lipid synthesis and transport Flashcards

1
Q

how FA is synthesised

A

in mitochondria, acetyl coa + oxaloacetate-> citrate
citrate moves out of mito into cytosol
citrate-> acetyl coa + oxaloacetate
acetyl coa + hco3- -> malonyl coa by ACETYL COA CARBOXYLASE; USING ATP
malonyl coa + acetyl coa-> 4C FA + co2 by FATTY ACID SYNTHETASE; USING NADPH
malonyl coa + 4C FA -> 6C FA + co2 USING NADPH

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2
Q

How is NADPH produced

A

hexose monophosphate shunt

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3
Q

what are lipoproteins made of? are they polar or non polar

A

inner core of TAG + cholesterol esters
outer shell of apoproteins + cholesterol + phospholipids
polar on outside, non-polar on inside

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4
Q

apoprotein function

A

structural role in lipoproteins
recognised by receptors
activate enzymes in lipid metabolism

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5
Q

types of lipoproteins, from greatest amount of TAG to least, from least dense to most dense. What does each of them do

A
chylomicron: carries dietary TAG
VLDL: endogenous TAG
LDL: liver-> tissues
IDL
HDL : tissues-> liver
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6
Q

chylomicron transport

A

IN GUT chylomicron + B48 -> IN BS chylomicron+B48+E+C2-> (Lipoprotein lipase activated by C2):
FA-> TAG IN ADIPOCYTES
glycerol-> LIVER
chylomicron+B48+E-> E receptor in LIVER

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7
Q

VLDL transport

A

IN LIVER VLDL-TAG + B100-> IN BS VLDL-TAG+B100+E+C2-> (lipoprotein lipase activated by c2):
FA-> TAG IN ADIPOCYTES
glycerol-> LIVER
IDL-TAG + B100 + C2 + E -> HDL + C2 + E in BS/ LDL-TAG + B100 -> B100 receptor in LIVER OR PERIPHERAL TISSUE

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8
Q

HDL transport

A

IN SMALL INTESTINE HDL+A1 + IN PERIPHERAL TISSUE C-> HDL + A1 + C by LCAT(activated by a1) -> C IN LIVER/ HDL+A1 IN BS

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9
Q

cholesterol synthesis regulation

A

B100 receptor + LDL -> endocytosis-> cholesterol formed-> receptor synthesis + cholesterol synthesis enzymes inhibited

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10
Q

cholesterol synthesis steps

A

acetyl coa + acetoacetyl coa -> HMG coa -> mevalonate by HMG COA REDUCTASE -> cholesterol

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11
Q

types of hyperlipoproteinaemias/hyperlipidaemias

A

hypertriglyceridaemia

hypercholesterolaemia

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12
Q

indications of defective LDL receptor

A

hypercholesterolaemia

high ldl in blood

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13
Q

indications of LPL deficiency

A

high chylomicrons + vldl

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14
Q

indications of c2 deficienct

A

high chylomicrons + vldl

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15
Q

indications of deficiency of apoproteins involved in remnant uptake

A

high chylomicrons + ldl

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16
Q

what’s lipoprotein a made of? what is it associated with? how can its levels be increased or decreased? what does it do?

A

ldl + apoprotein a
CHD
increased by trans fat; decreased by oestrogen
slows down breakdown of blood clots

17
Q

how does oxidised LDL lead to hypercholesterolaemia

A

oxidised LDL is not recognised by normal receptors and not metabolised by liver/peripheral tissues. instead, it is taken up by scavenger receptors on foam cells. These receptors are not down regulated-> accumulation of cholesterol

18
Q

how does atherosclerosis come about

A

starts as fatty streak from accumulation of foam cells (macrophages filled with lipid)-> plaque