Lipids and lipid metabolism Flashcards
What are the eight types of dietary fats?
SCFAs; SCFAs (C12-C18); MUFAs; PUFAs (n-6); PUFAs (n-3); cholesterol; phospholipids; trans fats
What are sources of SCFAs?
Milk, milk products, butter
What are sources of SCFAs (C12-C18)?
Meat, animal foods and fats, coconut and palm oils
What are sources of MUFAs?
Olive and rapeseed oils
What are sources of PUFAs (n-6)?
Sunflower and soybean oils, meat, eggs, nuts
What are sources of PUFAs (n-3)?
Oily fish
What are sources of cholesterol?
Eggs, organ meats
What are sources of phospholipids?
Animal foods, eggs
What are sources of trans-fats?
Ruminant animals, hydrogenated fats in manufactured goods
Where are fats stored?
Muscle fibres; within circulation; adipose tissues (subcutaneous and internal fats); adipocytes / lipocytes
How much ATP is released per TG?
~400ATP
How does fat energy storage compare to carbohydrate energy storage?
Fat accounts for ~80% (50,000-100,000kcal) of energy stored in body; carb energy reserve is just 2% of fat energy reserve (2000kcal)
Where is most glycogen stored?
In muscles
What is the order of quantity of energy storage?
Fats > proteins > carbs
What are the three classes of lipids?
Neutral, compound, and derived lipids
What are neutral lipids?
FAs and TGs; comprise of glycerol backbone + 3FAs
What are compound lipids?
Plipids; are ampithatic (hydrophobic and philic)
What are derived lipids?
Steroids and sterols; cholesterol (6C ring + 5C ring)
What is the implication of a longer chain FA?
More solid @RTP
What do saturated FAs stimulate?
Stimulates liver to form cholesterol
What are trans fats?
Form due to processing (heat, light, hydrogenation); have rigid double bonds; trans fats are trans (H and C on opposite sides @ C=C double bond); trans nature means chain is straight and less likely to be liquid; have structure of unsaturated, with properties of saturated; proposed to be better for health
What are examples of
essential FAs?
3-linolenic (n-3) and linoleic (n-6) acid
What do 3-linolenic and linoleic acids do?
Play a role in regulation of gene expression; involved in signal transduction; metabolites produce compounds involved in cell function, inflammation, and immune function
What are plipids?
Glycerol + 2FAs + Pi; are amphipathic; have hydrophobic tail and hydrophilic head; can be unsaturated or saturated; form plipid bilayer and lipoproteins
What do lipoproteins do (general)?
Carry TGs around in blood within them
What are four types of lipoproteins?
Chylomicrons, VLDL, LDL, HDL
What do chylomicrons do?
Have TGs packaged into them; allow absorption of TGs in small intestines; main transport of FAs to body tissues
What do VLDLs do?
Collect lipid droplets; transport FAs to body tissues
What do LDLs do?
Transports large amounts of cholesterol
What do HDLs do?
Collect excess cholesterol and take back to liver; have more protein and less lipid than LDLs
What are three ways that lipids can be mobilised?
Diet –> TGs –> chylomicrons –> lipolysis by lipoprotein lipase –> energy freed from lipids.
Adipose cells/ tissue –> released by hormone sensitive lipase –> form glucagon –> more FFAs and albumin.
Synthesised from liver –> convert excess glucose –> FFAs –> TGs and cholesterol
How are lipids metabolised within the post-prandial period?
In mouth, saliva contains lipase; FAs cleaves off TGs; slow process due to watery environment. In stomach, acid-stable lipase further hydrolyses TGs. In small intestine, TGs form past-like substance (lipid droplets) due to hydrophobic nature; gall bladder releases bile salts; bile salts emulsify droplets; pancreatic lipase into duodenum; pancreatic lipase further hydrolyses TGs; LCFA + MGs liberated; MGs and FFAs form micelles; micelles release FFAs and MGs into lining of epithelial cells; FAs and MGs diffuse into villi epithelial cells; FAs + MGs –> TGs due to watery environment; TGs packaged into chylomicrons; chylomicrons diffuse into lymph; lymph deposits chylomicrons in circulatory system within subclavian veins
What happens to lipids once in the blood?
Chylomicrons travel to tissues; lipoprotein lipase of extrahepatic tissues release FAs within chlyomicrons; FAs are: taken up by adipose for storage/ taken into muscle for fuel or storage as intramuscular TG/ excess FAs cleaved and trasported back to liver, carried by albumin and recycled in a VLDL –> TG
What occurs to lipids in the post-absorptive state/ when fasting?
