Pregled bibliografske jedinice broj: 771355
Non-alcoholic fatty liver disease and obesity : Biochemical, metabolic and clinical presentations
Non-alcoholic fatty liver disease and obesity : Biochemical, metabolic and clinical presentations // World journal of gastroenterology, 20 (2014), 28; 9330-9337 doi:10.3748/wjg.v20.i28.9330 (međunarodna recenzija, pregledni rad, znanstveni)
CROSBI ID: 771355 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Non-alcoholic fatty liver disease and obesity : Biochemical, metabolic and clinical presentations
Autori
Milić, Sandra ; Lulić, Davorka ; Štimac, Davor
Izvornik
World journal of gastroenterology (1007-9327) 20
(2014), 28;
9330-9337
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, pregledni rad, znanstveni
Ključne riječi
Fatty liver; Insulin resistance; Intra-abdominal fat; Metabolism; Non-alcoholic fatty liver disease; Obesity
Sažetak
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Presentation of the disease ranges from simple steatosis to non-alcoholic steatohepatitis (NASH). NAFLD is a hepatic manifestation of metabolic syndrome that includes central abdominal obesity along with other components. Up to 80% of patients with NAFLD are obese, defined as a body mass index (BMI) > 30 kg/m2. However, the distribution of fat tissue plays a greater role in insulin resistance than the BMI. The large amount of visceral adipose tissue (VAT) in morbidly obese (BMI > 40 kg/m2) individuals contributes to a high prevalence of NAFLD. Free fatty acids derived from VAT tissue, as well as from dietary sources and de novo lipogenesis, are released to the portal venous system. Excess free fatty acids and chronic low- grade inflammation from VAT are considered to be two of the most important factors contributing to liver injury progression in NAFLD. In addition, secretion of adipokines from VAT as well as lipid accumulation in the liver further promotes inflammation through nuclear factor kappa B signaling pathways, which are also activated by free fatty acids, and contribute to insulin resistance. Most NAFLD patients are asymptomatic on clinical presentation, even though some may present with fatigue, dyspepsia, dull pain in the liver and hepatosplenomegaly. Treatment for NAFLD and NASH involves weight reduction through lifestyle modifications, anti-obesity medication and bariatric surgery. This article reviews the available information on the biochemical and metabolic phenotypes associated with obesity and fatty liver disease. The relative contribution of visceral and liver fat to insulin resistance is discussed, and recommendations for clinical evaluation of affected individuals is provided.
Izvorni jezik
Engleski
Znanstvena područja
Kliničke medicinske znanosti
POVEZANOST RADA
Ustanove:
Klinički bolnički centar Rijeka
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE