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Biochem 102 > Lipids and Fatty Acids > Flashcards

Lipids and Fatty Acids Flashcards

1
Q

Define lipids, their properties, their functions, and what would result due to lipid deficiencies or imbalances.

A

Lipids are heterogenous, hydrophobic organic molecules.

Insolubility in water results in their compartmentalization. Example, in membranes, as oil droplets or adipocytes, or associated with proteins in the blood.

Functions:
- major source of energy
- structural component of cell membranes
- may serve as fat soluble vitamins
- structural component of some signaling molecules (e.g steroids)

Deficiencies and imbalances lead to diseases such as atherosclerosis, diabetes, and obesity.

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2
Q

Classify the biochemically important lipids and their roles in the cell.

A
  1. Free fatty acids
    - chains of hydrocarbons
    - simplest lipids
    - most common fuel source for lipids
    - also building blocks for membrane
    - e.g vitamins from fatty acids
    - they are ionized at ph7
  2. Triacylglycerols (TAG)
    - glycerol backbone and linked to 3 fatty acid chains through ester linkages
    - stored in adipose cells (adipocytes/fat droplets)
    - hydrophobic
    - primary energy storage molecule
    - insulation
  3. Phospholipids
    - major class of membrane lipds
    - amphipathic (hydrophobic and hydrophilic), can interact with water on one side
  4. Glycolipids
    - contains sugar, bound to carbohydrates
    - found in cell membrane
    - role in cell-cell interactions
    - the sugar is always on the extracellular side, for communication
  5. Steroids
    - multiring structure, the groups that are added to it are what make it different
    - have a steroid nucleus
    - plays roles in signaling (hormones) and digestion
    - important for maintaining membrane fluidity
    - cholesterol is a type of steroid
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3
Q

Naming fatty acids

A

Look at lecture 17 page 13 on your notes to see

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4
Q

What is important to know about omega-3 and omega-6 fatty acids?

A

humans cannot make them, they essential amino acids; must come from our diet

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5
Q

Membranes become rigid in
a) unsaturated fats
b) saturated fats

A

UNSATURATED FATS

membranes need fluidity so they ain’t gonna be too happy about this!

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6
Q

How do saturation/unsaturation and chain length affect melting temperature of the fatty acid?

A

Unsaturation decreases the melting point

Chain length; if its longer there is a higher temperature threshold.

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7
Q

What are dietary lipids, how are they digested and where?

A

90% TAG (fat storage molecule) and 10% cholesterol, cholesterol ethers, phospholipid and unesterified (free) fatty acids.

*lipase breaks down lipids
Digestion begins in the stomach. It is catalyzed by acid stable enzymes; lingual lipase (release from glands behind the tongue), and gastric lipase (released from mucosal cells lining the stomach)

Short/medium length TAGs are degraded to glycerol and free FAs. Mechanical mixing (peristalsis) begins emulsification.
- creates larger SA for lipids (more accessible for lipases)

In the small intestine, dietary lipids mixed with bile salts that also increase SA.

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8
Q

Describe TAG digestion.

A
  • TAG molecules are too big for mucosal cellular uptake
  • Lipase breaks it down into free fatty acids
  • Micelles (mix of digestion products and bile) take the free fatty acids + monoacylglycerols into intestinal cells
  • In the intestinal cells lipid digestion products are RESYNTHESIZED into TAG and packaged for transport
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9
Q

Describe how TAG is delivered to tissues!

A
  • Chylomicrons and VLDL release TAG to tissues
  • LDL (found on surface of tissues) releases FA from TAG to tissues
  • Chylomicron remnants return to the liver
  • VLDL BECOMES LDL to deliver cholesterol to tissues
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10
Q

What are apolipoproteins?

A

Proteins that bind to lipids since they CANNOT travel alone (they maintain the shape of the lipoproteins and add hydrophilicity)

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11
Q

What are lipoproteins, the four main classes, as well as general function?

A

Lipoproteins are complexes of lipids and apolipoproteins found in blood and plasma.

Four main classes are
- Chylomicrons
- VLDL
- LDL
- HDL

Their function is to maintain lipids in soluble form in blood and deliver lipids to tissues.

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12
Q

Chylomicrons composition, and what it carries…

A
  • Largest, lowest density
  • Highest lipid, lowest protein
  • Carry dietary fats
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13
Q

VLDL composition, and what it carries…

A

“Very low density lipoproteins”
- more dense
- higher protein, lower lipid
- carry de novo synthesized fats (newly synthesized fats)

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14
Q

LDL composition, and what it carries…

A

“Low density lipoproteins”
- more dense
- higher protein, lower lipid
- transporter of BAD cholesterol
- formed from VLDL
- after TAG is delivered to tissues from VLDL, LDL is what remains

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15
Q

HDL composition, and what it carries…

A

“High density lipoproteins”
- transports GOOD cholesterol
- smallest and most dense
- highest protein, lowest lipid (apolipoprotein storage molecule in the blood)
- picks up cholesterol when there’s too much and transports it back to liver to be disposed
- rich in phospholipids and apolipoproteins

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16
Q

What happens when you got too much cholesterol (hypercholesterolemia)?

A
  • inhibits HMG coA reductase (sterol dependent degradation) HMG CoA reductase catalyzes the rate-limiting step in
    cholesterol biosynthesis.
  • reduces # of LDL receptors = less intake, so buildup of LDL
  • if cholesterol, which is normally stored as cholesterol esters, is stored unesterified this means we have free cholesterol which is toxic
17
Q

Describe atherosclerosis:

A
  • LDL accumulates in the plasma and blood
  • it can become oxidized which triggers an immune response
  • macrophages (a type of white blood cell) come in and take up LDL
  • this forms a “foam cell” which gets trapped in vessel walls leading to plaque formation which can lead to heart attack/stroke
18
Q

Describe the release of fatty acids from TAG storage in adipose.

