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FoM - normal function > lipids > Flashcards

lipids Flashcards

1
Q

what are the biological functions of lipids?

A

Stored form of energy

Structural element of membranes

Enzyme cofactors

Steroid Hormones

Vitamins A, D, E, K

Signalling molecules

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2
Q

what are the 5 lipid classes?

A

fatty acids - hydrophobic hydrocarbons and a terminal carboxyl group

Triacylglycerol - glycerol head bonded to three fatty acid chains

Phospholipid - makes up cell membrane

Glycolipid - carbohydrate and lipid & source of blood group antigen

Steroids e.g. cholesterol

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3
Q

what are the different types of fat?

A

Essential fatty acids: Linoleic and a-linolenic;

  • must get these from plants

“Good fats”: high in polyunsaturated fatty acids: (Good for CV system)

e.g. vegetable oils, olive oil, sunflower oil, etc..

“Bad fats”: high in saturated fatty acids: (excess bad for CV system)

e.g. stearic (beef)

(huge role in myelination of nerve fibres and hormone production important in maintaining health)

“really bad fats”: trans fatty acids, result from hydrogenation of vegetable oils.

e.g. hard margarine (man-made)

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4
Q

what are the 2 essential fatty acids?

A

Ingested from plants, they are:

[1] Linoleic Acid
- Precursor of omega-6 arachidonic acid, which is the substrate for prostaglandin (eicosanoids) synthesis.

[2] Linolenic Acid
- Precursor of omega-3 fatty acids.

Omega-3 FA:

  • Lowers plasma cholesterol
  • Prevents atherosclerosis
  • Lowers triacylglycerols
  • Reduce inflammation

EFA Deficiency → ADHD, scaly dernatitis, alopecia, thrombocytopenia, chronic intestinal disorders

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4
Q

Triacylglycerols vs Phospholipids vs Glycolipids.

What’s the difference?

A

Triacylglycerols:

  • Esters derived from three fatty acids and glycerol
  • Water insoluble → lipid droplets in adipose tissue
  • Dietary fuel and insulation

Phospholipids:

  • Glycerol bond to two fatty acids and a phosphate group
  • Amphipathic: hydrophilic phosphate head, hydrophobic tails

Glycolipids:

  • Contain carbohydrate and lipid.
  • Components of membranes and high amounts in nerve tissues.
  • They are also source of blood group antigens
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5
Q

describe the digestion and uptake of dietary lipids:

A

[A] Beginning of partial digestion in Stomach & Oral cavity using Acid lipases
(partially digest short chain lipid, fewer than 12-C)

Acid lipases are important in neonate’s digestion of milk fat.

[B] Emulsification of dietary lipids using bile salts and peristalsis in Small Intestine

Bile salts, released by Gallbladder, act as biological detergents to form emulsions and micelles around lipids, prevents uniting by dispersing them, they are also derivatives of cholesterol.

[C] Degradation of emulsified dietary lipids by pancreatic lipase

Break down of TAG to monoacylglycerols and free fatty acids

Break down of CE to cholesterol and free fatty acids

Break down of PL to lysophospholipid and free fatty acids

[D] Absorption of lipids by intestinal mucosal cells (enterocytes)

Mixed micelles are amphipathic, they contain the hydrophobic lipid products inside them, while having a hydrophilic surface.

They facilitate the transport of the products to enterocytes.

Short- and medium-chain fatty acids do not require miscelles to help them, they diffuse.

[E] Resynthesis of TAG, PL, and CE for export into the Lymph then bloodstream

They are insoluble so they are packaged up into chlyomicrons, then released through exocytosis into the Lymph then the bloodstream.

[F] Use of dietary lipids contained in chlyomicrons by the tissues by lipoprotein lipase

Lipoprotein lipase, found in capillaries of skeletal muscle and adipose tissue converts:

Triacylglycerol → free fatty acid + glycerols

Free fatty acids are used for energy or reesterified for storage as TAG

Glycerols are used by liver to produce glycerol 3-phosphate which is used for glycolysis or gluconeogenesis by oxidation to dihydroxy acetone phosphate (DHAP)

Chylomicron remnants (depleted of TAG) go to the liver

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6
Q

what is steatorrhea?

A

it’s an illness that causes lipid malabsorption due to defects in bile secretion, pancreatic function or intestinal cell uptake.

It is characterized by excess fat in faeces and foul smell.

Cystic fibrosis patients are prone to this disease because they have thickened pancreatic secretions, which disable pancreatic enzymes from reaching the small intestine.

