TY - JOUR
T1 - Mechanisms of non-Alcoholic fatty liver disease development in normal-weight individuals
AU - Muriel, Pablo
AU - Cardoso-Lezama, Irina
AU - Vargas-Pozada, Eduardo E.
AU - Ramos-Tovar, Erika
N1 - Publisher Copyright:
© 2023 Lippincott Williams and Wilkins. All rights reserved.
PY - 2023/5/1
Y1 - 2023/5/1
N2 - While non-Alcoholic fatty liver disease (NAFLD) without inflammation or fibrosis is considered a relatively 'benign' disease, non-Alcoholic steatohepatitis (NASH), by contrast, is characterized by marked inflammation in addition to lipid accumulation, and may include fibrosis, progression to cirrhosis and hepatocellular carcinoma. Obesity and type II diabetes are frequently associated with NAFLD/NASH; however, a significant number of lean individuals may develop these diseases. Little attention has been paid to the causes and mechanisms contributing to NAFLD development in normal-weight individuals. One of the main causes of NAFLD in normal-weight individuals is the accumulation of visceral and muscular fat and its interaction with the liver. Myosteatosis (triglyceride accumulation in the muscle) induces a loss of muscle by reducing blood flow and insulin diffusion, contributing to NAFLD. Normal-weight patients with NAFLD exhibit higher serum markers of liver damage and C-reactive protein levels, as well as more pronounced insulin resistance, compared to healthy controls. Notably, increased levels of C-reactive protein and insulin resistance are strongly correlated with the risk of developing NAFLD/NASH. Gut dysbiosis has also been associated with NAFLD/NASH progression in normal-weight individuals. More investigation is required to elucidate the mechanisms leading to NAFLD in normal-weight individuals.
AB - While non-Alcoholic fatty liver disease (NAFLD) without inflammation or fibrosis is considered a relatively 'benign' disease, non-Alcoholic steatohepatitis (NASH), by contrast, is characterized by marked inflammation in addition to lipid accumulation, and may include fibrosis, progression to cirrhosis and hepatocellular carcinoma. Obesity and type II diabetes are frequently associated with NAFLD/NASH; however, a significant number of lean individuals may develop these diseases. Little attention has been paid to the causes and mechanisms contributing to NAFLD development in normal-weight individuals. One of the main causes of NAFLD in normal-weight individuals is the accumulation of visceral and muscular fat and its interaction with the liver. Myosteatosis (triglyceride accumulation in the muscle) induces a loss of muscle by reducing blood flow and insulin diffusion, contributing to NAFLD. Normal-weight patients with NAFLD exhibit higher serum markers of liver damage and C-reactive protein levels, as well as more pronounced insulin resistance, compared to healthy controls. Notably, increased levels of C-reactive protein and insulin resistance are strongly correlated with the risk of developing NAFLD/NASH. Gut dysbiosis has also been associated with NAFLD/NASH progression in normal-weight individuals. More investigation is required to elucidate the mechanisms leading to NAFLD in normal-weight individuals.
KW - adipose tissue
KW - inflammation
KW - liver
KW - normal weight
UR - http://www.scopus.com/inward/record.url?scp=85158847411&partnerID=8YFLogxK
U2 - 10.1097/MEG.0000000000002530
DO - 10.1097/MEG.0000000000002530
M3 - Artículo de revisión
C2 - 36966767
AN - SCOPUS:85158847411
SN - 0954-691X
VL - 35
SP - 521
EP - 529
JO - European Journal of Gastroenterology and Hepatology
JF - European Journal of Gastroenterology and Hepatology
IS - 5
ER -