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NSF > lipids > Flashcards

lipids Flashcards

1
Q

fatty acid general structure + saturated vs unsaturated

A

O-C=O at one end hydrocarbon chain
saturated = no double bonds in chain, unsaturated = at least 1

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2
Q

structure triglyceride storage lipids

= triacylglycerols

A

1 glycerol mol w 3 fatty acids attached by ester bonds

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3
Q

structure phospholipids

A

glycerol w 2 fatty acids + a phosphate mol attached
OR
sphingosine w fatty acid + phosphate attached

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4
Q

glycolipid structure

A

glycerol + 2 fatty acids + saccharide bound SO4
sphingosine + fatty acid + saccharide

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5
Q

structure cholesterol

chemish

A
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6
Q

cholesterol main role

A

precursor for lipid soluble hormones
* steroid hormone itself + can diff thru bilayer into cell
* bc lipid soluble + not much charge = hydrophobic

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7
Q

main biological roles lipids

A
  • lipid bilayers cell mems cont phospholipids, glycolipids, cholesterol
  • signalling mols, e.g. hormones
  • fuel
  • heat insulation
  • vitamins
  • nervous sys
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8
Q

lipid digestion monogastrics

A
  1. cholesterol precursor to bile salts
  2. bile salts emulsify fats = smaller droplets
  3. intestinal lipases removing FAs
  4. FAs (w other breakdown products) taken up by intestinal mucosa
  5. fats reformed
  6. packaged into chylomicrons
  7. chylomicrons secreted to lymph -> blood
  8. lipoprot lipase activated in caps releasing FAs + glycerol
  9. FAs enter myocytes or adipocytes
  10. oxidised as fuel or reesterified for storage
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9
Q

lipid digestion ruminants

A
  1. rumen bac enzs hydrolyse glycerol backbone fast
  2. glycerol ferments to volatile FAs -> gluconeogenesis
  3. polyunsaturated FAs (PUFA) most common in diet + toxic rumen bac so biohydrogenated to saturated FAs
  4. lysolecithin aids formation micelles w/o glycerol for absorption free FAs in SI
  5. phospholipids from breakdown rumen microbes leave rumen for absorption asw

some PUFA escape hydrogenation = mix polyun + sated

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10
Q

transport lipids w/in bod

A
  1. chylomicrons in blood, FAs -> adipose tiss + muscle
  2. remnants not absorbed (mostly prot, bit lipid) -> specific receptor liver
  3. dietary cholesterol added = VLDL (very low density lipoprots)
  4. released blood, broken down lipoprot lipase again, free FAs taken up adipose + muscle
  5. now IDL (intermediate), converted LDL, bind liver receptors - recycle cholesterol, e.g. making bile salts
  6. some LDL converted HDL - pick up cholesterol to go liver for processing (make VLDL)
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11
Q

how are lipids stored adipocytes

A

FAs absorbed + new glycerol made from glucose, so fats reformed

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12
Q

insulin + glucagon in fat storage

A

insulin promotes fat storage (use glucose so can take up more)
glucagon = hormone-sensitive triacylglycerol lipase breaks down fats + FAs + glucose to blood for E

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13
Q

what is beta-oxidation

A

process FA mols broken down in mitochond, gening several mols acetyl-CoA from each (depends chain length)
* beta (2nd) C oxidised to carbonyl grp
* acetyl-CoA mols prgressively removed from chain, making FADH2 + NADH from e- transport chain

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14
Q

odd vs even no. Cs FA chain beta-oxidation difference

A

even = gens only acetyl CoA
odd = gens acetyl CoA + 1 succinyl-CoA, used TCA cycle

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15
Q

how does beta-ox related to TCA cycle

A

acetyl CoA + succinyl CoA enter to gen NADH + FADH2 for oxidative phosphorylation + gen ATP

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16
Q

E available carbs vs fats

A

glycolysis = 30ATP
beta-ox = 106ATP (palmitic acid)

after TCA cycle + oxidative phosphorylation

17
Q

when + how ketone bodies made

A

gluconeogenesis in liver uses intermediates Krebs cycle so slowed + not turning much = acetyl CoA no enter
* in mitochond in liver acetyl CoA converted acetone, acetoacetate + D-3-hydroxybutrate

acetone exhaled

18
Q

ketosis/ketacidosis is + why

A

abnormally high levels acidic ketone bodies in blood = pH buffer syss exhausted = metabolic acidosis

due starvation as lots gluconeogenesis + ketone bodies created for use as fuel

19
Q

diseases caused by ketosis

A
  • pregnancy toxemia in late gestation (high metabolic demand) in sheep - ruminants susceptible bc primarily obtain glucose from gluconeogenesis (excessive fat = risk factor)
  • acetonomia soon after calving in dairy cattle
  • type 1 diabetes - no insulin = lots FA release -> liver + metabolised to ket bods
20
Q

how are fatty acids synthed

A

acetyl CoA (2C) -> acetyl-ACP + malonyl CoA (3C) -> acyl-ACP (4C) + CO2
AND REPEAT = sequential addition ethyl grps
* uses NADPH = uses E (giving e-)

carried out by multi-enz complex fatty acid synthase (FAS)

21
Q

diffs bet FA biosynth + breakdown

A

basically reverse processes

22
Q

triglyceride synth

A

sequential addition FAs to glycerol mol

23
Q

phospholipid synth

A

addition sep grps to build up larger mol

NSF (22 decks)

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