Hepatic steatosis as a marker of metabolic dysfunction
Research output: Contribution to journal › Review › Research › peer-review
Standard
Hepatic steatosis as a marker of metabolic dysfunction. / Fabbrini, Elisa; Magkos, Faidon.
In: Nutrients, Vol. 7, No. 6, 2015, p. 4995-5019.Research output: Contribution to journal › Review › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Hepatic steatosis as a marker of metabolic dysfunction
AU - Fabbrini, Elisa
AU - Magkos, Faidon
N1 - (Ekstern)
PY - 2015
Y1 - 2015
N2 - Nonalcoholic fatty liver disease (NAFLD) is the liver manifestation of the complex metabolic derangements associated with obesity. NAFLD is characterized by excessive deposition of fat in the liver (steatosis) and develops when hepatic fatty acid availability from plasma and de novo synthesis exceeds hepatic fatty acid disposal by oxidation and triglyceride export. Hepatic steatosis is therefore the biochemical result of an imbalance between complex pathways of lipid metabolism, and is associated with an array of adverse changes in glucose, fatty acid, and lipoprotein metabolism across all tissues of the body. Intrahepatic triglyceride (IHTG) content is therefore a very good marker (and in some cases may be the cause) of the presence and the degree of multiple-organ metabolic dysfunction. These metabolic abnormalities are likely responsible for many cardiometabolic risk factors associated with NAFLD, such as insulin resistance, type 2 diabetes mellitus, and dyslipidemia. Understanding the factors involved in the pathogenesis and pathophysiology of NAFLD will lead to a better understanding of the mechanisms responsible for the metabolic complications of obesity, and hopefully to the discovery of novel effective treatments for their reversal.
AB - Nonalcoholic fatty liver disease (NAFLD) is the liver manifestation of the complex metabolic derangements associated with obesity. NAFLD is characterized by excessive deposition of fat in the liver (steatosis) and develops when hepatic fatty acid availability from plasma and de novo synthesis exceeds hepatic fatty acid disposal by oxidation and triglyceride export. Hepatic steatosis is therefore the biochemical result of an imbalance between complex pathways of lipid metabolism, and is associated with an array of adverse changes in glucose, fatty acid, and lipoprotein metabolism across all tissues of the body. Intrahepatic triglyceride (IHTG) content is therefore a very good marker (and in some cases may be the cause) of the presence and the degree of multiple-organ metabolic dysfunction. These metabolic abnormalities are likely responsible for many cardiometabolic risk factors associated with NAFLD, such as insulin resistance, type 2 diabetes mellitus, and dyslipidemia. Understanding the factors involved in the pathogenesis and pathophysiology of NAFLD will lead to a better understanding of the mechanisms responsible for the metabolic complications of obesity, and hopefully to the discovery of novel effective treatments for their reversal.
KW - Blood Glucose/metabolism
KW - Diabetes Mellitus, Type 2/complications
KW - Fatty acid metabolism
KW - Lipolysis
KW - Insulin Resistance
KW - Lipid Metabolism
KW - Liver steatosis
KW - Glucose metabolism
KW - Non-alcoholic fatty liver disease (NAFLD)/steaotohepatitis (NASH)
KW - Obesity
KW - Prevalence
KW - Triglycerides/blood
KW - NAFLD
KW - VLDL secretion
U2 - 10.3390/nu7064995
DO - 10.3390/nu7064995
M3 - Review
C2 - 26102213
VL - 7
SP - 4995
EP - 5019
JO - Nutrients
JF - Nutrients
SN - 2072-6643
IS - 6
ER -
ID: 289962150