Are no chlyomicrons; liver produces VLDLs; VLDLs carry TG; drop in glucose = drop in insulin, increase in glucagon; glucagon stimulates (via hormone sensitive lipase) adipose cells to release FAs into blood; albumin is released by liver; FAs bind to albumin; liver takes up FAs which are picked up by LDL and HDL; liver breaks down fats for gluconeogenesis
How is FA utilisation regulated?
Transport of acyl-CoA esters into mitochondria; availability of FAD and NAD for beta-oxidation; lipolysis of TG –> FFAs (analogous to mobilisation of glycogen); resterification of FAs; mobilisation from adipose tissue
What is beta oxidation?
The separation of C chain at the 2nd (beta) carbon
How are FAs transported to target cells?
Adipose stores TGs; lipase breaks down TGs –> MG + FAs; FAs enter blood; FA enters cell via transporter; FA enters mitochondrion
What cells cannot metabolise FAs?
Brain cell or RBCs
How do FAs enter the mitochondrial matrix of the target cell?
Acyl-CoA synthase catalyses FFA –> acyl-CoA; acyl-CoA through porins of outer membrane; acyl-CoA into intermembrane space; carnitine palmitoyl transferase 1 on outer membrane attaches carnitine + acyl-CoA –> acyl carnitine (carnitine shuttle); CoA back into cytoplasm; acyl carnitine through carnitine acylcarnitine translocase on inner membrane into matrix; carnitine palmitoyl transferase 2 attaches CoA + acyl –> acyl-CoA; carnitine regenerated and back to intermembrane space
What regulates rate of FAO at CAPT1?
Glycolytic flux
How does beta oxidation occur?
Fatty acyl CoA has two C atoms removed from FA –> acetyl CoA + remaining FA: involves dehydrogenation (simultaneously reducing FAD); hydration; dehydrogenation (simultaneously reducing NAD); thiolysis (cleavage reaction catalysed by thiolase). Remaining FA re-enters pathway
Why is the actual energy yield from FAs not as much as the theorised?
Due to activation of FAs and processes in Krebs and ETC
Roughly how many ATP are produced from each acetyl-CoA, NADH, and FADH2?
Acetyl-CoA ~10ATP (perfect would be 12).
NADH ~2.5 (perfect would be 3).
FADH2 ~1.5 (perfect would be 2)
How many ATP are used in FA activation?
2
How nutrients interconverted?
Gluconeogenesis at the liver: glycerol, lactate and certain amino acids –> glucose; Lipogenesis at the liver and adipose cells: glucose and amino acids –> lipids
How is lactate converted to glucose?
Cori cycle: 2 lactate –> 2 pyruvate + glucose
How does carb oxidation change during prolonged exercise?
Significantly reduces over a three hour time span
How does fat oxidation change during prolonged exercise?
Significantly increases from onset of exercise
What substrate is responsible to largest energy expenditure?
Muscle glycogen - is used until it runs out
What is maximal fat oxidation?
Fat max: consume most fat @65% VO2max
Where does the range of fat max lie in regards to HR?
~60-80% HRmax
How does training status affect fat max?
%VO2max where fat max lies remains the same; fat max rate is increased in higher trained individuals
How does training affect substrate utilisation?
Endurance training increases use of intramuscular fat stores; less carbs are used
How does gender affect fat max?
Females’ fat max occurs at higher %HRmax; females’ fat max rate is higher
How does carb intake affect fat oxidation?
Consumption of carbs pre-exercise significantly reduces fat oxidation, particularly on intramuscular TGs
How does cycling affect fat max compared to running on a treadmill?
Oxidise much lower fats; fat max similar both when on treadmill and bike
How does exercise affect glycogenolysis?
Increased exercise intensity increases glycogenolysis in almost a linear relationship
Why is fat oxidation not sufficient at high intensity?
70-90% VO2max needs ~1mol ATP/min, but maximal rate of rate oxidation is only ~0.4 mol ATP/min
How does carb oxidation reduce fat oxidation at increased exercise intensity?
Increased plasma FAs does not increase fat oxidation during high intensity + main effect is on IMTG = limitation within muscle cell. Only oxidation of LCFAs is impaired = carnitine shuttle and beta oxidation are limiting = CoA, NAD, carnitine all needed for processes. CoA, NAD, carnitine reduced during high intensity exercise with increase in carb oxidation = source of reduced fat oxidation
