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Biochem BLOCK 2 > YOUNGER BLOCK 2 > Flashcards

YOUNGER BLOCK 2 Flashcards

1
Q

Unsaturated FA

A

Double bonds present

  • cause kinks
  • three carbon intervals
  • reduces melting temp, increases fluidity
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2
Q

Why do membrane phospholipids often contain double bonds?

A

Because they are LCFA (the longer the chain, the higher the melting temp) and needs the double bonds there to lower the melting temp and increase fluidity

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3
Q

What are 2 essential FA?

A
  • a-linolenic acid

- linoleic acid

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4
Q

Arachidonic acid

A

Becomes essential is linoleic acid is deficient in the diet

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5
Q

Linoleic acid

A
  • essential FA
  • omega 6
  • precursor for other omega 6 FA
  • arachidonic acid becomes essential if this is deficient
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6
Q

A-linoleic acid

A
  • precursor for omega 3 FA
  • important for growth and development
  • essential FA
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7
Q

Arachidonic acid

A
  • substrate for prostaglandin

- becomes essential id linoleic acid is deficient in diet

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8
Q

FA less than 12 carbons

A

-short and medium chain

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9
Q

FA greater than 22 C

A

VLCFA

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10
Q

Where are LCFA synthesized>

A

de novo synthesis

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11
Q

Where are VLCFA synthesized ?

A

Brain tissue

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12
Q

Dietary lipids

A
  • TAG
  • phospholipids
  • free FA
  • cholesterol
  • cholesterol esters
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13
Q

Acid lipase

A
  • lingual lipase
  • gastric lipase
  • target TAG containing short and medium chain FA
    • can get through to blood stream without micelle
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14
Q

What are the two complimentary actions of emulsification in the small intestines?

A
  • mechanical agitation
  • bile salts secretion
    • detergent
    • don’t coalesce
    • allows pancreatic enzymes more surface area
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15
Q

What are the pancreatic enzymes responsible for TAG digestion

A
  • pancreatic lipase

- colipase

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16
Q

Phospholipase A2

A
  • phospholipid digestion

- removes the fatty acid from position 2 from arachidonic acid

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17
Q

What do gut endocrine cells sense?

A

CCK senses lipids and proteins, causes reduction of gut motility

Secretin senses low pH and secretes bicarbonate

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18
Q

Micelles

A
  • amphipathic lipids

- DEAK

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19
Q

How do short and medium chain FA get into blood stream?

A

They don’t need a micelle

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20
Q

Fatty acyl-CoA synthetase (thiokinase)

A

-loads fatty acyl-CoA for entry into chylomicron

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21
Q

Chylomicron

A
  • ER—lymph system—-blood
  • contain B-48
  • carries neutral lipids such as TAG and DEAK vitamins
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22
Q

Lipoprotein lipase

A
  • clip FA from chylomicron
  • synthesized and secreted by muscle and adipose

Remnants interact with liver cells and are endocytosed, this is where the vitamins get absorbed into the body

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23
Q

Lipid malabsorption

A

Poor digestion such as inability to secrete the proper amount of bile.
Shortened bowel disease

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24
Q

Cystic fibrosis

A
  • cant take up fat soluble vitamins
  • pancreatic insufficiency, significant reduction in dietary calories, decrease fat soluble vitamin up take
  • treatment includes: enzyme replacement, and fat soluble vit supplements
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25
Q

De novo synthesis

A
  • well fed
  • cytosol of liver and mammary glands of lactating mammals
  • cytosolic acetyl CoA is carbon source for growing FA chain (originate in mitochondria)
  • energy source: ATP and NADPH
26
Q

Which membrane of the mitochondria is hard to get across?

