Energy Production-lipids Flashcards
What are the general properties of lipids?
Generally hydrophobic
Mostly contain C,H and O
More reduced than carbs=release more energy when oxidised + complete oxidation requires more O2
List the 3 classes of lipids.
Fatty acid derivatives
Hydroxy-methyl-glutaric acid derivatives (C6 compounds)
Vitamins
List some fatty acid derivatives and their functions.
Fatty acids=fuel molecules
Triacylglycerols=fuel store and insulation
Phospholipids=membrane and plasma lipoproteins
Eicosanoids=local Mediator (messenger)
List some HMG (C6 compounds) derivatives and their functions.
Ketone bodies (C4)= water soluble fuel molecules (STarve)
Cholesterol=membrane + steroid hormone synth
Cholesterol ester=store cholesterol
Bile acid+salt=lipid digestion
List some lipid vitamins and their source.
A, D ,E and K
Dietary we cant make them
What are some characteristics of triacylglycerols?
Hydrophobic Stored in anhydrous form (a blob) Stored in adipose tissue Used in prolonged exercise, starvation and pregnancy Storage/mobilisation hormonal controlled
Where does lipid metabolisms start and where does it go from there?
It begins as hydrolysis in the small intestine (using pancreatic lipases) it becomes fatty acids and glycerol.
Then recombined and transported by TAG by lipoprotein chylomicrons.
Either oxidised to energy in consumer tissues or stored as TAG in adipose tissues.
How does TAG move from adipose tissue to consumer tissues when needed?
It travels as the FA albumin. In fat mobilisation
What drives fat mobilisation?
Hormone sensitive lipase controls fat mobilisation from adipose tissues.
High glucagon/Adrenalin increases fat mobilisation
Low insulin increases fat mobilisation.
How are FA transported and stored across the body?
Converted back tot riglycerides in GI tract
Packaged into lipoprotein particle (CHylomicrons)
Released into circulation via lymphatic
Carried to adipose tissues
Stored as triglycerides
Released as FA when needed
Carried to tissues as albumin-fatty complex
What happens to the fatty acid cycle in adipose tiki cue when extracellular glucose is low?
The fatty acids are not recombined with Co-A to then act upon glycerol-1-P as there will be no glycerol-1-P to act upon.
Instead they are released for use, travelling on albumin.
What is the normal fatty acid cycle in adipose tissue?
Glycerol-1-P from glycolysis esterifies fatty acyl-CoA to a triglyceride. This is then broken down into glycerol (which is released) and fatty acids.
These fatty acids re-enter the cycle and join acy-CoA.
Define amphipathic.
The molecule contains both hydrophilic and hydrophobic groups.
Why are certain polyunsaturated fats needed in our diet.
As mammals cannot make them themselves as we cannot introduce a double bond beyond C9.
Summarise fatty acid catabolism (the second stage of FA metabolism).
Occurs in mitochondria
FA activated by linking to coenzyme A outside mitochondria
Transported across inner mitochondrial membrane using carnitine shuttle
FA cycles through sequence of oxidative reaction (C2 removed each cycle) until al C’s removed.
Summarise FA activation.
Occurs in cytoplasms
FA activated by linking to Coenzyme A, via high energy bond, in fatty acyl CoA synthase
Activated FA’s do not readily cross inner mitochondrial membrane (large and hydrophobic) so use carnitine shuttle.
List some key feature of the carnitine shuttle.
Regulated = controls rate of FA oxidation
Inhibited by malonyl-CoA (a biosynth intermediate)
Defects can occur causing exercise intolerance or lipid droplet s in muscles.
See image for mechanism
What are the key point of fatty acid metabolism?
Occurs in most tissues and rbc’s (not those without mitochondria or the brain) Mitochondrial A cycle of Reactions Remove 2C per cycle Oxidation H+ and e- transferred to NAD and FAD Stops in absence of O2 No direct ATP synth
Where is glycerol metabolised?
The liver
What is the main mechanism for glycerol.
It’s turned to glycerol phosphate by glycerol kinase enzyme nd one ATP.
Then enters either triacylglycerols synth or glycolysis depending on signal received.
What is the main function of acetyl-CoA?
The most important intermediate in both anabolic and catabolic pathways.
Synths fatty acids for triacylglycerols + phospholipids
Releases CO2 in krebbs
Synthesis’s HMG for ketone bodies and cholesterol
What is the normal threshold for ketones in the blood and what raises this?
Normal plasma ketone conc <1 mM
In starvation 2-10mM (physiological ketosis) energy supply
Untreated type 1 diabetes >10mM (pathological ketosis)-fruit breath
What stimulates ketone body production? Nd how?
Low NAD+ substrate availability or NADH production is inhibited.
This diverts Acetyl-CoA from the TCA cycle to ketone production.
How are ketone bodies produced?
???
How does starvation link to keton bodies?
When insulin/glucagon ratio is low (starvation) then lyase is activated, and reductase is inhibited beginingketon body synth
Acetyl CoA becomes HMG-CoA. What decides whether this molecule then forms cholesterol or ketone bodies?
If exposed to high insulin it becomes cholesterol (storage)
If exposed to high glucagon it becomes ketone bodies (energy source)
How do ketone bodies help the brain survive starvation?
In starvation less glucose is available, the brain needs glucose for metabolism. Therefore in starvation muscles try to use other sources of energy to divert any glucose to the brain. The muscles can use FA and ketone bodies as energy
What happens in long term starvation
We run out of amino acids in diet and they are needed to produce new blood glucose that’s no longer provided in the diet. Therefore the muscles are broken down releasing amino acids to then enter gluconeogenisis.
What is some key info about ketone bodies?
Water soluble
Permit relatively high plasma conc
Alternative substrate
If above renal threshold, excrete in urine = ketonuria
Acetoacetat and B-hydroxybutyrate are strong Organic acids= ketoacidosis-low blood pH
Volatile acetone excreted via lungs-fruity breath
What 3 ketone bodies can the body produce?
Acacetoacetate - from liver
Acetone- from spontaneous breakdown of the above
B-hydroxybutyrate- from liver
