Nutrition module 7- non alcoholic fatty
liver disease Final Exam And Accurate
Answers.
Non-alcholic fatty liver disease (NAFLD) - Answer broad term to describe liver diseases that
aren't caused by excessive alcohol consumption
T/F: NAFLD is strongly associated with features of the metabolic syndrome (obesity, T2D, IR) -
Answer true
4 stages of NAFLD - Answer 1. steatosis; liver accumulation in hepatocytes
2. non alcoholic steastohepatits (NASH); fat accumulation is accompanied by inflammation and/
or ballooning
3. cirrohsis; severe fibrosis (scaring ) of the live r
4. hepatocellular carcinoma (HCC) liver cancer
how long does it take NAFLD to progress? - Answer depends on the individual could take many
years 15-20 before becoming cancer
what are the reversible and irreversible stages of NAFLD? - Answer reversible- steatosis and
NASH
irreversible- chirrhosis and HCC
what are the 3 risk factors for NAFLD? - Answer 1. T2D and obesity
2. age and biological sex
-NAFLD occurs more in males, middle aged men and elderly post menopausal women (estrogen
is protective)
3. polymorphisms in PNPLA3 and TM6SF2,
what is the 2 hit hypothesis for NAFLD developement? - Answer hit 1: lipid accumulation in
hepatocytes, increases vulnerability of the liver to other damaging factors
hit 2: inflammation, oxidative stress --> drives the progression from steatosis to NASH
, what are the 3 main sources of hepatic FFA contributing to steatosis? - Answer 1. circulating
FFA (60)
-most come from dysfunctional adipose tissue
-vsiceral aipose affects liver fat accumulation more bc its linked to portal vein
2 de novo lipogeneis (26%)
-hepatic IR increases lipogeneis in the liver
3. dietary fat (14%)
-not the main issue
what are the 2 major contributers to steatosis? - Answer insulin resistance and dysfunctional
adipose tissues
what is the insulin pathway for a healthy liver? - Answer insulin--> Insulin receptor
-increases FOX01 phospohrylation (when phosphorylated it can't go into nucleus)--> decrease
G6Pase--> decrease gluconeogensis
insulin--> IR-->activates LXRa--> increase SREBP1c activation--> increases de novo lipogenesis
how does the insulin pathway work in an insulin resistant liver? - Answer insulin fails to
supress gluconeogensis but contineus to activate de novo lipogensis pathways leading to an
increase in FFA and TAG accumulation in the liver
how is dysfunctional adipose tissue related to steatosis? - Answer 1. adipose tissue IR causes
increase in FFA/ NEFA release leading to increase hepatic FFA uptake
2. IR in adipose tissue is associated with an increase in TAG lipolysis which is catalyzed by
Hormone sensitive lipase HSL
-HSL breaks down TAG--> FFA and is supressed by insulin so when the adipose is insulin ressitant
HSL is always on
how is steatosis converted to NASH? - Answer -FFA accumulation in the liver lead to
lipotoxicity--> induces inflammation --> NASH
lipotoxicity--> damages mitochondria--> increase oxidative stress--> oxidative stress and
inflammation further promote eachtoher
2. dysfunctional adipose tissue also releases large amounts of pro inflammatory cytokines that
promote inflammation in the liver (IL-1, IL-6, TNFa)
liver disease Final Exam And Accurate
Answers.
Non-alcholic fatty liver disease (NAFLD) - Answer broad term to describe liver diseases that
aren't caused by excessive alcohol consumption
T/F: NAFLD is strongly associated with features of the metabolic syndrome (obesity, T2D, IR) -
Answer true
4 stages of NAFLD - Answer 1. steatosis; liver accumulation in hepatocytes
2. non alcoholic steastohepatits (NASH); fat accumulation is accompanied by inflammation and/
or ballooning
3. cirrohsis; severe fibrosis (scaring ) of the live r
4. hepatocellular carcinoma (HCC) liver cancer
how long does it take NAFLD to progress? - Answer depends on the individual could take many
years 15-20 before becoming cancer
what are the reversible and irreversible stages of NAFLD? - Answer reversible- steatosis and
NASH
irreversible- chirrhosis and HCC
what are the 3 risk factors for NAFLD? - Answer 1. T2D and obesity
2. age and biological sex
-NAFLD occurs more in males, middle aged men and elderly post menopausal women (estrogen
is protective)
3. polymorphisms in PNPLA3 and TM6SF2,
what is the 2 hit hypothesis for NAFLD developement? - Answer hit 1: lipid accumulation in
hepatocytes, increases vulnerability of the liver to other damaging factors
hit 2: inflammation, oxidative stress --> drives the progression from steatosis to NASH
, what are the 3 main sources of hepatic FFA contributing to steatosis? - Answer 1. circulating
FFA (60)
-most come from dysfunctional adipose tissue
-vsiceral aipose affects liver fat accumulation more bc its linked to portal vein
2 de novo lipogeneis (26%)
-hepatic IR increases lipogeneis in the liver
3. dietary fat (14%)
-not the main issue
what are the 2 major contributers to steatosis? - Answer insulin resistance and dysfunctional
adipose tissues
what is the insulin pathway for a healthy liver? - Answer insulin--> Insulin receptor
-increases FOX01 phospohrylation (when phosphorylated it can't go into nucleus)--> decrease
G6Pase--> decrease gluconeogensis
insulin--> IR-->activates LXRa--> increase SREBP1c activation--> increases de novo lipogenesis
how does the insulin pathway work in an insulin resistant liver? - Answer insulin fails to
supress gluconeogensis but contineus to activate de novo lipogensis pathways leading to an
increase in FFA and TAG accumulation in the liver
how is dysfunctional adipose tissue related to steatosis? - Answer 1. adipose tissue IR causes
increase in FFA/ NEFA release leading to increase hepatic FFA uptake
2. IR in adipose tissue is associated with an increase in TAG lipolysis which is catalyzed by
Hormone sensitive lipase HSL
-HSL breaks down TAG--> FFA and is supressed by insulin so when the adipose is insulin ressitant
HSL is always on
how is steatosis converted to NASH? - Answer -FFA accumulation in the liver lead to
lipotoxicity--> induces inflammation --> NASH
lipotoxicity--> damages mitochondria--> increase oxidative stress--> oxidative stress and
inflammation further promote eachtoher
2. dysfunctional adipose tissue also releases large amounts of pro inflammatory cytokines that
promote inflammation in the liver (IL-1, IL-6, TNFa)
