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1. Foundations of Medicine PoNF > Lipids > Flashcards

Lipids Flashcards

1
Q

What are lipids

A

Heterogeneous organic molecules - hydrophobic (soluble in organic solvents)

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2
Q

Where do lipids exist

A
  • cell membranes
  • as lipid droplets in adipocytes (adipose tissue)
  • in blood lipoproteins
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3
Q

What are the biological functions of lipids (6)

A
  • Stored form of energy
  • structural element of membranes
  • enzyme cofactors
  • steroid hormones
  • vitamins A,D,E,K
  • signalling molecules
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4
Q

What can imbalances/deficiencies in lipid metabolism lead to

A

Major clinical problems e.g. obesity, metabolic diseases…

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5
Q

Lipid classes (5)

A
  • Fatty acids
  • Triacylglycerol
  • Phospholipid
  • Glycolipid
  • Steroids
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6
Q

What can FA be classed as?

A
  • Saturated - no C=C double bonds
  • Unsaturated - one/more C=C double bonds that kink the hydrocarbon chain
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7
Q

What “types” of FA are there

A
  • Essential FA
  • Good fats (cardiovascular)
  • bad fats (cardiovascular)
  • really bad fats
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8
Q

Essential FA

A

Must get these from plants - linoleic and a-linolenic

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9
Q

“goof fats” (cardiovascular)

A

high in polyunsaturated fatty acids (e.g. vegetable oils; sunflower/olive oil etc.)

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10
Q

“bad fats” (cardiovascular)

A

high in saturated FA (e.g. stearic (beef))
Saturated fats play a role in myelination of nerve fibres and hormone production.

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11
Q

“really bad fats”

A

trans FA, results from hydrogenation of vegetable oils (e.g. hard margarine (man-made))

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12
Q

Why must we ingest essential FA

A

Humans cannot introduce double bonds beyond carbon 9

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13
Q

Omega-3 FA (essential FA)

A

Derived from linolenic acid as essential FAs. Lowers plasma cholesterol, prevents atherosclerosis, lowers TAG, prevents obesity, reduces inflammation.

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14
Q

Arachindonic acid (essential FA)

A

Precursor of eicosanoids that can be synthesized from linoleic acid

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15
Q

Essential FA deficinecies

A

Rare, occuring mostly in infants caused by bad diet. Signs: scaly dermatitis, alopecia, thrombocytopenia, and intellectual disability.
can result in depresssion - deficincy of lipid signalling molecules
ADHD - lower levels of omega3 lead to behavioral problems.

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16
Q

Triacylglycerols (TAG)

A

Esters of fatty acids and glycerol. Dietary fuel and insulation. Water soluble TAG coalesce into lipid droplets in adipose tissue (major component)

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17
Q

Phospholipids

A

Amphiphatic - glycerol bound to two fatty acids and phosphate. Hydrophilic head and hydrophobic tail.

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18
Q

What are phospholipids critical for

A

Aqueous/non-aqueous interfaces:
* Membranes
* Lipid droplets
* Local signalling molecules

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19
Q

Steroids (inc 3 main classes)

A

Lipids with ring system, 3 main classes:
* Cholesterol - tarting material for synthesis of bile salts, steroid hormones and other components
* Steroid hormones - chemical messengers (sex hormones…)
* Bile salts - sodium salts of steroids used for emulsification

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20
Q

Cholesterol

A

Component of cell membranes, precursor to sterol hormones, bile acids and vitamin D. Made in liver, found only in animal foods.

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21
Q

What can cholesterol be made from

A

Acetyl CoA

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22
Q

how is synthesis of cholesterol regulated?

A

Statins inhibit HMG-CoA reductase that is essential in cholesterol synthesis, lowers LDL levels, reduce risk of cardiovascular disease.