A

Glucagon/epinephrine (produced in response to low blood sugar) stimulate FA release in adipose

These hormones bind to a receptor and a cascade of events starts that ends with a lipid.

The FA are activated by being linked to acetyl-coA, which transports them to the mitochondria

19
Q

What are the stages of fatty acid degradation

A
  1. release of FA from TAG storage (in adipose)
  2. activation of FA by linkage to acetyl-coA (transports them to mitochondria)
  3. FA oxidation generates acetyl-coA, NADH and FADH2 (all high energy molecules resulting in ATP production)
20
Q

What is hormone sensitive lipase and adipose triglyceride lipase, how are they activated, and what do they do?

A
  • Glucagon and/or epinephrine stimulate FA release in adipose tissue
  • Signaling cascade results in activation of the two lipases (HS-lipase) and (ATGL). They cleave FA off of triglycerol which releases free fatty acids and glycerol into the blood
21
Q

What are signaling cascades and transduction benefits, and some benefits of them?

A
  • Allow cells to respond to hormone or environmental stimuli
  • Activation of a receptor in a cell membrane results in reactions to produce second messengers
  • Once the hormone is released cascade turns off which allows for “on” and “off” function.
  • Water soluble molecules rely on cascades
22
Q

Where are FA and glycerol released from, and transported by?

A
  • Released from TAG
  • FA are hydrophobic thus require binding to albumin (a protein) to be transported to wherever they need to be used
  • Glycerol is transported to the liver (used in gluconeogenesis)
23
Q

‎‎‎‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ —> _____ —-> ________, ________
TAG
(fat cell)
‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ —> _____ —-> _______

A

‎‎‎‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ —> Glycerol —-> glycolysis & ‎‎‎‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ gluconeogenesis
TAG
(fat cell)
‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ ‎ —> FA —-> FA oxidation

24
Q

What is done to prepare fatty acids for oxidation?

A

Oxidation occurs in the mitochondrial matrix, so these FA must be transported there. In order to do this they need to be activated:
- by attaching coA to FA
- ATP dependent reaction, takes 2P off to form AMP (takes a lot of energy)

25
Q

After fatty acids get activated (into activated fatty acyl-coA) how does it get transported into the mitochondrial matrix?

A
  • coA CANNOT cross the membrane
  • coA makes the activated fatty acid so that it can attach to carnitine
  • carnitine takes the fatty acyl off of coA and attaches it to acyl carnitine, this can then cross the membrane and form acyl coA
26
Q

Do degradation and synthesis of fatty acids occur at the same time?

A

NO

27
Q

What is the carnitine shuttle inhibited by and why?

A

Inhibited by malonyl coA

Inhibited when FA synthesis occurs; FAs are not transferred to the mitochondria.

28
Q

What happens with carnitine deficiencies?

A
  • We can’t get FA into the mitochondria to break it down
  • These people rely more heavily on glucose
  • There is an accumulation of toxic amounts of free FAs and acyl groups
29
Q

What are the steps of FA synthesis?

A
  1. Transport of acetyl coA from mitochondrial matrix to cytoplasm
  2. Conversion of acetyl coA to malonyl coA
  3. Synthesis of FA by FA synthase
30
Q

Explain how acetyl coA is transported to the cytoplasm from the mitochondrion.

A
  • coA CANNOT cross the inner mitochondrial membrane
  • this is why acetyl-coA is converted into citrate to cross, then back to acetyl coA in the cytoplasm for the COST of 1 ATP
31
Q

How does the level of citrate affect glycolysis, FA synthesis, and the rate of TCA?

A
  • In addition to being a precursor for fatty acid synthesis, citrate serves as a signal molecule. It inhibits phosphofructokinase, which controls the rate of glycolysis:
    Citrate indicates an energy rich state (high ATP), it turns off glycolysis, and provides substrate for FA synthesis (to store the energy that has been made)

The citric acid cycle is slowing down (citrate is being pumped out)

32
Q

When does FA synthesis occur?

A

Fed state (increased blood glucose), therefore also means increased insulin, also when there’s high levels of ATP (because the body doesn’t wanna keep breaking them down so stores them instead as FA)

33
Q

Explain the three main stages of FA synthesis.

A
  1. In a preparatory step, acetyl CoA is transferred from mitochondria, where it is produced, to the cytoplasm, the site of fatty acid synthesis. Acetyl CoA is transported in the form of citrate, which is cleaved to yield acetyl CoA and oxaloacetate.
  2. Fatty acid synthesis begins in the cytoplasm with the activation of acetyl CoA, in a two-step reaction, to malonyl CoA.
  3. The reaction intermediates are attached to an acyl carrier protein, which serves as the molecular foundation for the fatty acid being constructed. Fatty acid is synthesized, two
    carbon atoms at a time, in a five-step elongation cycle.
34
Q

Explain how fatty acid metabolism is regulated

A

Fatty acid synthesis is maximal when carbohydrates and energy are plentiful and when fatty acids are scarce.
Acetyl carboxylase is a key regulator
- activated by insulin
- inhibited by glucagon and epinephrine
It gains a phosphate when inhibited (covalently inhibited by phosphorylation)

35
Q

What does acetyl coA carboxylase do?

A

Acetyl CoA play essential roles in regulating fatty acid synthesis and degradation.
- catalyzes the committed step in fatty acid synthesis: the production of malonyl CoA (the activated two-carbon donor)
- responds to changes in its immediate
environment and is switched off by phosphorylation and activated by dephosphorylation
The carboxylase is also allosterically stimulated by citrate.
The level of citrate is high when both acetyl CoA and ATP are abundant

Biochem 102 (4 decks)

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