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2024 SEM 1 BIOCHEMISTRY (LEC) > lipid metabolism > Flashcards

lipid metabolism Flashcards

1
Q

what process does the lipid undergo and what are the products

A

Metabolic oxidation of lipids releases large quantities of energy
Products: acetyl-CoA, NADH, and FADH2

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2
Q

it represents an efficient way of storing chemical energy

A

Lipids

[Fats, store a lot of energy in a compact form. They’re super efficient because they pack more energy per gram than carbohydrates or proteins. Think of them as dense fuel reserves.]

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3
Q

true or false:
lipids burn more fats compared to sugar

A

true

  • more fats = more energy
  • sugar is a short term energy while carbs is long term energy
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4
Q

It is the chief source of energy in the catabolism of lipids

A

fatty acids
- it comes from TAG & phosphoacylglycerol

*lipids are just not for energy, they also make cell membranes, these lipids have multiple sites where they can be cleaved for diff tasks

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5
Q

why is lipids the main storage of the chemical energy for most organisms

A
  • Carbon chains are in a highly reduced form (packed w electrons)
  • So, the OXIDATION (energy-producing reactions) occurs more frequently from these molecules. (the electrons are released, producing lots of energy)
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6
Q

true or false:
Energy yield per gram of carbohydrate oxidized is GREATER THAN that per gram of fatty acids oxidized

A

false - fatty acid oxidized is greater
bcs fatty acids have more chemical bonds that release energy when broken

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7
Q

what are main storage forms of lipids

A

triacylglycerol and phosphoacylglycerol

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8
Q

overview catabolism of lipids

A

TAG —> Free fatty acids —> phosphoacylglycerol (also called as phospholipids)

enzyme used respectively:
lipase (remove glycerol) and phospholipase

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9
Q

storage of the triacylglycerol

A

adipose cells or adipocytes in the adipose tissue

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10
Q

what hormones signal the body that it needs energy

A

Glucagon and epinephrine (main hormone)

-those interact with fat cells, sending a message to start breaking down TAGs.

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11
Q

it is the process of breaking down stored fats into smaller molecules (fatty acids and glycerol) that the body can use for energy.

A

hydrolysis of triacylglycerols (TAGs)

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12
Q

it is a secondary messenger, a product when the hormonal interaction with adipocytes

A

cyclic AMP (cAMP)

  • the signal triggers that production
  • cAMP signals the enzymes to start breaking down TAGs into fatty acids and glycerol
  • FA released into bloodstream
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13
Q

what happen when when the glucagon and epinephrine binds with the adipose cells

A

it activates a signaling pathway
= increases cAMP, which activates protein kinase
= which then activates
1. enzyme called hormone-sensitive lipase (HSL) by adding a phosphate group to it, phosphorylation and
- breakdown TAG in adipose cells

2.phopholipase
- breakdown phospholipids

  • both release FA after the breakdown

[the hormones tell the fat cells to start breaking down their stored fat, and cAMP is the molecule inside the cells that translates that external hormonal signal into action. The cAMP acts as a messenger, relaying the instruction to start fat breakdown]

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14
Q

what is the function of the HSL, hormone-sensitive lipase

A

once activated, it breaks down the fat (TAG) stored in the fat cells (adipocytes), releasing fatty acids

those fatty acids can be used as energy source, released in the bloodstream

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15
Q

why do competitive runners often drink caffeine the morning of a race.

A

caffeine mimics epinephrine

[Caffeine tricks your body into thinking it’s being signaled by epinephrine, the hormone that gets you ready for action.
This starts the process of breaking down stored fats (like epinephrine does)]

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16
Q

why do runners drink caffeine

A

[Distance runners want to use their fat stores for energy early in a race.
This helps them save their carbohydrate stores (which are limited) for when they really need a quick energy boost in the later stages of the race.]

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17
Q

Hydrolysis of triacylglycerols in adipose tissue is triggered by hormones that stimulate _____ production within adipose cells that stimulate lipases in these cells.

