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NUTR3360 > module 6 part 2 NAFLD > Flashcards

module 6 part 2 NAFLD Flashcards

1
Q

T/F: NAFLD is a broad term used to describe liver diseases caused by alcohol consumption

A

F; theyre NOT caused by it

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2
Q

T/F: NAFLD is not completely related/associated with obesity, IR, and T2D

A

False; strong association

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3
Q

4 stages of NAFLD:

A
  1. Steatosis: lipid accumulation in hepatocytes
  2. NASH: fat accumulation accompanied by inflammation/ballooning
  3. Cirrhosis: severe fibrosis of liver (scarring)
  4. HCC; liver cancer (hepatocellular carcinoma)
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4
Q

In what stage of NAFLD do you see symptoms such as inflammation/ballooning?
a) Steatosis
b) non-alcoholic steatohepatitis
c) cirrhosis
d) hepatocellular carcinoma (HCC)

A

b

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5
Q

In what stage of NAFLD do you see scarring?

A
  1. cirrhosis
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6
Q

Which stages of NAFLD are reversible?
a. steatosis
b. NASH
c. cirrhosis
d. HCC
e. a&c
f. just a
g. c& d
h. a&b
i. none of the abov

A

a & b

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7
Q

3 risk factors for NAFLD

A
  1. T2D/obesity
  2. age & biological sex: males middle aged, females post menopausal
  3. genetic variants: PNPLA3, TM6SF2
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8
Q

What does the inc in NAFLD in post-menopausal women suggest?

A

that estrogen may have a protective effect

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9
Q

Polymorphisms in two genes have been identified as potential modifiers of NAFLD progression, which 2?

A

PNPLA3
TM6SF2

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10
Q

Two hit hypothesis: most common theory about underlying mechanisms for NAFLD development

A

First Hit (between stage 1&2) — lipid accumulation in hepatocytes = inc vulnerability of liver to other damaging factors
Second Hit (between stage 2&3) — inflammation, oxidative stress, derives from progression of steatosis to NASH, if left untreated, NASH progress into more severe liver diseases

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11
Q

why does steatosis happen

A
  • imbalance in FFA levels due inc in hepatic FFA uptake and dec in FFA oxidation/VLDL export
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12
Q

What is the biggest contributor (60%) to steatosis
What is second (26%) and third (14%)

A

OVERALL IR and dysfunction adipose tissue: specifically:
circulating FFA 60%- from dysfunction adipose affecting liver fat bc of portal vein
de novo lipogensis 26%- hepatic insulin resistance increases this in liver
Dietary fat 14%

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13
Q

If an individual has hepatic insulin resistance, it means that they have
a) failed suppression of gluconeogenesis
b) suppressed ability to use dietary fats
c) suppressed de novo lipogenesis
d) continued activation of de novo lipogenesis
e) increased FFA and TAG accumulation in liver
f) 2 of the above
g) 3 of the above
h) none of the above
(SAY WHICH ONES)

A

g) 3 of above; a,d,e
- failed suppression of gluconeo
- continued activation of de novo
- inc FFA and TAG accumulation

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14
Q

What does failed suppression of gluconeogenesis pathway lead to?

A

increased gluconeogenesis, FFA and TAG

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15
Q

Adipose tissue insulin resistance causes
a) inc FFA release and TAG lipolysis
c) inc FFA release and dec TAG lipolysis
d) inc hepatic FFA uptake
e) Dec HSL activation, breaks down TAG into FFA
e) inc HSL activation

A

a, c, e

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16
Q

Is HSL suppressed or activated by insulin ?

A

suppressed

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17
Q

NASH:

A

FFA accumulation in liver —> lipotoxicity
—> inflammation, damage to mitochondria, inc oxidative stress

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18
Q

T/F: oxidative stress and inflammation further promote eachother

A

true

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19
Q

Why does dysfunctional adipose tissue promote liver inflammation?

A

release large amounts of proinflammatory cytokines (IL1, IL6, TNF-alpha)

20
Q

Why does the western diet contribute to NAFLD development?

