We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Non-Alcoholic Fatty Liver Disease: From Pathogenesis to Clinical Impact.
- Authors
Caturano, Alfredo; Acierno, Carlo; Nevola, Riccardo; Pafundi, Pia Clara; Galiero, Raffaele; Rinaldi, Luca; Salvatore, Teresa; Adinolfi, Luigi Elio; Sasso, Ferdinando Carlo
- Abstract
Non-Alcoholic Fatty Liver Disease (NAFLD) is caused by the accumulation of fat in over 5% of hepatocytes in the absence of alcohol consumption. NAFLD is considered the hepatic manifestation of metabolic syndrome (MS). Recently, an expert consensus suggested as more appropriate the term MAFLD (metabolic-associated fatty liver disease). Insulin resistance (IR) plays a key role in the development of NAFLD, as it causes an increase in hepatic lipogenesis and an inhibition of adipose tissue lipolysis. Beyond the imbalance of adipokine levels, the increase in the mass of visceral adipose tissue also determines an increase in free fatty acid (FFA) levels. In turn, an excess of FFA is able to determine IR through the inhibition of the post-receptor insulin signal. Adipocytes secrete chemokines, which are able to enroll macrophages inside the adipose tissue, responsible, in turn, for the increased levels of TNF-α. The latter, as well as resistin and other pro-inflammatory cytokines such as IL-6, enhances insulin resistance and correlates with endothelial dysfunction and an increased cardiovascular (CV) risk. In this review, the role of diet, intestinal microbiota, genetic and epigenetic factors, low-degree chronic systemic inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress on NAFLD have been addressed. Finally, the clinical impact of NAFLD on cardiovascular and renal outcomes, and its direct link with type 2 diabetes have been discussed.
- Subjects
NON-alcoholic fatty liver disease; LIPOLYSIS; SPLANCHNIC nerves; FREE fatty acids; TYPE 2 diabetes; ADIPOSE tissues; INSULIN resistance
- Publication
Processes, 2021, Vol 9, Issue 1, p135
- ISSN
2227-9717
- Publication type
Article
- DOI
10.3390/pr9010135