A

cyclic AMP (cAMP)

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18
Q

the process of fatty acid transport and activation within the mitochondria

A

FA enters mitochondria
then undergoes activation by binding to coenzyme A (CoA-SH) = acylCoA

acylCoA is then used by the acyl-CoA synthetase enzyme to further process the FA for use in energy production

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19
Q

how to activate the FA molecule

A

activation involves forming a special chemical bond called a thioester bond
which forms btwn carboxyl grp and a sulfur containing grp called CoA-SH

the enzyme that catalyzes this activation reaction is called acyl CoA synthetase (it takes the free fatty acid and attaches the CoA-SH group to it, creating a new molecule called acyl CoA.)

*activation step requires the use of ATP

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20
Q

what is the first step in the process of FA oxidation

A

FA activation
which is how cells break down FA to produce energy

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21
Q

how are thioester bond formed

A

btwn carboxyl grp of the FA and a molecule called coenzyme A (CoA-SH)

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22
Q

what enzyme that catalyzed this activation reaction

A

acyl-CoA synthetase, and it requires the use of ATP (the cell’s energy currency) to form the thioester bond.

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23
Q

where is the location of the activation

A

esterification (activation) happens in the cytosol, which is the fluid outside the mitochondria
but the rest of the FA oxidation reaction occur inside the mitochondrial matrix

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24
Q

true or false:
Acyl-CoA can cross the outer mitochondrial membrane and the inner membrane

A

false - but not the inner membrane

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25
Q

activated form of FA

A

Acetyl-CoA

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26
Q

molecule used in fatty acid metabolism to shuttle acyl groups across the inner mitochondrial membrane

A

carnitine

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27
Q

briefly explain the acyl carnitine/ carnitine shuttle

A

index card

28
Q

Carnitine Acyltransferase I (CAT-I) vs Carnitine Acyltransferase II (CAT-II)

  • specific name
  • location
  • function
A
  1. Carnitine Acyltransferase I (CAT-I):
    Specific Name: Carnitine Palmitoyltransferase I (CPT-I).

Location: On the cytosolic side (outer side) of the inner mitochondrial membrane.

Function: Transfers the fatty acid from Acyl CoA to carnitine. This creates acyl-carnitine, which can cross the membrane.

  1. Carnitine Acyltransferase II (CAT-II):
    Specific Name: Carnitine Palmitoyltransferase II (CPT-II).

Location: Inside the mitochondria, on the matrix side of the inner membrane.

Function: Transfers the fatty acid from carnitine back to CoA, forming mitochondrial Acyl CoA, which is ready for energy production.

29
Q

what happens after the acyl-CoA enters the matrix

A

undergo beta oxidation

30
Q

in the repeated series of reaction that cleaves carbon units from the carboxyl end of a fatty acid.

A

beta oxidation\
* it cleaves 2 carbon units

31
Q

why is it called beta oxidation

A

it’s called “beta-oxidation”—the focus is on the beta carbon, which is the second carbon from the carboxyl end of the fatty acid.

32
Q

what are the 4 steps where the second carbon from the carboxyl group (the beta carbon) is oxidized

A
  1. First Reaction: Oxidation
    The fatty acid (acyl-CoA) is slightly modified by removing hydrogen atoms, creating a double bond between the second and third carbons (α and β carbons).
    This reaction is powered by FAD, a molecule that carries away the removed hydrogen atoms.
    Enzyme: Acyl-CoA dehydrogenase.
  2. Second Reaction: Hydration
    Water is added to the molecule, which removes the double bond and creates a new structure called β-hydroxyacyl-CoA (with an -OH group on the β carbon).
    Enzyme: Enoyl-CoA hydratase.
  3. Third Reaction: Oxidation Again
    The -OH group on the β carbon is converted into a ketone group (-C=O) by removing more hydrogen atoms.
    This step uses NAD+, which carries the hydrogen atoms away.
    Enzyme: β-hydroxyacyl-CoA dehydrogenase.
  4. Fourth Reaction: Cleavage
    The fatty acid is “chopped” at the β carbon, producing two products:
    Acetyl CoA (a 2-carbon unit that goes to the Krebs cycle for energy).
    A shortened fatty acid (acyl-CoA), which goes back into the cycle.
    Enzyme: Thiolase.
33
Q

in each repetition of the 4 step process in beta oxidation, what was used and produced