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23
Q

LDL

A

Low Density Lipoprotein

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24
Q

Eicosanoids

A

Class of lipids derived from 20 carbon unsaturated fatty acids and are synthesized throughout body. Signaling molecules derived from omega 3/6 FAs. Precursors to prostaglandins, thromboxanes, leukotrienes. Short half life (metabolised rapidly), produced and act locally

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25
Q

What do eicosanoids regulate

A
  • Lipid infalmatory response
  • Other… (see more questions on sub-types of eicosanoids)
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26
Q

What do prostaglandins regulate

A

Pain and fever, reproductive functions, mucus production in stomach.

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27
Q

What do prostacyclin regulate

A

Blood pressure

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28
Q

What do thromboxanes regulate

A

Blood clotting induction / platelet homeostatis

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29
Q

What do leukotrienes regulate

A

SMC constrictions and bronchioconstriction

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30
Q

What dose asprin do?

A

Inhibits COX enzymes and prostaglandin synthesis which reduces inflammation and fever. Also inhibits thromboxanes which cause clotting.

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31
Q

Zadirlukast

A

orally administered leukotriene receptor antagonist

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32
Q

Zileuton

A

orally active inhibitor of 5-lipoxygenase (inhibits leukotrines formation)

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33
Q

How does degree of unsaturation affect melting point of FA

A

More unsaturated = lower mp (less intermolecular forces)

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34
Q

Whats a glycolipid

A

lipids with a carbohydrate attached by a glycosidic (covalent) bond

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35
Q

What are steroids synthesised from

A

cholesterol

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36
Q

What are eicosanoids precursers of?

A

Prostaglandins, thromboxanes and leukotrienes

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37
Q

What are our diatery lipids

A

TAG (main one), phospholipids, cholesterol, cholesterol ester, free FA

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38
Q

What is the main site of lipid digestion

A

small intestine

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39
Q

Lipid digestion of pancreatic enzymes (lipases)

A

Promoted by emulsification (dispersion) by bile salts and peristalsis (mixing)

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40
Q

Bile salts

A

Derivative of cholesterol, act as biological detergents to form emulsions and micelles, saves lipids coalescing in aqueous environment

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41
Q

Digestion of TAG

A

Degraded in small intestine by pancreatic lipase to monoacylglycerol and two fatty acids

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42
Q

Digestion of cholesterol esters

A

Digested to cholesterol and free fatty acids.

43
Q

Digestion of phospholipids

A

Hydrolysed to fatty acids and lysophospholipids.

44
Q

Summarise the process of the digestion of lipids

A

Fat –bile acids (duodenum)–> emulsified fats –lipases(small/large intestine)–> FA and glycerol

45
Q

Uptake of digested lipids

A

Products of lipid digestion form mixed micelles with bile salts. Mixed micelles approach brush border membranes of enterocytes and release lipid products which enter cells by diffusion. However, (short/med chain) fatty acids don’t need micelles for absorption

46
Q

Steatorrhea

A

Illness caused by lipid malabsorption due to defects in bile secretion, pancreatic function or intestinal cell uptake. Excess fat in faeces - float

47
Q

Effect of removal of gall bladder

A

inhibits digestion/absorption of fats

48
Q

What do intestinal cells do to TAG/PL/CE

A

resynthesise them for export

49
Q

How are insoluble FA utilised/digested

A

Packaged with apoB-48 (solubilising protien) into chylomicrons for export

50
Q

What happens with chylomicrons

A

Released by exoxytosis into lymph then blood

51
Q

What happens when blood chylomicrons reach tissue?

A

TAG in chylomicrons is hydrolysed to fatty acids and glycerol by lipoprotein lipase. This enzyme is found mainly in capillaries of skeletal muscle and adipose tissue. Leftover FAs used for energy or turned into TAG for storage. Glycerol used in liver to make G3P (glycolysis and gluconeogenesis)

52
Q

What are chylomicrons depleated of TAG called

A

Chylomicron remnants - go to liver

53
Q

how are free FA transported in blood?

A

In complex with serum albumin (aka NEFA). This is the most abundant plasma protein with 2-7 binding sites for FA.

54
Q

What are the majority of FA and how are they transported?