A

The inner mitochondrial membrane

27
Q

ACC

A
  • dimers in cytosol
  • coalesce to larger molecule which is active
  • takes CO2/energy and carboxylase acetyl CoA to malonyl CoA
  • RATE LIMITING STEP
28
Q

Presence of citrate

A

Signals ACC

29
Q

Short term regulation of ACC

A
  • AMPK reversibly phosphorylates and inhibits ACC

- LCFA presence also inhibits it (substrate)

30
Q

Long term regulation of ACC

A
  • prolonged high calorie, high carb increases ACC synthesis

- low calorie or high fat diet reduces ACC synthesis

31
Q

FAS

A
  • multifunctional dimeric enzyme
  • 7 different enzymatic activities
  • acyl carrier protein (ACP)
  • holding site for cysteine

2 C from malonyl CoA
ATP
NADPH

32
Q

Predominant source of the NADPH required for FA synthesis

A

HMP shunt

33
Q

Palmitate

A

Elongated at the smooth ER
Reduction of NADPH
2 C from malonyl CoA

34
Q

Desaturation of FA chains

A

Add double bonds to maintain fluidity at body temp

35
Q

Carbon 2 on TAG

A

Unsaturated FA of varied length

36
Q

Where is TAG generated ?

A

In liver and adipose

37
Q

TAG generation in liver

A

Glycerol kinase converts free glycerol to glycerol phosphate simply by adding a phosphate group

38
Q

What do chylomicrons deliver?

A

Exogenous dietary lipids

39
Q

What do VLDLS deliver?

A

De novo synthesized lipids

40
Q

Adipose lipase

A

-constitutive, low level release of FA

41
Q

Hormone sensitive lipase

A
  • major role in regulated TAY lipolysis and release
  • much more than adipose lipase
  • heavily influenced by insulin
42
Q

What is the major pathway for obtaining energy from FA

A

B-oxidation in the mitochondria

FA must be in the fatty acyl CoA

43
Q

Products of B oxidation

A

Acetyl CoA, NADH, FADH2q

44
Q

Carnitine shuttle

A
  • imports LCFAs into the mitochondria
  • CATI on outer mitochondrial membrane acyl groups transferred from CoA to carnitine. Regulated by malonyl CoA
  • CATII on matrix side acyl group transfer from carnitine to CoA
45
Q

CAT I inhibition

A

Malonyl CoA

-preventing LCFA transfer from CoA to carnitine

46
Q

Source of carnitine

A

Diet

Synthesized in liver/ kidney

47
Q

Where is most of the carnitine

A

Skeletal muscle

48
Q

Secondary carnitine deficiency

A
  • liver disease
  • malnutrition
  • dialysis
  • pregnancy
49
Q

Primary carnitine deficiency

A

congenital deficiencies

CAT I and CAT II defect

50
Q

Energy molecules for B oX

A

NADH
FADH2
Acetyl CoA–produce ketone bodies in liver to be used by peripheral tissue

51
Q

What vitamin is required for odd number of carbon degeneration?

A

Vitamin B12

52
Q

Saturated or unasturated FA release less energy?

A

Unsaturated

-require additional enzymes

53
Q

MCAD deficiency

A

Decreased oxidation of 6 to 10 carbon FA

-hypoglycemia

54
Q

Ketone bodies

A
  • produced in liver from B-oxidation derived acetyl CoA
  • acetoacetate and 3-hydroxybutarate transported in the blood to peripheral tissues
  • peripheral cells convert ketone bodies back into acetyl CoA, a substrate for the TCA cycle
  • decrease the demand on blood glucose
55
Q

Hypoketosis

A

-fatty acid oxidation disorder due to decreased acetyl CoA availability

56
Q

Hypoglycemia

A

-fatty acid disorder due to increased reliance on glucose for energy

57
Q

HMG CoA synthase=

A
  • rate limiting step in ketone body synthesis and is present only in the liver to significant amounts
  • makes 6-C chain to make ketone
58
Q

Can liver uses ketone bodies as fuel?

A

No because it lacks thiophorase

-extrahepatic cells having mitochondria can conduct this process

59
Q

Imbalances in use and production of ketone bodies

A

Cause ketone ketone bodies to rise

  • blood (ketonemia)
  • urine (Ketonuria)
60
Q

How can ketoacidosis be caused?

A

Fasting

-decreases blood volume increases H+ concentration causing severe acidosis

61
Q

Why is thromboxane synthesis more severely affected by NSAIDs and how does it affect coagulation?

A

Inhibits the COX step in the formation of both prostacyclin and thromboxanes
-platelets cannot synthesize new COX because no nucleus and significantly limits the thermogensis potential

62
Q

Glucocorticoids and inhibited phospholipase A2

A
  • inhalers
  • steroidal anti-inflammatory drug
  • promotes gene level up-regulating of phsopholipase A2 inhibitor

Biochem BLOCK 2 (14 decks)

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