Lipid Metabolism and Ketones Flashcards

1
Q

consequences of increased fat intake without appropriate energy expenditature

A

increase in number of adipocytes
more fat in adipocytes
obesity

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2
Q

what is the energy balance dependent on

A

genetically linked factors - protein messengers regulating appetite
environmental factors - food abundance, fashionable food

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3
Q

requirements for fat

A

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

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4
Q

structure of lipids

A

predominantly hydrocarbon
long chain fatty acid
insoluble in water - important for biological function

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5
Q

examples of lipids

A

simple
compound
steroids

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6
Q

describe triglycerides

A

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

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7
Q

structure of fatty acids

A

mainly straight chains
aliphatic - no rings
even number of carbon atoms - branched and odd numbers of carbon atoms are rare

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8
Q

saturated fatty acid

A

no double bond

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9
Q

unsaturated fatty acid

A

double bond - cis figuration

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10
Q

polyunsaturated fatty acid

A

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

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11
Q

examples of natural fatty acids

A

palmitic acid - saturated
stearic acid - saturated
oleic acid - unsaturated

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12
Q

melting point of fatty acids

A

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

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13
Q

products of fat digestion

A

glycerol - readily absorbed in intestinal epithelial cells
fatty acids
monoglycerides

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14
Q

fat absorption

A

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

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15
Q

chylomicrons

A

fat coated with a layer of protein, phospholipid and cholesterol

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16
Q

action of a chylomicron

A

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

17
Q

describe lipolysis

A

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

18
Q

activation of fatty acids prior to oxidation

A

they have to first be converted to CoA derivatives - fatty acid + CoA –> acyl-CoA –> carnitine
occurs in cytoplasm
requires energy - 2ATP

19
Q

how and why are fatty acids transported to mitochondrial matrix

A

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

20
Q

beta-oxidation of fatty acids

A

occurs in mitochondrial matrix

4 steps in each cycle

21
Q

products of beta oxidation

A

acetyl-CoA
FADH2
NADH + H+
fatty acyl-CoA - shortened by 2 carbon atoms

products then go to TCA cycle

22
Q

how to calculate the number of oxidations required for complete catalysis of a saturated fat

A

(x/2) - 1

23
Q

breakdown of glycerol

A

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

24
Q

where are ketone bodies formed

A

formed in liver mitochondria - from acetyl-CoA from beta oxidation

25
Q

ketosis

A

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

26
Q

ketosis in starvation and diabetes

A

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