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103-theme 3 > introduction to lipids > Flashcards

introduction to lipids Flashcards

1
Q

what are the functions of lipids? 3

A
  • phospholipids and cholesterol: cell membranes
  • triglyceride is a key energy store
  • steroids and fatty acids play regulatory roles as hormones, vitamins and bile acids
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2
Q

explain how cellular energy is stored short term? 4

A
  • ATP (and other phosphate bonds)
  • redox agents (NADH, FADH2)
  • ionic transmembrane gradients (H+ across the mitochondrial membrane can drive the formation of ATP)
  • all of the above are labile
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3
Q

how is some energy stored inside the cell when you can’t have anymore ATP?

A

creatine phosphate

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4
Q

how can energy be stored long term? 2

A
  • large, stable efficient energy precursors

- carbohydrates and fats

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5
Q

what is acetyl-CoA used as? 4

A
  • an energy mediator
  • converts glucose into cholesterol, citric acid+ amp and fatty acids
  • cannot be transported in plasma
  • instead organisms use Co-enzymeA
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6
Q

what can the production of cholesterol be blocked by?

A

statins

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7
Q

explain carbohydrates as energy? 4

A
  • starch is digested into sugars in the gut
  • sugars are absorbed from gut into the bloodstream
  • sugars are absorbed by the liver and stored as glycogen (via the hepatic portal vein)
  • sugars are stored through the body as glycogen
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8
Q

where is there no glycogen?

A

in the brain as it needs glucose or ketone bodies from plasma constantly

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9
Q

what is the citric acid cycle? 6

A
  • acetyl-CoA gets turned into energy by burning O2 and CO2
  • start with a 4 carbon chain
  • acetyl-CoA gets added to make citric acid ( a 6 chain carbon)
  • oxygen is then added
  • this releases carbon dioxide and ATP
  • the 4 carbon chain is then reformed and the cycle continues
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10
Q

what does fatty acid synthesis leads to? 2

A
  • fatty acids with an even number of carbons

- this consumes ATP

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11
Q

what is beta-oxidation? 2

A
  • breaking down fatty acids

- fat mobilisation which shortens fatty acid by 2 carbons at a time, this produces ATP and acetyl-CoA

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12
Q

what are fatty acids? 4

A
  • simple straight carbon chains +COOH
  • in humans they are mostly 16-20 carbons long
  • 50% have double bonds
  • acyl group
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13
Q

explain double bonds in fatty acids and what they mean? 3

A
  • 0 double bonds= saturated
  • 1 double bond=monounsaturated
  • 2 or more double bonds= polyunsaturated
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14
Q

what is cholesterol? 5

A
  • essential component of cell membranes
  • precursor of bile acids, steroid hormones and vitamin D
  • ring system makes it very rigid
  • from the diet or made in the liver
  • major emphasis on recycling- a lot is used in bile salts- endogenous pathway needs cholesterol
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15
Q

what are cholesterol esters? 3

A
  • a large portion of plasma cholesterol is esterified (75%)
  • broken down by lipases to free cholesterol and fatty acids
  • cholesterol is amphipathic (both hydrophilic and hydrophobic parts) as the alcohol group is hydrophobic when esterified
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16
Q

what are steroids? 4

A
  • cholesterol
  • vitamin D - produced by skin by the action of light on a cholesterol derivative
  • cortisol- hormone secreted by the adrenal cortex
  • testosterone- male sex hormone
17
Q

what are ketone bodies? 6

A
  • soluble chemicals
  • made from acetyl-coA during fasting, by the liver
  • lasts for 5 hours
  • ‘use it or lose it’
  • during fasting they are the main energy source especially by the brain and the heart
  • acetone is a waste product made spontaneously by decarboxylation and is eliminated by the kidney
  • Acetoacetic acid and beta-hydroxybutyric acid
18
Q

what is special about the melting point of unsaturated fatty acids? 2

A
  • lower

- more liquid at room temperature which increases the fluidity of cell membranes

19
Q

why do manufacturers use saturated fats?

A
  • they are less vulnerable to rancidity and are, in general, more solid at room temperature than unsaturated fats
20
Q

explain cis and trans carbon chains? 4

A
  • cis carbon-carbon double bonds (cis unsaturated fats) create a kink
  • the kink lowers the melting temperature
  • saturated fats and trans unsaturated fats lack this kink
  • the kink interferes with stacking and solidification, making it liquid
21
Q

what do fatty acids in diet affect? 6

A
  • cholesterol levels
  • triglyceride levels
  • trans unsaturated fats are bad
  • saturated fats are bad and increase LDL
  • cis unsaturated fats are either monounsaturated or polyunsaturated, and are probably good for you
  • high melting temperature= soluble and non mobilisable
22
Q

what are the 4 pathways for lipid transport?