A

USED
1 fatty acid
1 FAD
1 NAD+
CoA-SH

PRODUCED
1 acetyl CoA
1 new acyl CoA that is two carbons shorter (Cn-2)
1 FADH2
1 NADH

34
Q

how to find the
no. of actyl CoA molecules
no. of cycles of beta-oxidation

A

index card

35
Q

true or false:
odd carbon fatty acids does not go through beta-oxidation

A

false - it goes through just like regular fatty acids with an even number of carbons

36
Q

what is the difference between even and odd no. of carbon fatty acids

A

For odd carbon, instead of producing a 2-carbon unit (acetyl-CoA), the final product is a 3-carbon unit called propionyl-CoA.

  • the last step produces propionyl-CoA, a 3-carbon molecule, instead of acetyl-CoA.
37
Q

why is monosaturated fatty acid hard to break down directly in beta-oxidation

A

as it has one double bond = hard to break
bcs the enzymes involved dont work on double bonds in the cis configuration

38
Q

what is the solution for monounsaturated fatty acids in order for it undergo beta oxidation

A

Solution: Cis-Trans Isomerization
an enzyme rearranges the double bond into trans that can be processed by beta oxidation

39
Q

why is it when the Cis-Trans Isomerization occur, it produces less energy

A

The rearranging of the double bond skips some steps in beta-oxidation.

These skipped steps mean less FADH2 is produced, which leads to fewer ATP molecules being generated compared to a saturated fatty acid with the same number of carbons.

[Summary:
Monounsaturated fatty acids need extra processing (cis-trans isomerization) before beta-oxidation. This extra step makes them slightly less efficient at producing energy (less ATP) than saturated fatty acids.]

40
Q

Why Does the Body Prefer Glucose in Many Situations?

A

Quick Energy: Glucose is the body’s go-to energy source because it can be used quickly and efficiently, especially when immediate energy is needed.

41
Q

what does the brain primarily relies on its fuel source

A

glucose

42
Q

During intense physical activity, why does carbohydrates are the main fuel source instead of fats

A

as fats cant be mobilized quickly enough

43
Q

what is the state of fat when you are in a well-fed state

A

When you eat a lot of food, especially sugars, your body stores excess energy as fat.
Fat burning is slowed down because glucose is available and the body prefers to use it first.

44
Q

what happens if you are fasting or starving and your body needs energy

A

your body needs an alternative energy source.
Fat is used because it’s stored in large amounts and can be broken down into energy through beta-oxidation

[Summary:
Glucose is used first because it’s quick and efficient, especially for the brain and intense activities.
Fats are stored for later use, mainly during fasting or when glucose isn’t available.]

45
Q

why does the citric acid cycle slows down when glucose is low

A

as it needs OAA
OAA is taken out of the cycle and used to make more glucose in a process called gluconeogenesis

  • however, w/o enough OAA, the acetylCoA cant enter the citric acid cycle = excess acetyl-CoA starts to accumulate

the solution:
liver solves this problem by using the extra acetyl-CoA in a process called ketogenesis

46
Q

what happens in ketogenesis

A

Two acetyl-CoA molecules combine to form = acetoacetyl-CoA, which is the start of creating ketone bodies.
*Ketone bodies are alternative fuel sources for the brain and other organs during starvation.

47
Q

where does ketone bodies formed

A

liver mitochondria

48
Q

what are the 3 ketone bodies

A

Acetone
B-hydroxybutyrate
Acetoacetate (used as a fuel in most tissues and organs)

49
Q

why does the body make ketone bodies

A

The brain and other organs normally rely on glucose for energy.

During starvation or in diabetes (when glucose isn’t available or used properly), the body breaks down fats into ketone bodies to provide energy.

This helps keep the brain and body functioning when glucose is scarce.

50
Q

this occurs when ketone bodies build up in the blood, making it too acidic.

