into TAG Fatty acids are combined with cholesterol and glycerol to form chylomicrons These are surrounded by apoproteins to make them hydrophilic
Release of NEFA by lipoprotein lipase	LPL sits on surface of endothelial cells Hydrolyses TAG in the chylomicron into NEFA This releases NEFA for uptake by adipose and muscle LPL is activated by insulin
Adipose tissue	Organelles squashed to the outside Majority is a lipid droplet Adipose triglyceride is a mixture of saturated and unsaturated fatty acids
Transport of NEFA in the blood	NEFA is re-esterified into TAG to be stored NEFA is remobilised by lipase enzymes - Adipose triglyceride lipase, hormone sensitive lipase and monoacylglycerol lipase Hydrophobic NEFA transported in blood bound to albumin protein
Regulation of Hormone sensitive lipases	Activate by phosphorylation via adrenaline activating cAMP and PKA This increases fuel to the muscles and heart Inactivated by dephosphorylation by protein phosphatase, activated by insulin signalling
Plasma NEFA concentrations	Fed state - 0.3-0.6 mmol/L Prolonged exercise - 2 mmol/L Stress - 0.8-1.8 mmol/L Fasting - 0.5-2 mmol/L Thyroxine - 0.6-0.8 mmol/L
Storage in non-adipose tissue	Many cells have TAG stores Provides a source of energy is need to suddenly produce ATP TAG stores must be kept low to avoid damaging normal function Too much TAG leads to non-alcoholic fatty liver disease etc
Fatty acid metabolism in the heart	Fats are more energy rich than glucose - the heart needs more ATP per gram than any other organ Its use of TAG leaves glucose for cells which must use it 60-70% of ATP comes from fatty acid oxidation Contains intrinsic TAG stores
Fatty acid metabolism in the renal cortex	Kidneys require large amounts of energy to accomplish reabsorption Cortex is highly reliant on fatty acids Medulla has a poor oxygen supply - limited mitochondrial respiration so rely on glucose
Skeletal muscle and metabolism	Type 1 - slow twitch - oxidative - higher reliance on fatty acids Type 2 - slower fast twitch and faster fast twitch - glycolytic - rely on glucose In exercise initially use glycogen stores, then switch to fatty acids when these run out
Steps of fatty acid oxidation	Uptake Activation Carnitine shuffle Beta oxidation
Transport across the plasma membrane	Can diffuse across the membrane by a flip flop mechanism Transporter mediated uptake by fatty acid translocase - regulates uptake Intercellular FA is bound to cytoplasmic fatty acid binding protein
Activation	Fatty acids are activated in the cytosol by adding a CoA molecule to form Fatty acyl CoA Catalysed by Acetyl CoA synthetase Uses ATP Traps them in the cell and makes them a substrate for further enzymes
Transport into mitochondria	Need to cross highly impermeable inner membrane - no transporter Conjugated with carnitine which can be transported Achieved by 2 enzymes and one transporter
Carnitine Shuffle	Fatty acyl CoA conjugated with carnitine to form fatty acyl carnitine by CPT1 This crosses the membrane in CAT Fatty acyl carnitine is then converted back to fatty acyl CoA
Stages of beta oxidation	Oxidation of FACoA to trans enoyl Coa Hydration to Hydroxyacyl CoA dehydrogenase Oxidation to ketoacyl CoA thiolase Thiolysis to FACoA and Acetyl CoA
Isoforms of Acyl CoA dehydrogenase	Each breaks down different lengths of fatty acyl CoA Very long chain Long chain Medium chain Short chain
Products of Beta oxidation	Multiple acetyl CoA units Multiple NADH Multiple FADH2 There will be half the acetyl CoA as carbons in the FA e.g. 8 in a 16 C FA These feed into krebs cycle and oxidative phosphorylation
Dealing with unsaturated fatty acids	Contain a cis double bond Isomerase converts cis to trans double bond Reductase makes it a substrate for ongoing oxidation
Dealing with fatty acids with an odd number of carbons	B oxidation produces acetyl CoA with 2 carbons, so if an odd chain FA enters this is not possible The last cycle generates 1 Acetyl CoA and 1 propionyl CoA This can then be metabolised to succinyl CoA and enter the krebs cycle
Dealing with short chain fatty acids	Less than 6 carbons Enter mitochondria directly Bypass the carnitine shuffle
Dealing with very long chain fatty acids	20-22 carbons Must be shortened in the peroxisomes to 16-18 carbons Then transferred to mitochondria This does not generate ATP but produces H2O2
Dealing with branched chain fatty acids	Starts in peroxisomes with alpha oxidation before transfer to mitochondria for beta oxidation
Regulation of beta oxidation	Hormone sensitive lipase - regulated by hormonal phosphorylation as an external signal The carnitine shuffle - regulated intracellularly via allosteric control - inhibited by malonyl CoA from lipogenesis to prevent futile cycling
Systemic Carnitine deficiency	Relatively rare genetic disorder Unable to take carnitine up into cells, shutting down the carnitine shuffle Cardiomyopathy, fatty infiltration of organs, muscle weakness and hypoglycaemia Caused by switch from FAs to glucose as a fuel
Jamaican Vomiting Sickness	Poisoning - inhibition of Acyl CoA dehydrogenase Hypoglycin A is metabolised into a product that inhibits the first step of beta oxidation The body switches to using glucose Hypoglycaemia, coma and death