Steatosis and insulin resistance in hepatitis C: A way out for the virus?

Campo, J.A. Del; Romero‐Gómez, Manuel

doi:10.3748/wjg.15.5014

Cited by 64 publications

(63 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…HCV also directly provokes insulin resistance. In HCV infection, insulin resistance is more closely related to viral load than to obesity, supporting a direct effect of HCV on insulin metabolism [66] . In fact, diabetes is more frequently observed among HCV patients [67] .…”

Section: Insulin Resistancementioning

confidence: 95%

Liver steatosis in hepatitis C patients

González‐Reimers¹

2015

WJH

View full text Add to dashboard Cite

would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in "pure" steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients. Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory elementbinding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements. AbstractThere is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which REVIEWSubmit a

show abstract

Section: Insulin Resistancementioning

confidence: 95%

Liver steatosis in hepatitis C patients

González‐Reimers¹

2015

WJH

View full text Add to dashboard Cite

show abstract

“…Additionally, the presence of coexistent nonalcoholic steatohepatitis, the more aggressive form of NAFLD, is found in about 10% of liver biopsies from patients with CHC [42]. Viral and metabolic factors have been shown to contribute to the formation of steatosis in patients with CHC.…”

Section: Hcv and Hepatic Steatosismentioning

confidence: 98%

Metabolic Syndrome and HCV: Where Do We Stand in 2010?

Lamb

Harrison

2010

Curr Hepatitis Rep

View full text Add to dashboard Cite

Hepatitis C virus (HCV) infection and metabolic syndrome are common worldwide. Insulin resistance, an inherent part of metabolic syndrome, may result from HCV infection and has been shown to affect outcomes for chronic hepatitis C (CHC) virus infection. Various host and virally mediated factors contribute to insulin resistance and ultimately the metabolic syndrome. The metabolic derangements in combination with CHC virus affect disease natural history and treatment outcomes. The ideal treatment strategy for patients with features of metabolic syndrome and CHC virus infection is unknown, but most would agree to treat the components of the metabolic syndrome.

show abstract

“…Ponadto HOMA-IR był niezależ-nym czynnikiem progresji włóknienia w PZWC [13]. Stopień insulinooporności ściśle wiąże się z zasięgiem włóknienia i jego progresją [14][15][16]. Insulinooporność występowała głównie u pacjentów zakażonych genotypem 1 lub 4 i z wyższą wiremią [10,17,18].…”

Section: Wprowadzenieunclassified