A

ketoacidosis

High ketone levels can cause symptoms like nausea, dehydration, and confusion.
The excess ketone bodies are excreted in urine, which is why checking urine for ketones can help diagnose diabetes.

51
Q

what type of process is the fatty acid biosynthesis

A

anabolic process that takes place in the cytosol

52
Q

fatty acid biosynthesis

A

index card

53
Q

difference between beta oxidation and fatty acid biosynthesis
- goal
- location
- direction
- energy use
- key molecules involved
- enzymes
- oxidation vs reduction

A
  1. Goal:
    Beta-Oxidation: Breaks down fatty acids to release energy.
    Fatty Acid Synthesis: Builds fatty acids to store energy.
  2. Location:
    Beta-Oxidation: Happens in the mitochondria (the cell’s powerhouse).
    Fatty Acid Synthesis: Happens in the cytosol (the fluid part of the cell).
  3. Direction:
    Beta-Oxidation: Cuts fatty acids into smaller pieces (2-carbon units as acetyl-CoA).
    Fatty Acid Synthesis: Joins small pieces (acetyl-CoA + malonyl-CoA) to make a longer chain.
  4. Energy Use:
    Beta-Oxidation: Produces energy in the form of NADH, FADH₂, and acetyl-CoA.
    Fatty Acid Synthesis: Consumes energy in the form of ATP and NADPH.
  5. Key Molecules Involved:
    Beta-Oxidation: Uses CoA and produces acetyl-CoA.
    Fatty Acid Synthesis: Uses malonyl-CoA and acyl-carrier protein (ACP).
  6. Enzymes:
    Beta-Oxidation: Uses a series of separate enzymes for each step.
    Fatty Acid Synthesis: Uses a single multi-enzyme complex called fatty acid synthase.
  7. Oxidation vs. Reduction:
    Beta-Oxidation: Oxidizes fatty acids (removes electrons and hydrogen).
    Fatty Acid Synthesis: Reduces molecules (adds electrons and hydrogen).
54
Q

it is the blockage of arteries due to cholesterol plaque buildup, leading to heart disease and heart attacks.

A

Atherosclerosis

55
Q

what are the contributing factors of atherosclerosis

A
  1. Diet
    - Eating too much cholesterol
    - Saturated fats
    - Other unhealthy fats increases the risk of plaque buildup
  2. Genetics
    Some people inherit defective genes that make the condition worse:

Familial Hypercholesterolemia: A genetic condition caused by a faulty LDL receptor gene (the receptor that removes “bad cholesterol” from the blood).
- Heterozygotes: People with one defective gene may have higher cholesterol and increased heart disease risk.
- Homozygotes: People with two defective genes have extremely high cholesterol from birth and can suffer heart attacks as early as 2 years old.

  1. Apolipoprotein E Problems
    - Apolipoprotein E (ApoE) is a protein that helps clear certain fats (IDL and VLDL) from the blood.
    - If ApoE is defective, fats aren’t removed properly, leading to more cholesterol buildup.
56
Q

what are the different types of lipoproteins and its function

A

Chylomicrons:
- Carry fats and cholesterol from the food you eat (dietary lipids) into your bloodstream.
Think of them as delivery trucks for the fats you just ate.

VLDL (Very Low-Density Lipoproteins)
- Transport fats and cholesterol made by your liver (endogenous lipids) to your body tissues.
These are like cargo ships carrying the body’s own produced fats.

IDL (Intermediate-Density Lipoproteins)
- A middle stage lipoprotein created when VLDL starts losing its fat cargo.
It’s like an emptying truck halfway through its delivery route.

LDL (Low-Density Lipoproteins) – “Bad Cholesterol”
- Delivers cholesterol to your body’s cells for use.
Problem: When there’s too much LDL, it deposits cholesterol in the arteries, forming plaques that can lead to heart disease.

HDL (High-Density Lipoproteins) – “Good Cholesterol”
- Picks up extra cholesterol from your blood and takes it back to the liver to be broken down and removed.
Think of HDL as a clean-up crew that prevents cholesterol buildup in your arteries.

[Too much LDL (“bad cholesterol”) can clog arteries, leading to heart disease.
High HDL (“good cholesterol”) helps clear excess cholesterol, keeping your heart and arteries healthy.]