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7
Q

what is used for the partial digestion of lipids (fewer than 12C) done in the stomach?

A

acid lipases

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8
Q

what are bile salts?

A

Bile salts, released by Gallbladder, act as biological detergents to form emulsions of lipids with the aqueous solution by forming micelles around them, prevents uniting by dispersing lipids into smaller units, they are also derivatives of cholesterol.

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9
Q

what is Triacylglycerols, Cholesterol Ester, Phospholipids broken down and degraded in the small intestine using?

A

pancreatic lipase, secreted by the pancreas

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10
Q

what do enterocytes do?

A

Degraded long-chain lipids are absorbed through the intestinal mucosal cells when they are inside an amphipathic transport structure called a mixed micelle

While degraded short- and medium-chain fatty acids simply diffuse through the cell wall.

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10
Q

what are chlyomicrons?

A

TAG, PL, and CE are resynthesized after entering the intestinal cells for export into the Lymphatic system then to the bloodstream, they are packaged up into these amphipathic structures.

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10
Q

what lipoprotein lipase do and is found?

A

a lipase found in capillaries of skeletal muscle and adipose tissue that converts:

Triacylglycerol → free fatty acid + glycerols

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10
Q

What are the fates of Free fatty acids, Glycerols, and Chlyomicron remnants after the process of lipid absorption?

A

Free fatty acids are used for energy in beta-oxidation or reesterified for storage as TAG (for later use)

Glycerols are used by liver to produce glycerol 3-phosphate which is used for glycolysis or gluconeogenesis by oxidation to dihydroxy acetone phosphate (DHAP)

Chylomicron remnants (depleted of TAG but contain other components) go to the liver to be used.

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11
Q

Why are free fatty acids reesterified as TAG?

A

1- To be stored in adipose cells as droplets that make up the depot fat

2- Because TAG is the most efficient storage form of fuel (highly reduced, nearly anhydrous)

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12
Q

how are fatty acids released from stored TAG in adipose tissue?
e.g. when body energy supply is low - ↓ plasma glucose and insulin.

A

FA released from stored TAG by hormone sensitive lipase (HSL)

  • HSL activated by phosphorylation in response to epinephrine
  • High plasma glucose and insulin promote dephosphorylation (inactivation) of lipase
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13
Q

how free and esterfied fatty acids transported?

A

free fatty acids are transported in the blood through serum albumin

Albumin is the most abundant plasma protein with 2-7 binding sites for fatty acids.

Esterfied fatty acids e.g. TAG/CE are transported in the blood through lipoproteins which are a mixture of lipids and proteins, with hydrophilic surfaces and hydrophobic cores i.e. amphipathic.

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14
Q

what is the 4 classifications of lipoproteins?

A

1- Chlyomicrons - rich in triacylglycerols,

transports it from intestine to tissue
(largest size, lowest density)

2- VLDL - rich in triacylglycerols,

transports it from liver to tissue

3- LDL - cholesterol rich,

transports cholesterol to extrahepatic tissue

excess is bad

4- HDL - protein/cholesterol rich,

transports cholesterol from tissues to liver for elimination
(smallest size, highest density)

good cholesterol

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15
Q

Why is LDL ‘bad cholesterol’ and HDL ‘good cholesterol’ ?

A

Because excess LDL (transports cholesterol to extrahepatic tissues) causes build-up of foam cells and atherosclerotic plaques in the arteries. (atherosclerosis)

Because HDL removes cholesterol out of the plaque and provides cholesterol for bile and hormone synthesis

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16
Q

describe the Beta-oxidation pathway of fatty acids: (Catabolism of fatty acids)

A

Occurs in Mitochondrial Matrix

Provides energy for skeletal/heart muscle, kidneys when glucose/glycogen/gluconeogenic precursors ↓

Produces: Acetyl CoA, NADH, FADH2

[0] Release of fatty acids from adipose tissue via epinephrine and glucagon

[1] Activation of fatty acids in the cytosol & Diffusion

Fatty Acid + CoA → Fatty Acyl CoA in cytoplasm which diffuses through
the Outer Mitochondrial Membrane (OMM).

[2] Transport into the mitochondria by Carnitine Shuttle

This transport step is only required for Long-Chain Fatty Acids

Reaction 1: Fatty Acyl CoA → Fatty Acyl Carnitine
Catalyst - Carnitine palmitoyl transferase I (CPT1) or Carnitine acyl-transferase I (CAT1)

To move through the Inner Mitochondrial Membrane (IMM) into the Mitochondrial Matrix,
CoA is removed and Carnitine is added.