A

high fat/sugar/carb/fructose/cholesterol= obesity= dysfunctional adipose
low fibre/antioxidants/omega3 fats

21
Q

Saturated FA’s tend to be incorporated into _____, which contribute to _____, while MUFA and PUFA tend to be incorporated into _____, which is more stable and less toxic

A

ceramides
lipotoxicity
TAG

22
Q

High saturated fat induces inflammation and oxidative stress by activating _____
a) ChREBP
b) TNFalpha
c) IL-6
d) NF kB
e) SREBP1c

A

d) NF kB

23
Q

High dietary sugars and carbs promote lipogenesis by activating
a) NF-kB
b) TNFalpha
c) IL-6
d) ChREBP
e) SREBP1c

A

d) ChREBP

24
Q

How do fructose levels contribute to NAFLD development?

A
  • most potent promoter of NAFLD
  • strongly promotes hepatic de novo lipogenesis
  • broken down into pyruvate more quickly than glucose because the rate-limiting step of glycolysis is bypassed
25
Q

Where is glucose metabolized? where is fructose?

A

widely in body
almost entirely in liver

26
Q

T/F unregulated metabolism of fructose leads to less acetyl coA production, which promotes DNL.

A

false
it leads to EXCESS

27
Q

T/F fructose induces DNL by INC ChREBP gene expression and promoting SREBP1c activity in liver

A

true

28
Q

What are the two key transcription factors controlling DNL

A

ChREBP and SREBP1c

29
Q

Which generates more ROS ? glucose or fructose

A

fructose by 100x

30
Q

An excess of fructose causes:
a) hepatic phosphate deficiency, dec uric acid synthesis, dec production of ROS
b) hepatic phosphate deficiency, inc uric acid synthesis, inc production of ROS
c) oxidative stress, dec uric acid synthesis, inc production of ROS
d) dec ChREBP expression and SREBP1c activity in liver

A

b) hepatic phosphate deficiency, inc uric acid, inc ROS

31
Q

Western diet and NAFLD summary

A

Diets high in fructose and saturated fat promote the “two hits” required to promote the development of NAFLD

32
Q

PNPLA3 as a potential modifier of NAFLD

A

greater NAFLD risk
involved in energy mobilization and storage in lipid droplets
greater severity of symptoms of stages
greater response to an intervention

33
Q

T/F; TM6SF2 E167K was independently associated with histological severity of steatosis and liver damage independent of age sex BMI diabetes or PNPLA3

A

true

34
Q

Is NAFLD more commonly undiagnosed in early or late stages?

A

early- it is asymptomatic until severe

35
Q

What is a limitation in the diagnosis of NAFLD?

A
  • non-invasive diagnostic methods lack sensitivity and accuracy
    i.e
    ultrasound:
  • steatosis = >5% liver fat, ultrasound only sensitive to >12.5%
  • doesnt detect inflammation/fibrosis
    Serum biomarkers:
  • ALT & AST can tell you its unhealthy but not the cause
    Proton magnetic resonance spectrometry:
  • provides quantitative estimate of liver fat but is expensive and not common in clinical setting
36
Q

why can we not use ultrasounds to detect NAFLD in early stages?
a) shows ALT & AST levels which only tell you its unhealthy
b) expensive
c) doesnt measure liver fat accumulation
d) only sensitive to very high levels of liver fat
e) doesnt detect inflammation/fibrosis
f) only shows liver scarring

A

d & e

37
Q

What is the gold standard method to diagnose NASH?

A

liver biopsy

38
Q

What is the curative treatment for NAFLD currently? at what stage would we do this?

A

liver transplantation, in cirrhosis and HCC (stages 3&4)

39
Q

What are some methods used to treat NAFLD?

A
  • insulin sensitizers
  • bile acid modulation
  • vitamin E
40
Q

Can vitamin E be used to treat NAFLD in patients with T2D?

A

no

41
Q

t/f: FXR agonists improve metabolic homeostasis and reduces hepatic inflammation

A

true

42
Q

in obese individuals with NAFLD, a 7-10% weight loss is the target of most lifestyle interventions and results in improvement of:

A

serum biomarkers and liver histology

43
Q

Can exercise decrease hepatic fat content without weight loss?

A

yes, has direct effect on liver health

44
Q

What diet style can slow NAFLD progresssion from mild to moderate?

A

intermittent fasting

45
Q

WHat effect did an omega 3 PUFA-enriched diet have?

A

decreased severity of NASH by:
- suppressing lipogenic gene expression
- inhibiting SREBP1 and ChREBP
- activate PPAR alpha- inc expression of enzymes involved in fat oxidation
- strong anti inflammatory properties

46
Q
A

NUTR3360 (6 decks)

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