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Open AccessJournal ArticleDOI

Obesity and Nonalcoholic Fatty Liver Disease: Biochemical, Metabolic and Clinical Implications

Elisa Fabbrini, +2 more
- 01 Feb 2010 - 
- Vol. 51, Iss: 2, pp 679-689
TLDR
It is not clear whether NAFLD causes metabolic dysfunction or whether metabolic dysfunction is responsible for IHTG accumulation, or possibly both, but it is likely that abnormalities in fatty acid metabolism are key factors involved in the development of insulin resistance, dyslipidemia, and other cardiometabolic risk factors associated withNAFLD.
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This article is published in Hepatology.The article was published on 2010-02-01 and is currently open access. It has received 1668 citations till now. The article focuses on the topics: Nonalcoholic fatty liver disease & Fatty acid metabolism.

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2019 ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD

TL;DR: The second iteration of the European Society of Cardiology (ESC) and European Association for the Study of Diabetes (EASD) joining forces to write guidelines on the management of diabetes mellitus (DM), pre-diabetes, and cardiovascular disease (CVD), designed to assist clinicians and other healthcare workers to make evidence-based management decisions.
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Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis†

TL;DR: Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.
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Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis.

TL;DR: The evidence that suggests NAFLD is a multisystem disease and the factors that might determine interindividual variation in the development and progression of its major hepatic and extrahepatic manifestations are reviewed.
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The role of hepatic lipids in hepatic insulin resistance and type 2 diabetes

TL;DR: Therapeutic approaches based on a key role for hepatic diacylglycerol activation of protein kinase Cε in triggering hepatic insulin resistance could alleviate the related epidemics of non-alcoholic fatty liver disease and type 2 diabetes.
References
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Obesity is associated with macrophage accumulation in adipose tissue

TL;DR: Transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob) found that the expression of 1,304 transcripts correlated significantly with body mass.
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Inflammation and metabolic disorders

TL;DR: Dysfunction of the immune response and metabolic regulation interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease.
Journal ArticleDOI

Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes

TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).
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