The Role of Insulin Resistance and Diabetes in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) consists of the entire spectrum of fatty liver disease in patients without significant alcohol consumption, ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) to cirrhosis, with NASH recently shown as an important cause of hep...

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Bibliographic Details
Published in:International journal of molecular sciences 2020-05, Vol.21 (11), p.3863
Main Authors: Fujii, Hideki, Kawada, Norifumi, Japan Study Group Of Nafld Jsg-Nafld
Format: Article
Language:English
Subjects:
Animals
Biopsy
Cell activation
Cirrhosis
Cytokines
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus - epidemiology
Diabetes Mellitus - genetics
Diabetes Mellitus - metabolism
Energy metabolism
Extracellular matrix
Fatty liver
Fibrosis
Genetic factors
Glucose
hepatic fibrosis
Hepatocellular carcinoma
Humans
Hyperglycemia
Immune system
Inflammation
Insulin
Insulin Resistance
Kinases
Liver
Liver cancer
Liver cirrhosis
Liver diseases
Metabolism
Molecular modelling
Mortality
Non-alcoholic Fatty Liver Disease - epidemiology
Non-alcoholic Fatty Liver Disease - genetics
Non-alcoholic Fatty Liver Disease - metabolism
Obesity
Proteins
Review
Steatosis
stellate cell
Tumor necrosis factor-TNF
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Summary:Nonalcoholic fatty liver disease (NAFLD) consists of the entire spectrum of fatty liver disease in patients without significant alcohol consumption, ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) to cirrhosis, with NASH recently shown as an important cause of hepatocellular carcinoma (HCC). There is a close relationship between insulin resistance (IR) and NAFLD, with a five-fold higher prevalence of NAFLD in patients with type 2 diabetes (T2DM) compared to that in patients without T2DM. IR is involved in the progression of disease conditions such as steatosis and NASH, as well as hepatic fibrosis progression. The mechanisms underlying these processes involve genetic factors, hepatic fat accumulation, alterations in energy metabolism, and inflammatory signals derived from various cell types including immune cells. In NASH-associated fibrosis, the principal cell type responsible for extracellular matrix production is the hepatic stellate cell (HSC). HSC activation by IR involves "direct" and "indirect" pathways. This review will describe the molecular mechanisms of inflammation and hepatic fibrosis in IR, the relationship between T2DM and hepatic fibrosis, and the relationship between T2DM and HCC in patients with NAFLD.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21113863