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module 103 - theme 3 > introduction to lipids > Flashcards

introduction to lipids Flashcards

1
Q

how is energy stored long term?

A

as large, stable, efficient energy precursors

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2
Q

how is energy stored when the lipid of stored ATP is reached?

A

stored intracell as creatin phosphate

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3
Q

how are carbohydrates used as energy?

A
  • starch is digested into glucose in gut
  • glucose is absorbed from gut into blood stream
  • glucose absorbed by liver and stored as glycogen via hepatic portal vein
  • glucose stored throughout the body as glycogen
  • later when more energy is needed glycogen is broken down into glucose
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4
Q

what energy resource does the brain need?

A

glucose or ketone bodies from plasma constantly

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5
Q

what does fatty acid synthesis do?

A

leads to fatty acids with even number of carbons and consumes ATP

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6
Q

what does beta oxidation lead do?

A

fat mobilisation - shortens fatty acid by 2 carbons at a time and produces ATP and acetyl-coA

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7
Q

how many carbons long are most fatty acids in humans?

A

16-20 carbons long

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8
Q

what is a fatty acid called if it has one double bond?

A

monounsaturated

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9
Q

what is a fatty acid called if it had 2 or more double bonds?

A

polyunsaturated

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10
Q

what is cholesterol?

A

a precursor of bile acids, steroid hormones & vitamin D

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11
Q

what makes cholesterol very rigid?

A

it’s ring structure

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12
Q

where do we get cholesterol from?

A

diet or it is made in the liver

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13
Q

what percentage or cholesterol is esterified?

A

75%

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14
Q

what is cholesterol broken down by and what is it broken into?

A

broken down by lipases into free cholesterol and fatty acids

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15
Q

why is cholesterol amphipathic?

A

the free alcohol is hydrophobic when esterified

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16
Q

name 4 steroids

A
  • cholesterol
  • vitamin D
  • cortisol
  • testosterone
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17
Q

what is acetyl-coenzyme A?

A

main energy production precursor

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18
Q

what are ketone bodies?

A

3 soluble chemicals made from acetyl-CoA during fasting

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19
Q

what is a waste product of ketone bodies?

A

acetone is always a waste product

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20
Q

why do unsaturated chains have a lower melting point?

A

as they are more liquid at body temperature so increase the fluidity of the cell membrane

21
Q

what are the most naturally occurring unsaturated fatty acids?

A

Cis

22
Q

which types of unsaturated fats are bad?

A

trans

23
Q

what can cis unsaturated fats be?

A
  • monounsaturated

- polyunsaturated

24
Q

why do cis unsaturated fats have a lower melting point?

A

due to the kink

25
Q

what are the 4 ways of lipid transport?

A
  • from gut to liver and periphery
  • from liver to periphery
  • from periphery to liver
  • from liver into digestive tract
26
Q

what is the exogenous pathway?

A
  • from gut to liver
  • exogenous = lipid from diet
  • lipids from diet packaged by small intestine into “chylomicrons”
  • chylomicrons taken up by liver
27
Q

what is the endogenous pathway?

A
  • from liver to periphery
  • endogenous = made by body
  • lipid from liver packaged into VLDL
28
Q

what is reverse cholesterol transport?

A
  • from periphery to liver
  • occurs when lipid supplies in liver are being exhausted
  • HDL in blood indicated reverse path activity
29
Q

how does lipoprotein work?

A
  • metabolises TG –> fatty acids + glycerol
  • cause TG cannot go through cell membrane
  • cell surface-linked enzyme in capillary walls
  • in order to remove triglycerides from VLDL and to move the TG across the capillary membrane, TG must be metabolised via lipoprotein lipase
30
Q

what are lipoprotein particles?

A
  • lipids are not soluble in plasma so they must be packaged to be transported
  • lipoprotein particles in plasma are soluble and can carry lipids
  • apolipoproteins are proteins in LP particles that can hold lipids
31
Q

why are lipoproteins lower in density?

A

they usually carry lots of lipids

32
Q

what is the list dangerous lipoprotein?

A

low density lipoproteins

33
Q

how do low density lipoproteins work?

A
  • LDL get incorporated into atheromas
  • LDL in blood may be storage for cholesterol that cannot be stored elsewhere
  • excess LDL accumulates in atheromas
  • LDL is eventually left over after periphery absorbs endogenous TG from VLDL from liver
34
Q

what is the good lipoprotein?

A

high density lipoprotein

35
Q

how does the high density lipoprotein work?

A
  • increased HDL lowers CV risk
  • HDL: lipid transport from fat cells to liver called reverse cholesterol transport and appears when cholesterol is being used up
36
Q

how to very low density lipoproteins work?

A
  • signifies a risk of atheroma
  • used to transport endogenous cholesterol and TG from liver to adipose and muscle
  • after TG is removed by periphery from VLDL leaves over IDL
37
Q

what is IDL?

A
  • intermediate density lipoprotein
  • results from VLDL losing TG to periphery
  • IDL will become LDL
  • is a sign of CV risk
38
Q

what is chylomicron?

A

it carries lipids from gut to periphery for exogenous lipids and they aren’t usually associated with CV risk

39
Q

what cells release insulin?

A

beta cells

40
Q

what cells release glucagon?

A

alpha cells

41
Q

what are the signalling errors of diabetes?

A
  • type 1 diabetes: no insulin made

- type 2 diabetes: absent or decreased response to insulin by target cells

42
Q

what is type 2 diabetes mellitus?

A
  • also called adult onset diabetes
  • high blood glucose: poor plasma glucose control
  • insulin resistance
  • relative insulin deficiency
  • cause: obesity and genetic predisposition
43
Q

what is hypercholesterolsemia?

A
  • high fasting levels of plasma cholesterol
  • increased risk of atherosclerosis
  • due to combination of environmental and genetic factors
44
Q

what are statins?

A

drugs used to treat hypercholesterolaemia

45
Q

how do statins work?

A

block endogenous cholesterol synthesis by blocking HMG-CoA reductase: the entry step into cholesterol synthesis

46
Q

what is an example of a statin?

A

simvastatin prescribed for CAD prophylaxis

47
Q

what is metabolic syndrome?

A

a group of risk factors that occur together leading to increased risk for CAD, stoke and type 2 diabetes

48
Q

what are the main causes of metabolic syndrome?

A

insulin resistance, central obesity (waist circumference)

module 103 - theme 3 (17 decks)

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