Reaction 2: Fatty Acyl Carnitine → Fatty Acyl CoA
Catalyst - Carnitine palmitoyl transferase II (CPT2) or Carnitine acyl-transferase II (CAT2)

Inside the Mitochondrial Matrix
Carnitine is removed and CoA is added.

[3] Degradation of Fatty Acyl CoA to Acetyl CoA

[A] Dehydrogenation aka Oxidation: FAD → FADH2

[B] Hydration: requires H2O

[C] Dehydrogenation aka Oxidation: NAD+ → NADH

[D] Thiolysis: cleavage of Acetyl CoA → TCA Cycle

  • Fatty Acid chain becomes two carbons shorter, then goes through the cycle again.
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17
Q

what is carnitine shuttle (CAT-1/CPT-1)?

A

is a major site of regulation during Fatty Acid Beta-Oxidation, which is inhibited by Malonyl CoA to prevent Acyl CoA from becoming Acyl Carnitine.

It also prevents synthesis and degradation from occuring simultaneously.

17
Q

what is malonyl CoA?

A

one of the control or regulation coenzymes in Fatty Acid Beta-oxidiation, which, in high amounts, inhibits the function of CAT1 or CPT1 to prevent the process of
Acyl CoA becoming Acyl Carnitine, so that it can’t be transported into the matrix.

It has a main role in the process of Fatty Acid Synthesis

18
Q

what is CAT-1/CPT-1 Deficiency?

A

it’s a deficiency that prevents beta-oxidation, leads to hypoglycemia.

Treatment:
eating food containing medium-chain fatty acids which do not require CAT-1 to transport, they simply diffuse through the mitochondria.

Deficiency in liver → impairs the liver’s capacity to use fatty acids as fuels, and puts an extra burden on its capacity to generate glucose through gluconeogenesis.

Deficiency in muscle → avoid strenous exercise and excessive fat.

19
Q

what happens to very long chained fatty acids in peroxisomes?

A

22 carbons undergo a preliminary b-oxidation in peroxisomes.

Then the shortened FA linked to carnitine diffuses from peroxisome into the mitochondria for further oxidation.

First step does not produce FADH2 and so less energy efficient than b-oxidation of long chained fatty acids

Defects in this pathway lead to VLC-FA accumulation in blood and tissue

19
Q

How many Acetyl CoA, FADH2, NADH, ATP result from the beta-oxidation of Palmitate (16-C)?

How many beta-oxidation cycles did it go through?

A

Each cycle produces one Acetyl coA and chain that is shorter by two carbons.

16/2 = 8 Acetyl CoA & then minus one = cycle numbers, FADH2, NADH

So the result is 8 Acetyl CoA & 7 FADH2 & 7 NADH

It went through 7 beta-oxidation cycles.

ATP approximate calcuation:

Each FADH2 = 2 ATP (2x7 = 14)

Each NADH = 3 ATP (3x7 = 21)

Each Acetyl CoA = 12 ATP (8x12 = 96)

However, 2 ATP are needed to produce Palmitoyl CoA so total is 131 - 2 = 129 ATP

Much more energy from fatty acids than from glucose

20
Q

what does gluconeogenic mean? e.g. animals

A

Animals cannot convert fatty acids to glucose i.e. they are not gluconeogenic, but they can convert glycerol to glucose.

21
Q

During fasting or starvation, there is an excess of Acetyl CoA
from Fatty acid breakdown:

A

Acetyl CoA ↑ inhibits {{c1::pyruvate dehydrogenase}}
(used in Transition Stage) because:

  • It uses Pyruvate to make Acetyl CoA (For Krebs Cycle)

Acetyl CoA ↑ activates {{c1::pyruvate carboxylase}}
(used in Gluconeogenesis) because:

  • It uses Pyruvate to form Oxaloacetate (For Krebs Cycle)
  • It forms Glucose (To raise BG levels)
21
Q

when does beta oxidation of fatty acids happen?

A

when blood glucose levels are down (Fasting/Starvation).

Two conflicting processes happen here:

[1] Excess levels of Acetyl CoA go through Krebs Cycle and bond with Oxaloacetate to make Citrate

[2] Oxaloacetate is used up in gluconeogenesis to form Glucose.

Then you have no Oxaloacetate left to bind with Acetyl CoA (starvation)

22
Q

What happens to the excess levels of Acetyl CoA?

