Lipids Flashcards
(44 cards)
Name the three classes of lipids.
Fatty acid derivatives
Hydroxy-methyl-glutaric acid derivatives
Vitamins
How are triacylglycerides formed?
They are formed from a glycerol backbone and three fatty acid molecules. They are a product of esterification reactions.
Give properties of TAG and state where in the body it can be found.
TAG is a hydrophobic molecule which is stored in its anhydrous form in adipose tissue.
What are the products of TAG breakdown and where are they metabolised?
Glycerol –> Liver. Metabolised by glycolysis.
Fatty Acids –> Adipose / Target Tissues. Fatty Acid oxidation releases energy.
What enzyme in the small intestine catalyses breakdown of TAG?
Pancreatic lipase.
What are the two tissues/ cells where Fatty acid oxidation cannot be used to release energy?
Red Blood Cells (these have no mitochondria) and the brain (cannot pass the blood-brain barrier)
Name two hormones which can activate fat mobilisation.
Adrenaline and Glucagon.
Explain why when there is low Extracellular glucose, FA are oxidised.
When glucose is low, there is less substrate for TAG synthesis (glycerol-1-phosphate) being produced from glycolysis, so this leads to an accumulation of FA in the tissues. These are oxidised to release energy.
Why are some fatty acids essential?
Fatty acids with a double bond after C9 cannot be synthesised by the body and therefore they must be sourced from the diet.
Where does activation of fatty acids occur and what is the enzyme responsible for this?
Activation occurs in the cytoplasm.
Fatty acyl coA synthase.
What transporter protein is used to transport activated fatty acids into the mitochondria for B oxidation?
Carnitine shuttle
Name the substance which inhibits the Carnitine shuttle to prevent breakdown of newly synthesised FA.
Malonyl~coA
When a Cn fatty acid enters B oxidation, what is the product?
A C(n-2) molecule and also a C2 which is acetyl~coA and enters the TCA cycle.
What is the enzyme which converts glycerol from TAG breakdown into glycerol phosphate?
Glycerol kinase.
Acetyl~coA is a useful intermediate for anabolism and catabolism. What anabolic processes is it a precursor for?
Hydroxymethylglutaric acid derivatives including Ketone Bodies and Cholestrol.
Fatty Acids
Name three ketone bodies
Acetoacetate, acetone and B hydroxybuturate.
How do statin drugs lower Cholestrol?
Statin drugs lower Cholestrol formation by inhibiting HMG~coA reductase which is a step in the metabolic pathway for Cholestrol synthesis.
How is production of ketone bodies regulated?
Ketone body production is regulated because the starting molecule is acetyl~coA which is diverted from the TCA cycle. When NADH is high this leads to product inhibition, and so acetyl~coA is diverted to alternative pathways.
What is the name of the enzyme which catalyses the reaction from HMG~coA to acetoacetate?
Lyase. This is inhibited when Insulin to Glucagon ratio is high as HMG~coA is used for Cholestrol synthesis. When this ratio is low, lyase is activated and ketone bodies form.
How does muscle protein breakdown provide glucose for the brain?
Protein - amino acids, Pyruvate, gluconeogenesis glucose
In prolonged starvation what fuel molecules do muscles use and why?
Fatty acids and ketone bodies. The prevent usage of glucose which is reserved for the brain.
What is a common condition seen in starvation and also in type one diabetes?
Ketoacidosis. This occurs because acetoacetate and B hydroxybuturate are both relatively strong acids. Ketouria will also be seen because ketone bodies are above the renal threshold.
What happens during fatty acid oxidation if the carbon chain has an odd number of carbons?
In this case, the cycle continues until 3 carbons remain. Carboxylase catalyses carboxylation and the production of methylmalonyl~coA which is then rearrange to succinyl~coA, a Kreb cycle intermediate.
When glucose is low, Pyruvate dehydrogenase is inhibited. How does this help to maintain glucose?
Inhibition of Pyruvate dehydrogenase slows acetyl~coA synthesis, and therefore acetyl~coA –> citrate which I inhibits phosphofructokinase. This leads to a build up of Glucose 6 phosphate which acts as product inhibition on hexokinase and so maintains glucose concentration.
