Lipid Metabolism and Ketones Flashcards
consequences of increased fat intake without appropriate energy expenditature
increase in number of adipocytes
more fat in adipocytes
obesity
what is the energy balance dependent on
genetically linked factors - protein messengers regulating appetite
environmental factors - food abundance, fashionable food
requirements for fat
energy source
essential fatty acids - polyunsaturated fats cannot be made in the body (deficiencies lead to membrane disorders, increased skin permeability, mitochondrial damage)
soluble vitamins - A, D, E, K stored in body fat
structure of lipids
predominantly hydrocarbon
long chain fatty acid
insoluble in water - important for biological function
examples of lipids
simple
compound
steroids
describe triglycerides
simple lipid - glycerol and 3 fatty acids
main energy storage form in adipose tissue
compact - doesn’t require concomitant storage of water
hydrophobic
high energy yield per gram
structure of fatty acids
mainly straight chains
aliphatic - no rings
even number of carbon atoms - branched and odd numbers of carbon atoms are rare
saturated fatty acid
no double bond
unsaturated fatty acid
double bond - cis figuration
polyunsaturated fatty acid
multiple double bond
lower the melting point
occur in small amounts - cannot be synthesised by body but is essential for living
e.g. linoleic acid
examples of natural fatty acids
palmitic acid - saturated
stearic acid - saturated
oleic acid - unsaturated
melting point of fatty acids
fatty acids with <8 carbon atoms - liquid at room temp
plants contain large proportions of unsaturated fatty acids - liquid
animal fats contain mostly palmitic and stearic acid - solid
products of fat digestion
glycerol - readily absorbed in intestinal epithelial cells
fatty acids
monoglycerides
fat absorption
absorbed into mucosal cells of intestine;
short and medium length fatty acids enter portal blood
longer chain fatty acids and monoglycerides are re-synthesised to triglycerides
chylomicrons
fat coated with a layer of protein, phospholipid and cholesterol
action of a chylomicron
enter lymph then enter the blood stream
at muscle and adipose tissue, chylomicrons are attacked and cleaved by lipoprotein lipases
there, fatty acids are;
re-synthesised into triacylglycerols (in adipose tissue, for storage)
oxidised to provide energy (in muscle)
depends on amount available
describe lipolysis
breakdown of lipids - initial cleavage by hormone sensitive lipases e.g. adrenaline-sensitive - releasing free fatty acids and glycerol, occurs when energy is needed
fat stored as adipose tissue
activation of fatty acids prior to oxidation
they have to first be converted to CoA derivatives - fatty acid + CoA –> acyl-CoA –> carnitine
occurs in cytoplasm
requires energy - 2ATP
how and why are fatty acids transported to mitochondrial matrix
for further oxidation, first they have to be transferred from acyl-CoA –> carnitine
transported via acyl-carnitine transport (carnitine shuttle) in inner membrane to mitochondrial matrix
beta-oxidation of fatty acids
occurs in mitochondrial matrix
4 steps in each cycle
products of beta oxidation
acetyl-CoA
FADH2
NADH + H+
fatty acyl-CoA - shortened by 2 carbon atoms
products then go to TCA cycle
how to calculate the number of oxidations required for complete catalysis of a saturated fat
(x/2) - 1
breakdown of glycerol
glycerol is activated to glycerol-3-phosphate by glycerol kinase - present in liver and kidney but absent from adipose tissue, skeletal and heart muscle
glycerol kinase then dehydrogenated to dihydroxyacetone phosphate
where are ketone bodies formed
formed in liver mitochondria - from acetyl-CoA from beta oxidation
ketosis
diffuse into the blood stream and to peripheral tissues
important for energy metabolism for heart muscle renal cortex - converted back to acetyl-CoA via fatty acid oxidation and enters TCA cycle
dependent on C4 compound (oxaloacetate) for formation of citrate
ketosis in starvation and diabetes
oxaloacetate is consumed for gluconeogenesis
fatty acids are oxidised to provide energy
acetyl-CoA is converted to ketone bodies
high levels in blood
too much for extrahepatic tissue (i.e. heart, brain, etc.)
ketone bodies are moderate acids
accumulation leads to severe acidosis (blood can’t buffer any more)
impairs tissue function, particularly central nervous system
smell of acetone can be detected in breath