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Medical Studies 2B > 4.3 Lipid Metabolism > Flashcards

4.3 Lipid Metabolism Flashcards

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USMLE® Step 1 flashcards
1
Q

What type of lipid is most commonly found in our diet? Of the plant and animal sources, which are saturated/unsaturated, and how does this affect naming?

A
  • Most common type is TAG
  • Animal: mostly saturated (“fats”)
  • Plant: mostly unsaturated (“oils”)
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2
Q

Where are bile salts made? Where are they stored? Where are they released into the GI tract, and how do they help us absorb lipids?

A
  • Made in liver
  • Stored in gall bladder
  • Released into duodenum, and form micelles with hydrophobic lipids to aid in solubility
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3
Q

What is the main lipase in the GI tract enzyme? Why is it lazy?

A
  • Pancreatic lipase
  • Converts TAGs into 2x free fatty acids and a monoacylglycerol; leaves one on the second carbon (since it’s lazy)
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4
Q

Which occurs first: lipase digestion or bile salt emulsification? Why does this make sense?

A
  • Bile salt emulsification
  • This increases the SA : V ratio, allowing enzymes to act more efficiently
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5
Q

Fully explain fat digestion and absorption

A
  1. Fat emulsified by bile salts
  2. Fat digested by pancreatic lipase to MAG + FFAs
  3. Absorbed into enterocytes, return to TAG, and packed into chylomicrons
  4. Enter lymphatic system through lacteals (too big for endothelium), drain into blood
  5. Lipoprotein lipase expressed on endothelium of blood vessels near muscle, heart, adipose, mammary glands etc.
  6. LL binds to apolipoproteins, hydrolyses TAGs, and sucks the FFAs out
  7. Eventually, empty chylomicrons (w/ glycerol in) recycled by liver
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6
Q

Which tissues express lipoprotein lipase? Which use the FFAs immediately, and which store them?

A
  • Immediately: skeletal muscle, heart
  • Store: adipose, mammary glands
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7
Q

True or false: the liver will begin lipogenesis as soon as we start eating

A
  • False
  • Lipogenesis kicks in as the body’s glycogen stores approach full capacity
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8
Q

What are the substrates for hepatic lipogenesis?

A
  • Ketogenic amino acids
  • Excess carbohydrates
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9
Q

Why do fatty acids have an even number of carbons in their chains?

A
  • They’re made via the assembly of acetyl coa
  • Acteyl = acetate = 2 carbons; therefore, must be even (2x is even)
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10
Q

What’s the difference between the TAGs found in chylomicrons vs VLDLs?

A
  • Chylomicrons carry exogenous TAGs into the body
  • VLDLs carry endogenous TAGs made in the liver
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11
Q

What happens to VLDLs as they circulate through the blood? What do we call the product, and how can we remember this using a science experiment from the Mathwin Centre?

A
  • Oils float on water; they are low density
  • Therefore, as lipoprotein lipase sucks the fatty acids (TAGs) out of VLDLs, they become denser
  • We call these LDLs once this has occurred
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12
Q

Chylomicrons are made by the ____, and VLDLs are made by the _____. But both of these organs make ___s.

A
  • Chylomicrons: small intestine
  • VLDLs: Liver
  • Both: HDLs
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13
Q

What are the two ways that HDLs can reduce cholesterol in the bloodstream?

A
  • Deposits into VLDLs (as they become LDLs)
  • Sent straight to the liver
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14
Q

The precursor to bile salts is…

A

Cholesterol

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15
Q

Cells can synthesise their own cholesterol from the precursor ____. Or, they can get it for free by…

A
  • Synthesised from Acetyl-CoA
  • Or, can be gotten for free by taking up LDLs (and phagocytosing components, like empty chylomicrons in liver)
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16
Q

What is the rate limiting enzyme in the production of cholesterol? What drugs inhibit this?

A
  • HmG-CoA Reductase
  • Inhibited by statins
17
Q

Can the body catabolise cholesterol? How does this affect the importance of reverse cholesterol transport?

A
  • The body cannot catabolise cholesterol
  • The only way to get rid of it is to turn it into bile salts, that are then secreted.
18
Q

Intermediate density lipoproteins are between…. in density

A

Between VLDL and LDL.

19
Q

Draw a diagram of the entire lipid handling system of the body

A
  • Dietary in by chylomicrons, endogenous in by VLDLs
  • VLDLs become LDLs, which are taken up by the liver and other tissues
  • HDLs bring cholesterol back to the liver, where it can be reused for VLDLs or turned into bile salts
20
Q

What organelle does beta oxidation occur in? What happens?

A
  • Occurs in mitochondria
  • Fatty acid jointed to CoA (fatty acyl CoA) shuttled into mitochondria
  • Broken down 2 carbons at a time (2 = beta), producing many Acetyl CoA
  • This process produces coenzymes for ETC (FADH2 and NADH), and Acetyl Coa for the citric acid cycle

Many ATP made as a result

21
Q

Which molecular process activates hormone sensitive lipase? What is its action?

A
  • Activated by phosphorylation
  • Fully hydrolyses TAGs in adipose cells for use in beta oxidation
22
Q

Which hormones activate/inactivate hormone sensitive lipase?

A

Activate: glucagon, adrenaline, cortisol
Inactivate: insulin

23
Q

What is one structural advantage of ketone bodies over free fatty acids? What organ does this give them unique access to?

A
  • Won’t damage cell membranes (FFAs are polar, like detergent)
  • This enables them to cross the blood brain barrier, for use as an alternative, non-glucose fuel source
24
Q

What is one disadvantage of ketone bodies as a fuel source? Link this to T1DM

A
  • Ketone bodies are very acidic
  • In T1DM, no insulin means the body cannot take up glucose
  • Therefore, we become too reliant on FFAs, producing many fatty acids that pull the pH out of safe ranges, causes DKA
25
Q

What are the effects of insulin, broadly, on the metabolism

A
  • Increased glucose uptake (muscle, adipose, liver)
  • Increased glycogenesis
  • Decreased glycogenolysis
  • Increased liopogenesis
  • Increased fatty acid synthesis
  • Increased glycolysis

(Make everything except glucose)

26
Q

Which channel protein carries insulin into muscle and adipose? Which enzyme aids hepatic glucose uptake?

A
  • In muscle and adipose, GLUT4 transporter is key
  • In the liver, glucokinase aids hepatic glucose uptake
27
Q

Which enzymes are rate limiting for producing/breaking down glycogen

A

Producing: glycogen synthase
Breaking down: glycogen phosphorylase

28
Q

Does a healthy liver store TAGs that are produced once glycogen stores are full?

A
  • No
  • This is fatty liver disease
29
Q

What are the effects of glucagon on adipose?

A
  • Mobilise hormone-sensitive lipase
  • Mobilise fatty acids
30
Q

Fatty acids are transported in the blood bound to…

A

Albumin

31
Q

Why does Acetyl-CoA accumulate in the liver when glucagon is high? What is produced as a result?

A
  • When glucagon is high, oxaloacetate is used for gluconeogenesis
  • This limits the citric acid cycle, and so Acetyl-CoA produced by beta oxidation builds up
  • As a result, we produced ketone bodies instead

Medical Studies 2B (57 decks)

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