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Biochem block 3 > lecture 3 lipid metabolism > Flashcards

lecture 3 lipid metabolism Flashcards

1
Q

Adipose tissue as an _____ and _____ organ

A

endocrine and secretory

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2
Q

There were two things that Dr. Williams underlined that adipocytes contribute to

A

Leptin, adiponectin, Resisting
-molecules regulating energy homeostasis

Molecules regulating innate immune system
-TNF a and IL-6

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3
Q

Fatty acids are taken up by ____, where they may serve as precursors in the synthesis

A

cells

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4
Q

after fatty acids are taken up by the cell, what are the different paths it can go

A

synthesis fatty acids for storage or export

mitochondria for energy or ketone bodies (export energy)

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5
Q

What is the major form of energy storage?

A

fat

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6
Q

what is the distribution fuel reserves in a typical individual

A

Fat: 100,000 kcal
Protein: 25,000 kcal
carbohydrate: 650 kcal

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7
Q

What are the intermediated if fatty acid metabolism

A

phospholipid (in membranes)

Eicosanoids, including prostaglandins and leukotrienes which play a role in physiological regulation

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8
Q

What are the diseases for fatty acid metabolism?

A

Diabetes mellitus
specific disorders of fatty acids oxidation like SIDS, Reye syndrome which might be related to a deficiency of medium chain acyl CoA, dehydrogenase, an important enzyme of fatty acid oxidation

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9
Q

For SIDS AND Reye syndrome, what might that be related to

A

related to a deficiency of medium chain acyl CoA, dehydrogenase, an important enzyme of fatty acid oxidation

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10
Q

What are two precursors of acetyl coA?

A

amino acids and glucose

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11
Q

Acetyl coA makes what?

A

Fatty acids
triglycerides
phospholipid
eicosanoids
CO2, H2O,ATP
Cholesterol–> steroid hormones
Ketone bodies

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12
Q

What is the structure of acetyl coA

A

1.Acetyl group
2.Coenzyme A
-Beta-mercaptoethylamine
-Pantothenic acid (not synthesized in man – an essential nutrient)
-Phosphate
-3’, 5’-adenosine diphosphate

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13
Q

What is the structure of fatty acid

A

A long hydrocarbon chain
A carboxylic acid group

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14
Q

What is the chain length and structure of fatty acids

A

Ranges from 4 to 30 carbons
Most common: 12-24 carbons
LINEAR
EVEN NUMBER OF CARBONS

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15
Q

What is one system of fatty acid classification

A

based on the number of double bonds

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16
Q

How many db are in saturated fatty acids

A

ZERO

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17
Q

What is an example of saturated fatty acid

A

Stearic acid

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18
Q

How many bonds are in monounsaturated fatty acids

A

ONE

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19
Q

what is an example of monounsaturated fatty acid

A

oleic acid

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20
Q

What does db in fatty acids cause and what is the result

A

db cause steric hinderance which affects the melting point

More dbs = lower melting point

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21
Q

The db in natural unsaturated fatty acids are in ____ configuration

A

CIS

22
Q

Fatty acids with ____ double bond are the most prevalent in the human body

A

one

23
Q

in saturated fatty acids, why is the melting point higher?

A

Hydrophobic interaction with packed tightly

Solid

24
Q

More double bonds=

A

lower melting point

25
Q

LISTEN TO LECTURE TO ADD QUESTION

A
26
Q

What are the five common fatty acids that we need to remember

A

palmitic acid
stearic acid
oleic acid
linoleic acid
linolenic acid

27
Q

For the five common fatty acids, list them with their carboxyl reference

A

palmitic acid—> 16:0
stearic acid—>18:0
oleic acid —> 18:1▵ 9
linoleic acid–> 18:2 ▵9, 12
linolenic acid–> 18:3 ▵9,12,15

28
Q

The first carbon numbers in the fatty acid is what?

