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NUTR 301 > Lipids 7: Essential Fatty Acids I > Flashcards

Lipids 7: Essential Fatty Acids I Flashcards

1
Q

Major functions of lipids

A
  • barriers
  • membranes
  • structural components
  • lubricate surfaces
  • act as signaling molecules
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2
Q

major function of linoleic acid

A

structural integrity and barrier function in skin ceramides
* If deficient get flaky skin and barrier breaks down so immune function decreases allowing entrance of pathogens

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3
Q

Major function of DHA

A

makes up a large portion of the myelin sheath (70-85% lipid) which is an ‘extended and modified plasma membrane’ that helps with insulation in nerve conduction

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4
Q

Functions of ecosanoids

A

EFAs are precursors for ecosanoids which have essential roles in processes such as inflammation, reproduction, gastric secretion, blood pressure

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4
Q

What are the major function categories od PUFAs?

A

1) Synthesis of lipid biomediators
2) Production of membrane phospholipids which had structural (fluidity) and signal transduction properties

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5
Q

Definition of essential fatty acids

A
  1. Fatty acids that must be consumed in our diet
  2. Cannot be synthesized in the body or in sufficent quantities
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6
Q

What are the 2 essential fatty acids? (name and notations)

A
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7
Q

What are common conditionally essential fatty acids?

A

body can synthesize from LA and ALA but in limitied quantities and need to consume when demand is high (fetal development and infants)

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8
Q

Full name and notation
* ALA
* EPA
* DHA
* LA
* AA

A
  • ALA - a-linolenic acid (18:3n-3)
  • EPA - eicosapentaenoic acid (20:5n-3)
  • DHA - Docosahexaenoic acid (22:6n-3)
  • LA - Linoleic acid (18:2n-6)
  • AA - Arachidonic acid (20:4n-6)
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9
Q

typical sources of ALA

A

flaxseed oil, canola oil, soybean oil, walnuts, hemp, chia

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10
Q

typical sources of EPA and DHA

A

fish especially oily fish (salmon, herring, anchovy, smelt and mackeral)

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11
Q

typical source of LA

A

vegetable oils

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12
Q

Typical sources of AA

A

animal fats, liver, egg lipids, fish

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13
Q

How do FAs differ between plants and animals

A

Shorter chains are plant sources and as they get longer become animal because they elongate and desaturate especially marine source. In ocean can get cold so colder the ocean the more of the longer to keep their membranes fluid and prevent freezing

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14
Q

Sources of SFA & MUFAs

A
  • diet
  • DNL
  • elongation and/ or desaturation of exongenous
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15
Q

sources of 18 C PUFAs

A

ALA and LA ONLY diet

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16
Q

source of LC-PUFAs

A
  • diet
  • elongation &/ or desaturation reactions of ALA/ LA
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17
Q

Enzymes involved in elongation (elongases) & desaturation (desaturases) have:

A
  • Substrate specificity
  • Tissue specific distribution
  • Regulation/modulation depending on a number of factors (e.g. diet, hormones, development, chronic disease)
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18
Q

What are the 2 pathways for LC-PUFA synthesis and metabolism?

A

n-6 fatty acids via LA & n-3 fatty acids via ALA
* pathways use the same enzymes but they are distinct and do not crossover so there is competition for the enzymes

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19
Q

How much of ALA can be converted to EPA and DHA?

A

higher in women due to reproduction

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20
Q

What ecosanoids come from AA?

A
21
Q

What ecosanoids come from EPA?

A
22
Q

What ecosanoids come from DHA?

A
  • docosatrienes
  • resolvins
  • neuroprotectins
23
Q

What is EFA deficiency usually a result of?

A

Usually due to dietary deficiency of LA but pretty rare (3-5g/d prevents deficiency)

24
Q

Who is at risk of LA deficiency?

A
  • infants fed low fat diets
  • preterm babies
  • patients unable to eat (cancer, injury, major surgery with EFA-free TPN for extended periods)
25
Q

clinical symptoms with LA deficiency

A
  • Scaly dermatitis (↑ permeability to water & sebum production)
  • Failure to grow in children
  • Suppressed immune function
  • Impaired reproduction
  • Degeneration/impaired organ function
26
Q

Clinical symptoms of n-3 deficiency

A
  • decreased visual acuity
  • peripheral neuropathy
27
Q

What happens with n-3 EFA deficiency?

A

the n-6 series gets upregulated

28
Q

What happens with both n-3 and n-6 EFA deficiency?