A

Excess levels of Acetyl CoA are stored as ketone bodies which are made in the liver (ketogenesis)

  • Acetone
  • Acetoacetate
  • D-Beta-Hydroxybutyrate

The amount of ketogenesis depends on the availability of acetyl CoA and the activity of rate limiting enzyme HMG CoA synthase.

23
Q

what is diabetic ketoacidosis?

A

it’s a condition characterized by excessive levels of ketone bodies in the blood and low blood pH, which can occur during uncontrolled diabetes or starvation, when the rate of ketone body production exceeds utilisation and insulin is absent.

It leads to a fruity odour in breath due to acetone.

23
Q

what are ketone bodies?

A

they are soluble, fuel molecules made from excess Acetyl CoA from fat metabolism during starvation or fasting.

They are used by the Brain (it can’t use fatty acids), Cardiac and Skeletal muscle as an energy source during starvation, because of low glucose levels.

They can’t be used by red blood cells.

They are formed in the liver, in the mitochondrial matrix, but cannot be used by the liver, they are transported in the blood to be used in other cells.

24
Q

what is ketonemia?

A

Ketonemia is the presence of an abnormally high concentration of ketone bodies in the blood.

No Oxalacetate = start making ketones
(because under starvation - no pyruvate to make OAA)

25
Q

what is ketouria?

A

Ketouria is the presence of an abnormally high concentration of ketone bodies in the urine (detected by presence of acetoacetate in it).

26
Q

what happens when there’s no oxalacetate?

A

start making ketoned

(because under starvation - no pyruvate to make OAA)

27
Q

describe the anabolism of fatty acids:

A

Occurs in the Cytosol

  • Uses: ATP and NADPH (Reducing Agents)
  • Fatty acid is synthesized from Acetyl CoA, which is derived from excess protein, fat and carbohydrates.
  • Fed state & ↑ Blood Glucose
  • Important Enzymes used:
    Acetyl CoA carboxylase (activation/regulation)
    Fatty acid synthase (multifunctional enzyme)
  • Product: Palmitic acid

[1] Condensation

[2] Reduction (NADPH → NADP+)

[3] Dehydration

[4] Reduction (NADPH → NADP+)

[E] Thioesterase Cleavage of the Palmityl-CoA from the ACP. (DONE ONCE AT THE END)

28
Q

what is the detailed anabolism of fatty acids?

A

[A] Production of cytosolic Acetyl CoA

Acetyl CoA (which is produced in many pathways) is moved from the mitochondria to the cytosol

But it is in another form - Citrate - it moves through Citrate Shuttle into the cytosol when Citrate concentration is high in the mitochondria, because of ↑ in ATP (inhibits isocitrate dehydrogenase).

[B] Carboxylation of Acetyl CoA (2-C) to form Malonyl CoA (3-C)
Catalyst - Acetyl CoA Carboxylase (ACC)

C-C bond needs high energy - which is supplied indirectly by synthesizing Malonyl CoA

[C] Elongation by condensation reaction, in addition to a decarboxylation.
Acetyl ACP (2-C) + Malonyl ACP (3-C)→ Acetoacetyl ACP (4-C) (one carbon pops off)

ACP = Acyl Carrier Protein

[D] Reverse of Fatty Acid Degradation, further elongation in a cycle repeated six times, using Malonyl-CoA every time, to finally produce palmityl-ACP (16-C)

29
Q

What metabolic and hormonal signals control the activity of Acetyl CoA Carboxylase (ACC)?

A

CC is a key regulatory enzyme in De Novo Synthesis

Activatory Regulation:

  • Citrate (signals that there is enough glucose - so make Fatty acids) (+) (Allosteric)
  • Insulin (activates protein phosphatase) (+)

Inhibitory Regulation:

  • Palmitoyl CoA (signals that there is enough fatty acids - so stop synthesis!) (-)
  • Long-chain fatty acyl CoA (-) (Allosteric)
  • Glucagon (phosphorylation of ACC making it inactive) (-)
  • Epinephrine (phosphorylation of ACC making it inactive) (-)

ACC (dimer form - inactive) → ACC (polymer form - active) using citrate as a stimulus

30
Q

what is fatty acid synthase?

A

Fatty Acid Synthase (FAS-1) is a multifunctional enzyme with 7 subunits that has an ACP arm for anchoring the chain as it moves around the subunits, it is used in the elongation period of the fatty acid synthesis.