A

The carboxyl carbon will always be one

29
Q

What is the carbon next to the the carboxyl carbon

A

alpha, then it goes to beta, gamma

30
Q

What is ALWAYS the last carbon, regardless of how many carbons we have

A

omega, ⍵

31
Q

Instead of starting with the carboxyl carbon for greek letters, what is the other way?

A

omega (⍵) subtracted by the number of carbons until we hit the db

Example: ⍵-3–> the db is 3 carbons from the end

32
Q

Where does fatty acid synthesis occurs primarily in ?

A

CYTOPLASM of these tissues:
-liver
-adipose (fat)
-central nervous system
-lactating mammary gland

33
Q

What are the major lipogenic tissues?

A

liver
adipose
CNS
lactating mammary gland

34
Q

What is the starting molecule of the de novo synthesis of fatty acids

A

glucose to pyruvate to then make acetyl coA

35
Q

What is the fatty acid created with the De Novo synthesis

A

palmitate (16:0)

36
Q

What is the process of glucose

A

Glucose is degraded to pyruvate by aerobic glycolysis in the cytoplasm.

Pyruvate is transported into mitochondria, where pyruvate dehydrogenase oxidatively decarboxylates pyruvate, forming acetyl CoA which can serve as a substrate for citrate synthesis.

Citrate transported out of the mitochondria to the cytoplasm (where fatty acid synthesis occurs), and split to generate acetyl CoA for fatty acid synthesis.

37
Q

what is another pathway that citrate can take besides fatty acid synthesis?

A

Citrate can be oxidized by TCA cycle in mitochondria to get energy

38
Q

What is the next step with acetyl CoA in fatty acid synthesis

A

Acetyl CoA + bicarbonate+ ATP with acetyl CoA carboxylase (biotin) to create malonyl CoA

39
Q

What is the RLS for de novo synthesis in fatty acid synthesis?

A

acetyl CoA carboxylase (biotin)

40
Q

What are the short term ways of regulating acetyl coA carboxylase?

A

Phosphorylation (inactive)
-mediated by AMP-dependent protein
-kinase and protein kinase A

Dephosphorylation (active)
-mediated by phosphoprotein phosphatase

Allosteric regulation
-citrate is a positive effector
-long chain fatty acids are negative effectors

41
Q

Increase insulin, decrease glycogen activates what

A

Phosphoprotein phosphatase

42
Q

decrease insulin, increase glycogen activates what

A

protein kinase A

43
Q

How do we long term regulate fatty acid synthesis in liver

A

Carbohydrate-responsive element binding protein (chREBP)

44
Q

What is Carbohydrate-responsive element binding protein (chREBP)

A

is a major glucose responsive transcription factor

45
Q

When is the expression of chREBP gene is induced in the liver?

A

in response to increased glucose uptake

46
Q

ChREBP acts _____ with ____

A

ChREBP acts synergistically with Sterol Response Element Binding Protein (SREBP)

47
Q

What happens when ChREBP acts synergistically with Sterol Response Element Binding Protein (SREBP)

A

to induce lipogenic genes such as acetyl CoA carboxylase and fatty acid synthase.

48
Q

What happens to ChREBP under low (basal) glucose concentration?

A

ChREBP is phosphorylated and resides in the cytosol.

49
Q

What happens to ChREBP when glucose concentration raise?

A

dephosphorylated and translocated to the nucleus where it binds to Carbohydrate Response Elements (ChoREs) to stimulate transcription of lipogenic genes

50
Q

Where does the dephosphorylated ChREBP translocate and cause?

A

translocated to the nucleus where it binds to Carbohydrate Response Elements (ChoREs)

stimulate transcription of lipogenic genes

51
Q

Besides ChREBP what also translocated to the nucleus

A

insulin, increases pSREBP-1c to bind to SRE for the stimulation of transcription of lipogenic genes

Biochem block 3 (6 decks)

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