Cell Metabolism II - Lipids Flashcards

1
Q

what are the three primary sources of fats?

A
  1. the diet
  2. the liver (cholesterol metabolism)
  3. storage depots in adipose tissues
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2
Q

where are bile salts generated and stored?

A

generated: liver
stored: gall bladder

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3
Q

what can bile salts do to fats?

A

they can emulsify the fats (to incr. their surface area for lipase to break down) and fat soluble vitamines = aids their digestion and absorption in intestine

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4
Q

what can a lack of bile salts lead to?

A

fats pass through gut unabsorbed = steatorrhea (fatty stool)

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5
Q

what does the term “ampiphatic” molecules?

A

can interact with both hydrophobic molecules and hydrophobic molecules

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6
Q

how does the structure of bile salts relate to their function?

A
  • they are flat
  • hydrophilic groups face outdoes and hydrophobic groups face inside so they can transport the otherwise non-water solute/hydrophobic fats
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7
Q

how can medications aid with obesity?

A

Orlistat → can be used as a potent inhibitor of gastric and pancreatic lipase = fats passed out unabsorbed.

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8
Q

how are lipids transported around the body?

A

lipoproteins in the plasma

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9
Q

where are chylomicrons produced?

A

(lipoprotein)

enterocytes cells that - line the small intestine

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10
Q

how do chylomicrons transport the dietary fats around the body?

A
  1. dietary products enter the enterocytes e.g. triglycerides
  2. the triglycerides are resynthesized using enzymes and incorporated into the chylomicrons
  3. transported in the lymphatic system → blood
  4. they take up apoproteins (from HDL) into their membrane once they have reached the blood stream

The hydrophilic phospholipid monolayer, and apoproteins allow for the transportation of the core hydrophobic fats

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11
Q

By what and where do chylomicrons get broken down?

A

They are broken down by lipoprotein lipases, found in the on the capillary endothelial cells lining e.g. adipose, heart and skeletal muscle

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12
Q

What happens once the chylomicrons are broken down?

A

Fatty acids undergo β-oxidation. Glycerol is returned to the liver for use in gluconeogenesis

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13
Q

why do chylomicrons have apoproteins?

A

so that they can be recognised by tissues

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14
Q

where are lipoproteins synthesised?

A

liver

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15
Q

what is the main role of lipoproteins?

A

they transport hydrophobic molecules in a aqueous environment

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16
Q

what is the structure of lipoproteins?

A
  • phospholipid monolayer
  • cholesterol (esterified them to make them more hydrophobic so that they pack more tightly)
  • apoproteins
17
Q

What are the lipoproteins that transport fat to and from the liver? (Chylomicrons are from the intestine)

A

VLDL (very low density lipoproteins) - found in the liver and are responsible for endogenous fat transport
IDL (intermediate density lipoproteins) - comes from VLDL and is an LDL precursor (substance from which LDL can be made)
LDL (low density lipoproteins) - comes from IDL and is responsible for cholestrol transport from liver to peripheral tissues
HDL (high density lipoproteins) - comes from LDL and is responsible for reverse cholestrol transport from peripheral tissues to liver

18
Q

What are cholestrol esters and where are they found?

A

Synthesized in the plasma from cholesterol

19
Q

What are the 3 main steps for making Acetyl CoA from Fatty Acids?

A
  1. fatty acid → acyl CoA
  2. Transfer Acyl CoA into mitochondria via carnitine shuttle
  3. Beta Oxidation - finally produces Acetyl CoA
20
Q

what is step 1 to make acetyl CoA?

A

fatty acid → acyl CoA

21
Q

describe the carnithine shuttle

A

cytoplasm → matrix of mitochondria

1) carnitine + acyl CoA→ acyl carnitine + CoA
2) acyl carnitine moved across outer membrane through translocase
3) acyl carnitine + CoA→ carnitine Acyl CoA

only carnitine and all carnitine can move across membrane through translocase

22
Q

What is Primary carnitine deficiency and what are the symptoms?

A
  • reduces cells ability to take up canitine which is needed for beta-oxidation of fatty acids
  • muscle weakness, cardiomyopathies hypoglycaemia
23
Q

describe the beta oxidation cycle

A

(OHOT) oxidation → hydration → oxidation → thiolysis

from acyl CoA to acetyl CoA which is two carbons shorter

24
Q

When can acetyl coA from beta oxidation enter TCA??

A

if β-oxidation = carbohydrate metabolism as oxaloacetate is needed for entry

25
Q

When is acetyl CoA from fatty acids used to make ketone bodies?

A

When fat breakdown predominates e.g. during fasting

-if not sufficient oxaloacetate is produced from carb metabolism

26
Q

Which ketone bodies does Acetyl CoA make?

A
  • acetoacetate
  • D-3-hydroxybutyrate
  • acetone
27
Q

How does fatty acid metabolism compare to glucose metabolism in terms of no. of ATP produced?

A

significantly more ATP/mole of substrate is produced in fatty acid metabolism

28
Q

Which family of enzymes catalyse the initial step in each cycle of fatty acid β -oxidation?

A

acyl-CoA-dehydrogenases (oxidation)

29
Q

What is a disease to do with lipid metabolism?

A

cancer → FA biosynthesis only happens in liver, adipose tissue and lactating breast

30
Q

What are the 4 reactions of lipogenesis? (and enzymes involved)

A

1) condensation
2) reduction
3) dehydration
4) reduction

CRDR (lengthening carbonchain by 2)

31
Q

why are HDLs referred as “good cholesterol” and LDLs bad?

A
  • HDL take the cholesterol bad k to the liver for disposal = lower cholesterol levels
  • LDL can lead to atherosclerosis (hardening of the arteries) as
32
Q

What are the 4 reactions of lipogenesis? (and enzymes involved)

A

1) condensation
2) reduction
3) dehydration
4) reduction

CRDR
(lengthening carbon chain by 2)

33
Q

What does the desaturation of fatty acids require?

A

fatty acyl-CoA-desaturases

34
Q

In adults, where is de novo FA biosynthesis restricted to?

A
  • liver
  • adipose tissue
  • lactating breast
35
Q

What occurs in certain cancer cells?

A

reactivation of FA synthesis