A

The n-9 series can compensate for n-6s but n-3s resulting in ↑ **triene:tetraene **
* oleic acid forms mead acid and if elevated indicates EFA deficiency

29
Q

DHA in normal development: last trimester to 18 months

A

DHA accumulates in neural tissues at a high rate

30
Q

DHA in normal development: prenatal

A

FAs are transferred through the placenta from maternal blood (from diet/ adipose tissue) via passive diffusion. High accretion rate results in “preferential” transfer of LC-PUFAs to the fetus

31
Q

DHA in normal development: postnatal

A

Human breast milk contains DHA, but adipose tissue provides both an E source (for rapidly growing grey matter) & greater [DHA]/ body wt than any other time in life

32
Q

Why are preterm infants at risk of EFA deficiency?

A

Do not have the proper stores yet accumulated

33
Q

Where do LC-PUFAs originate from?

A

majority originate from diet or liver synthesis

34
Q

Where do most LC-PUFAs go in the body?

A

transported in blood, enter brain by diffusion, highly conserved (low turnover)

35
Q

What LC-PUFA is the major component of the brain?

A

DHA is major component of cerebrum & myelin \ sheath & retinal photoreceptor membranes and is critical to proper function
* DHA&raquo_space;> EPA in brain tissue
* Balance of DHA & AA required for normal function

36
Q

How do infants get DHA?

A

INfants need preformed DHA to meet demand which typically comes from breast milk

37
Q

What is DHA replaced with in n-3 deficient?

A

DHA replaced by DPA (22:5n-6)
* changes retinal physiology, visual acuity, learning ability (difficult to detect ∴ measure)

38
Q

What is the fatty acid composition of human milk?

A

make up ~50% of energy but also the most variable macronutrient of human milk as it depends a lot on the moms diet

39
Q

What are the sources of fatty acids in human milk

A
  • maternal body stores (fat deposits from which the fatty acids are released)
  • endogenous synthesis (mammary gland)
  • uptake from maternal plasma
  • mothers diet
40
Q

What are the variations that can be seen with proportions of fatty acids?

A
  • ~25 to 40 fold variation in EPA and DHA
  • ~4 to 6 fold variation in n-6 and n-3 PUFAs
  • ~2 fold for MUFAs & SFAs
41
Q

What does variation of fatty acids in human milk depend on?

A
  • maternal diet
  • genetics (FADS1 &2 polymorphisms)
  • lactation stage
  • maternal and infant health status
42
Q

Major functions of n-6 FAs

A
  • AA is a major substrate for eicosanoid synthesis
  • AA is a major subsrate for signal transduction via phosphatidylinositols
  • LA important for skin ceramides
  • n-6 are ligands for transcription factors so can turn specific genes on and off involved in metabolism
43
Q

How do LC-PUFAs effect gene expression?

A

By binding to transcription factors, main effects via activity of 3 major classes of transcription factors:
* PPARs
* liver X receptor (LXR)
* sterol regulatory element binding protein (SREBP)

44
Q

Regulation of SREBP gene expression by PUFAs

A
  • SREBP inhibited from transport to nucleus by PUFAs
  • transcription & SREBP1c mRNA stability regulated by n-3 FAs
45
Q

Regulation of pro-inflammatory cytokines by PUFAs

A

EPA/DHA decrease gene expression (mRNA) levels of pro- inflammatory cytokines
* i.e. TNF-α, IL-1, IL-6

46
Q

Other gene expression regulations by highly unsaturated EFAs

A

genes that control:
* FA synthesis
* mitochondrial & peroxisomal FA oxidation
* SFA desaturation
* synthesis of FABPs
* insulin-mediated glucose utilization

47
Q

biological effects of n-3 FAs

A
  • EPA is the major n-3 precursor for eicosanoids - antithrombatic and anti-inflammatory via competitive inhibition of AA metabolism
  • Oxygenated derivatives of EPA and DHA have potent anti-inflammatory + pro-resolution effects (help with healing)
  • n-3 FAs can upregulate and downregulate the expression of different proteins
48
Q

What is the hypotriglyceridemic effect of EPA (fish oil)?

A

Results in ↓ production and ↑clearance of VLDL-TG from the blood in the fasted state mostly due to:
* ↑ FA uptake in adipose, heart, skeletal muscle
* ↑ β-oxidation of FA and ↓ DNL so ↓availability of FA in the liver for VLDL-TG production
* ↓ lipolysis from adipocytes (↓HSL, ↑LPL) partly by ↓adipose tissue inflammation so ↓plasma FFAs

Also ↓ production + ↑ clearance of CMs in fed state

49
Q

Role of Vascepa

A

icosapent ethyl (EPA ethyl ester) used to reduce plasma TG levels, as an adjunct to:
* Statin therapy in high risk or existing CVD patients with elevated TG (≥1.7 mmol/L)
* Diet in patients with severe hypertriglyceridemia (≥5.6 mmol/L)

NUTR 301 (32 decks)

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