Hepatic steatosis as a marker of metabolic dysfunction

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Standard

Hepatic steatosis as a marker of metabolic dysfunction. / Fabbrini, Elisa; Magkos, Faidon.

I: Nutrients, Bind 7, Nr. 6, 2015, s. 4995-5019.

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Harvard

Fabbrini, E & Magkos, F 2015, 'Hepatic steatosis as a marker of metabolic dysfunction', Nutrients, bind 7, nr. 6, s. 4995-5019. https://doi.org/10.3390/nu7064995

APA

Fabbrini, E., & Magkos, F. (2015). Hepatic steatosis as a marker of metabolic dysfunction. Nutrients, 7(6), 4995-5019. https://doi.org/10.3390/nu7064995

Vancouver

Fabbrini E, Magkos F. Hepatic steatosis as a marker of metabolic dysfunction. Nutrients. 2015;7(6):4995-5019. https://doi.org/10.3390/nu7064995

Author

Fabbrini, Elisa ; Magkos, Faidon. / Hepatic steatosis as a marker of metabolic dysfunction. I: Nutrients. 2015 ; Bind 7, Nr. 6. s. 4995-5019.

Bibtex

@article{aa119c4aac41432ea92e6702e7e9f65e,
title = "Hepatic steatosis as a marker of metabolic dysfunction",
abstract = "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. ",
keywords = "Blood Glucose/metabolism, Diabetes Mellitus, Type 2/complications, Fatty acid metabolism, Lipolysis, Insulin Resistance, Lipid Metabolism, Liver steatosis, Glucose metabolism, Non-alcoholic fatty liver disease (NAFLD)/steaotohepatitis (NASH), Obesity, Prevalence, Triglycerides/blood, NAFLD, VLDL secretion",
author = "Elisa Fabbrini and Faidon Magkos",
note = "(Ekstern)",
year = "2015",
doi = "10.3390/nu7064995",
language = "English",
volume = "7",
pages = "4995--5019",
journal = "Nutrients",
issn = "2072-6643",
publisher = "M D P I AG",
number = "6",

}

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