A
  • exogenous pathway (from gut to liver and periphery (muscle and adipose tissue))
  • endogenous pathway (from liver to periphery)
  • reverse cholesterol transport (from periphery to liver)
  • bile production (from lover into gut)
23
Q

explain the exogenous pathway? 3

A
  • lipids from diet
  • packaged by small intestine into chylomicrons (increased lipids in plasma after fatty meal)
  • chylomicrons taken up by the liver or periphery
24
Q

explain the endogenous pathway? 2

A
  • made in the body

- lipid from liver packaged into the VLDL

25
Q

explain the reverse cholesterol transport? 2

A
  • occurs when lipid supplies in liver are being exhausted- thus a sign of reduced body lipid
  • HDL in blood indicates reverse path activity
26
Q

explain bile production? 4

A
  • bile released into the cystic duct
  • cholesterol is converted into bile ducts
  • bile is necessary to digest fats in diet as it emulsifies fat
  • most bile acids are reabsorbed by the gut and returned to the liver and recycled
27
Q

what is needed for pathway to move fats in and out of blood vessels? 6

A
  • receptors and enzymes
  • lipoprotein lipase
  • metabolises triglycerides into fatty acids and glycerol
  • this is because TG cannot go through the cell membrane
  • cells surface-linked enzyme s in capillary walls
  • in order to remove TG from VLDL and to move the TG across the capillary membrane, the TG must be metabolised by lipoprotein lipase
28
Q

what are lipoprotein particles? 4

A
  • lipids are not soluble in plasma
  • they must be packaged to be transported
  • lipoprotein particles in plasma are soluble and carry lipids
  • apolipoproteins: proteins in LP particles that can hold lipids and they are amphipathic (detergent like)- apolipoprotein E (apoE)
29
Q

how are lipids identified? 4

A
  • lipid is much less dense than protein
  • triglycerides are very low density
  • cholesterol is mid-way between Tgs and proteins
  • bigger lipoprotein particles usually are carrying a lot of lipids thus are lower in density
30
Q

what are LDLs? 6

A
  • low density lipoprotein
  • most dangerous lipoprotein
  • LDL contents get incorporated in atheroma
  • LDL in blood may be storage for cholesterol that cannot be stored elsewhere
  • excess LDL accumulates in atheroma
  • LDL is eventually left over after periphery absorbs endogenous TG from VLDL from liver
31
Q

what are HDLs? 4

A
  • the good lipoprotein
  • increased HDL means lower cardiovascular risk
  • lipid reverse cholesterol transport
  • appears when cholesterol is being used up
32
Q

what are VLDLs? 4

A
  • very low density lipoprotein
  • signifies risk of atheroma
  • transport endogenous cholesterol and TG from liver to adipose and muscle
  • after TG is removed by periphery from VLVL, IDL is left
33
Q

what is IDL? 3

A
  • intermediate density lipoproteins
  • IDL will become LDL
  • is a sign of CV risk
34
Q

what is chylomicron? 3

A
  • not usually associated with CV risk
  • normally high after fat containing meals
  • carries lipids from gut to periphery for exogenous lipids
35
Q

what happens in the islet of langerhans in the pancreas? 2

A
  • beta cells release insulin when there is too much blood glucose
  • alpha cells release glucagon to convert glycogen into glucose
36
Q

what is type II diabetes mellitus? 6

A
  • adult onset diabetes
  • high blood glucose
  • poor plasma glucose control
  • insulin resistance
  • relative insulin deficiency
  • obesity/genetic predisposition
37
Q

what is hypercholesterolaemia? 5

A
  • high fasting levels of plasma cholesterol
  • hyperchol is a subclass
  • increased risk of ateriosclerosis
  • HDL reduces risk
  • due to combination of environmental and genetic factors
38
Q

what are statins? 4

A
  • drugs used to treat hypercholesterolaemia
  • block endogenous cholesterol synthesis by blocking HMG-CoA reductase
  • the entry step to cholesterol synthesis
  • simvastatin is one of the most commonly prescribed drugs especially in men over 50
39
Q

what is metabolic syndrome? 2

A
  • a group of risk factors that occur leading to increased risk for CAD, stroke and type 2 diabetes
  • main causes: insulin resistance, central obesity, waist circumference and high blood pressure

103-theme 3 (18 decks)

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