A

Esterified - lipoproteins

55
Q

Why are lipoproteins necessary

A

TAG/cholesterol esters (CE) are insoluble in water - can’t be transported in blood/lymph as free molecules

56
Q

Structure of lipoproteins

A

Hydrophobic core (hold CE…) with a hydrophilic surface (unesterfied cholesterol, pholsholipids…)

57
Q

How are lipoprotein classified and give the classes

A

By density (least to most):
* Chylomicrons
* VLDL
* LDL
* HDL

58
Q

Chylomicrons

A

type of lipoprotien: TAG rich (take TAG from intestine to tissues)

59
Q

VLDL

A

TAG rich. Transports TAG from liver to tissue

60
Q

LDL

A

Cholesterol rich. Brings cholesterol to extrahepatic tissue - Bad cholesterol but dec with staffin drugs

61
Q

HDL

A

Protein and cholesterol rich. Brings cholesterol from tissue to liver for elimination - Good cholesterol

62
Q

What happens if you have too much LDL

A

Caused by obesity or genetic defect. Leads to artherosclerosis - lipid develops into fatty straks and plaque in artery

63
Q

Summarise lipid digestion/absorption

A

Ingested lipids (e.g TAG) are cleaved by enzymes (e.g.,pancreatic lipase), absorbed in thesmall intestine, and then transported inchylomicronsviathe lymphatic systeminto the bloodstream, where they reach theliver (for lipoproteins), peripheral tissues (energy) andadipose tissue(storage)

64
Q

How are lipids transported?

A

Circulating lipids are transported in lipoproteins (containhydrophilicapolipoproteins) because the hydrophobic lipids are insoluble in plasma.

65
Q

What else is broken down and released in lipolysis

A

breakdown and release of adipocyte triglyceride (TAG to free FA and glycerol)

66
Q

Where does liver take up FA from

A

Plasma

67
Q

2 major fates of FA taken up from plasma in the liver

A
  1. Oxidation - energy source for liver and production of ketones - burn
  2. TAG or lipid formation - local store for liver energy, distributed to other tissues like VLDL - store
68
Q

What is reqired for long chain FA transport to michochondria

A

Carnitine shuttle

69
Q

Lipid metabolism/oxidation summary

A

FA + CoA —> Fatty acyl CoA —- TAG (synthesis) or B-oxidation to CO2/ketone bodies

70
Q

How are lipids metabolised in the fed state

A

Insulin elevated, stimulates ACC to convert acetyl CoA to malonyl CoA, which inhibits CPT-1 and means fatty acids accumulate and esterify to TAGs in cytosol.

71
Q

how are lipids metabolised in the fasted state

A

Glucagon is elevated which stimulateds CPT-1 expression increasing fatty acid transport to mitochondria. FA oxidation is favoured.

72
Q

Steps of Beta-oxidation

A

Dehydrogenation, hydration, dehydrogenation, thiolysis.

73
Q

What happens each B-oxidation cycle

A

1 acetly CoA and a species 2 carbons shorter than origional produced + 4 ATP

74
Q

where does beta oxidation primarily occur

A

mitochondria

75
Q

What is the purpose of B-oxidation

A

breakdown of FA for energy

76
Q

Explain B-oxidation in the peroxisomes

A

Less ATP efficient, only happens to very long chain fatty acids, shortened fatty acids then move to mitochondria for further oxiidation

77
Q

Can we use FA to make glucose?

A

No. Also can’t convert acetyl CoA into glucose due to irreversible reaction pathway to make acetyl CoA

78
Q

Ketone bodies

A
  • Metabolites of fat
  • energy source while fasting
  • excess production if no insulin
  • impaired use without insulin
  • leads to diabetic ketaoacidosis
79
Q

What happens when we have high levels of ketone bodies

A

Acidic - so make blood acidic (ketoacidosis)

80
Q

What are ketone bodies

A

metabolites that replace glucose as the main fuel of the brain in situations of glucose scarcity, including prolonged fasting, extenuating exercise, or pathological conditions such as diabetes

81
Q

When do we make ketone bodies

A

fasting (used by tissues as energy source - if not, then have sufficeint glucoes for glycolysis