31
Q

where does most of the NADPH that is use for a reducing agent for the synthesis of palmitoyl-CoA come from? 2 reactions

A

[1] Phosphate Pentose Pathway

[2] Reaction of Malate → Pyruvate
Catalysed by Malic Enzyme (NADP+ → NADPH)

32
Q

where does any modification (e.g. unsaturation, elongation, branching) of palmitate or other dietary fatty acids occur? in the mitochondria and endoplasmic reticulum?

A

in the mitochondria and endoplasmic reticulum

33
Q

what is the fate of synthesised fatty acids?

A

Formed fatty acids → combine them with glycerol to make TAGs(triacergylcerols) → TAGs + proteins + phospholipids + cholesterol → VLDLs → they can be stored in adipose tissue.

34
Q

what are the 3 main classes of steroids?

A

[1] Cholesterol is the starting material for the synthesis of bile salts, steroid hormones and other components.

[2] Steroid hormones are substances that serve as chemical messengers in the body
(corticosteroids, sex hormones).

[3] Bile salts - sodium salts of steroids used for emulsification

35
Q

what are cholesterols?

A

It is made from Acetyl CoA in the liver.

Functions:

  • Component to cell membrane
  • Precursor to other substances:
    > Sterol hormones
    > Vitamin D
    > Bile acids

Synthesis: (mainly in the liver)

Food sources: only animal foods

36
Q

what are statins?

A

Statins e.g. lovastatin, are drugs that inhibit HMG-CoA reductase, which is essential in cholesterol synthesis.

They are the most common cholesterol-lowering drugs.

  • They lower LDL levels
  • They decrease the risk of developing cardiovascular disease
37
Q

what are eicosanoids?

A

they are lipids derived from 20-carbon unsaturated fatty acids (eicosanoic acids) and are synthesized throughout the body.

  • They are signalling molecules derived from omega-3 or omega-6 fatty acids
  • Precursors to prostaglandins, thromboxanes, and leukotrienes.
  • Short half life (metabolised rapidly), produced and act locally.
38
Q

what are the roles of eicosanoids?

A

Inflammatory response (e.g. joints, skin, eyes)

  • Pain & fever (Prostaglandins)
  • Mucus production in the stomach (prostaglandins)
  • Many reproductive functions (e.g. labour induction) & menstrual cramps, sperm mobility (prostaglandins)
  • Blood pressure regulation (prostacyclin)
  • Blood clotting induction/platelet homeostasis (thromboxanes)
  • Smooth muscle cell constrictions & bronchioconstriction regulation (leukotrienes)
39
Q

what do anti inflammatory drugs do? give examples

A

Anti inflammatory drugs e.g. Steroids & NSAIDs (Non-Steroidal-Anti-Inflammatory-Drugs) inhibit Eicosanoid synthesis.

e.g.

Anti-inflammatory and fever-reducing property of Aspirin due to inhibition of COX enzymes and prostaglandin synthesis.

Aspirin inhibits thromboxanes that cause clotting – given to susceptible patients

40
Q

Why might patients taking NSAIDs, e.g. aspirin, suffer from stomach ulcers?

A

Because Aspirin inhibits prostaglandin synthesis which then stops mucus production in the stomach

41
Q

what are some eicosanoid analogues in medicine?

A
  • Leukotriene antagonists - asthma treatment
    (inhibit leukotrienes).
  • Prostaglandin analogue - induces labor.
  • :Corticosteroids - inhibit inflammation, pain, fever
    (inhibit Phospholipase A2 / prostaglandins)
  • NSAIDs - pain/inflammation, inhibit clotting
    (inhibit {{c2::prostaglandins}} / {{c2::thromboxanes}})
42
Q

Why do some patients with asthma take Zileuton or Zafirlukast?

A

Because leukotrienes cause bronchioconstriction and these drugs inhibit leukotrienes

Zileuton is an orally active inhibitor of 5-lipoxygenase, and thus inhibits leukotrienes formation.

Zafirlukast is an orally administered leukotriene receptor antagonist (ASTHMA)

43
Q

what are the 3 types of ketone bodies?

A

[1] Acetone

[2] Acetoacetate → only one detected in urine

[3] D-Beta-Hydroxybutyrate → found in blood

44
Q

when are ketone bodies made?

A

Ketone bodies are made when insulin is absent & no presence of OAA because of no pyruvate.

So TCA cycle doesn’t work = excess Acetyl CoA = make ketone bodies in liver.

FoM - normal function (20 decks)

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