57
Q

how does LDL get inside the cells

A

LDL (bad cholesterol) has a “key” called apoprotein B-100 that binds to “locks” on cells called LDL receptors.
Once bound, the cell pulls LDL inside through a process called endocytosis (like swallowing it).
Inside the cell, LDL is broken down in a structure called a lysosome, and cholesterol is released.

58
Q

How Cholesterol Regulates Itself

A

When the cell has enough cholesterol, it slows down or stops making more. It does this by:
Inhibiting HMG-CoA reductase, the enzyme needed to make cholesterol.
Reducing LDL receptor production, so less LDL is brought into the cell.

59
Q

Impact of Too Much Cholesterol

A

If there’s too much cholesterol in the blood and fewer LDL receptors on cells, LDL levels in the blood rise.
Excess LDL builds up in arteries, forming plaques that can block blood flow and lead to heart disease.

60
Q

Bad Cholesterol (LDL) vs. Good Cholesterol (HDL)

A

LDL (“bad cholesterol”) delivers cholesterol to your body’s cells, but too much LDL can cause cholesterol to build up in your arteries, leading to blockages.
HDL (“good cholesterol”) helps clear cholesterol from the bloodstream and sends it back to the liver to be broken down, reducing the risk of blockages.

61
Q

Why LDL and HDL Levels Matter:

A

High LDL + Low HDL = Higher Risk of Heart Disease.
Cholesterol buildup in the arteries can lead to heart disease or heart attacks.

62
Q

How Lifestyle Affects Cholesterol Levels

A

Exercise: Regular exercise boosts HDL (good cholesterol) and lowers the risk of heart disease.

Smoking: Smoking lowers HDL levels, which makes it harder for your body to clear cholesterol, increasing the risk of heart problems.

63
Q

it arises from excessive fat accumulation in adipocytes (fat cells).

A

obesity
- Leads to health problems like diabetes, heart attacks, strokes, and even some cancers

64
Q

How the Body Controls Hunger and Fat Storage

A

SHORT TERM CONTROL(Feeling Hungry or Full):

  1. Cholecystokinin (CCK):
    Released by the gut after eating.
    Sends a “you’re full” signal to the brain to stop eating.
  2. Ghrelin:
    Released by the stomach when it’s empty.
    Sends a “you’re hungry” signal to the brain.
    Levels drop after eating.

LONG TERM CONTROL (Managing Fat Levels Over Time):

  1. Insulin (Hormone from the Pancreas):
    Helps manage sugar and fat in the body.
    Encourages fat storage and increases leptin production.
    High insulin = more fat stored.
  2. Leptin (Hormone from Fat Cells):
    Released by fat cells to let the brain know how much fat is stored:
    - High leptin = You’re full (less appetite).
    - Low leptin = You’re starving (more appetite).
    Reduces hunger by lowering levels of neuropeptide Y (NPY), which triggers hunger.

[In summary:

Short-term signals (CCK and ghrelin) control hunger from meal to meal.
Long-term signals (insulin and leptin) manage fat storage and appetite over time. Keeping these hormones balanced is important for preventing obesity and related health problems.]

65
Q

How does the Brain Regulates Appetite

A

The arcuate nucleus is a part of your brain (in the hypothalamus) that controls whether you’re hungry or full. It uses two types of neurons:

  1. NPY/AgRP Neurons (Hunger Neurons):

What they do: Make you feel hungry.
Activated by:
Ghrelin (hormone released when your stomach is empty).
Other signals that tell the brain you need food.

  1. Melanocortin-Producing Neurons (Fullness Neurons):

What they do: Make you feel full and stop eating.
Activated by:
Leptin (from fat cells when your body has enough fat).
Insulin (from the pancreas after eating sugar or carbs).
Other signals that indicate you’re well-fed.

[Summary:
Hunger neurons (NPY/AgRP) say: “Eat more!”
Fullness neurons (Melanocortin) say: “Stop eating!”]

2024 SEM 1 BIOCHEMISTRY (LEC) (19 decks)

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