82
Q

Breakdown of ketone bodies for energy

A

Oxidised in mitochondria to give 2 GTP and 22 ATP. Transported from liver to other tissues (brain/skeletal muscle) and reconverted to acetyl CoA. Ketone bodies can’t be used by liver as fuel, as liver lacks b-ketoacyl-CoA transferase (however, brain does have it)

83
Q

What can happen when insulin is absent (diabetes)

A

Diabetic ketosis

84
Q

How is fatty acid oxidation regulated

A

The rate-limiting step of fatty acid oxidation is the transport of fatty acyl-CoA to the mitochondria matrix through the carnitine system. - entry into mitochondria and carnitine shuttle

85
Q

Where are ketone bodies made

A

liver

86
Q

Where does FA synthesis occur
(tissues not cellular location)

A
  • Liver
  • Lactating mammary gland
  • adipose tissue
87
Q

De novo synthesis of fatty acids

A
  • Occurs in cytosol, uses ADP and NADPH
  • Acetyl CoA formed in mitochondria needs to be transferred to cytosol
  • FA synthesised from acetyl CoA, derived from excess protein, fat and carbohydrate
88
Q

What controls formation of malyonyl CoA?

A

Acetyl CoA Carboxylase (ACC)

89
Q

Why is formation of Malonyl CoA important

A

It is a committed step in FA synthesis (stimulated by insulin) so no going back

90
Q

Describe ACC

A
  • Key regulatory enzyme
  • Activated by citrate (signals enough glucose so make FA)
  • deactivated by palmitoyl COA (enough FA made)
  • insulin signalling activates (phosphorylation)
  • glucagon, epinephrine deactivates (dephosphorylation) - inc levels of gucagon in fasting, want to break down FA, not synthesise them, hence deactivates
91
Q

Is the synthesis pathway of FA different from the degredation?

A

Yes, uses different intermediates too - allows for better/easier control

92
Q

Synthesis of fatty acids

A
  • Every time 2 carbons are added in cycle
  • carbons must come from malonyl CoA each time…
93
Q

Elongation and desaturation

A

Further modification of palmitate or dietary FAs (e.g. ybsaturation/elongation/branching) occur in mitochondria and ER by diverse enzymes

94
Q

What can’t happen to essential FA?

in terms of elongation and desaturation

A

Can’t be synthesised but are required to make other lipids (eicosanoids)

95
Q

Where are triglycerides generated

A

In the endoplasmic reticulum (ER) membrane

96
Q

Compare FA synthesis and degredation

A
  • Synthesis - cytosol, CoA, multiple enzymes used, Acetyl-CoA, NAD+/FAD
  • Degredation - mitochondrial matrix, ACP, Enzyme complex, Malonyl-CoA, NADPH
97
Q

Describe synthesis of free FA

A

fatty acid synthesis is the creation of fatty acids from acetyl-CoA and NADPH through the action of enzymes called fatty acid synthases. This process takes place in the cytoplasm of the cell.

98
Q

essential fatty acid definition

A

polyunsaturated fatty acids (PUFA) that must be provided by foods because these cannot be synthesized in the body yet are necessary for health.

99
Q

What kind of reaction is beta-oxidation

A

Catabolism

100
Q

Structure of cholesterol

A

Cholesterol is a 27 carbon compound with a unique structure with a hydrocarbon tail, a central sterol nucleus made of four hydrocarbon rings, and a hydroxyl group

101
Q

Function of cholesterol

A

helps your body make cell membranes, many hormones, and vitamin D. The cholesterol in your blood comes from two sources: the foods you eat and your liver. Your liver makes all the cholesterol your body needs.

102
Q

How many carbons at a time are FA degraded and where?

A

2C at a time in the mitochondrial matrix

(B-oxidation)

103
Q

3 main steps of B-Oxidation

Not dehydration… ect.

A
  1. Fatty acid activation
  2. transport into the mitochondrial matrix by the carnitine shuttle
  3. degradation which has 4 main enzyme reactions.
104
Q

What is cellular glycogen (in terms of movement)

A

Osmotically inactive - important benifit of storage

1. Foundations of Medicine PoNF (22 decks)

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