Chapter 17 Flashcards
(10 cards)
Why fatty acids are the preferred form of storage of metabolic energy?
Fatty acids are mainly composed of –CH2– groups which are fully reduced; high energy of complete oxidation
Fatty acids are hydrophobic – they DO NOT need to be solvated; they can be packed tightly and in large quantities in storage tissues
Lipases
Lipases hydrolyze triacylglycerols, releasing one fatty acid at a time and forming diacylglycerols, monoacylglycerols, and finally, glycerol
Pancreatic lipase hydrolyzes dietary triacylglycerols, lipoprotein lipase acts on lipoprotein triacylglycerols, hormone-sensitive lipase is responsible for mobilization of triacylglycerols from adipose tissue storage
LDL particles
( “bad cholesterol”) – have high lipid:protein ratio, their lipid is mainly cholesterol
HDL particles
(“good cholesterol”) – lipid-poor, protein-rich, the most dense of all lipoproteins
chylomicron
the largest lipoprotein
the least dense lipoprotein
has the highest lipid:protein ratio
Mobilization of triacylglycerols stored in adipose tissue
In response to hormones, hormone-sensitive lipase (HSL) is activated
HSL hydrolyzes stored triacylglycerols to release fatty acids
The mobilized fatty acids are released into the bloodstream where they associate with serum albumin and circulate to various tissues in need of fuel
Stages of complete fatty acid oxidation
Stage 1 consists of oxidative conversion of two-carbon units into acetyl-CoA via β-oxidation with concomitant generation of NADH and FADH2
Stage 2 involves oxidation of acetyl-CoA into CO2 via citric acid cycle with concomitant generation NADH and FADH2
Stage 3 generates ATP from NADH and FADH2 via the respiratory chain
Fate of excess acetyl-CoA
Entry of acetyl-CoA into citric acid cycle depends on availability of oxaloacetate (for formation of citrate)
Oxaloacetate is depleted during gluconeogenesis
If organism has a high intake of fat, low intake of carbohydrate, or is unable to metabolize glucose (diabetes), or during fasting/starvation, [acetyl-CoA]»[oxaloacetate]
Acetyl-CoA is diverted to formation of ketone bodies
Ketone bodies are formed when capacity of citric acid cycle is exceeded
Use of ketone bodies as fuel
Ketone bodies are formed in the liver mitochondria
Acetoacetate and b-hydroxybuterate are transported by the blood to extrahepatic tissues
Acetone is produced in smaller amounts and is exhaled
Ketone bodies are converted to acetyl-CoA and oxidized by the citric acid cycle for energy in skeletal and cardiac muscle and brain
The brain prefers glucose as fuel but can adapt to using ketones when glucose is not available
Oxidation of ketones by other tissues facilitates the continued oxidation of fatty acids in the liver
Ketone bodies and diabetes:
In uncontrolled diabetes and starvation
Glucose cannot enter cells and is not available for oxidation
Gluconeogenesis depletes intermediates for the citric acid cycle, citric acid cycle pauses
Fatty acid biosynthesis is inhibited (normally activated by sufficient levels of insulin)
Malonyl-CoA (first step of fatty acid synthesis) is not formed
Fatty acid b-oxidation is not inhibited (at carnitine acyl-transferase I)
Acetyl-CoA is in excess and ketones are formed
Uncontrolled diabetes results in diabetic ketoacidosis, the decrease in blood pH impairs some tissue functions and can be fatal
