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J Hepatol. 2006 Jan;44(1):190-6. Epub 2005 Jul 12.

Hepatic steatosis and insulin resistance: does etiology make a difference?

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  • 1Unità Operativa di Medicina Interna e Gastroenterologia, Nuovo Ospedale Civile-Estense, Via Giardini, Baggiovara, Modena 41100, Italy. a.lonardo@libero.it

Abstract

BACKGROUND/AIMS:

To ascertain whether the etiology of hepatic steatosis modulates insulin resistance (IR) and to determine the predictors of IR.

METHODS:

We studied IR through HOMA IR in 146 subjects, 99 of whom had ultrasonographic and/or histologic steatosis. Twenty-two had familial heterozygous hypobetalipoproteinemia (FHBL), 48 had non-alcoholic fatty liver disease (NAFLD), 34 HCV infection (17 with HCV1b, 17 with HCV3a) and 42 were healthy controls without steatosis.

RESULTS:

Steatosis was present in 77.3% of FHBL and, by enrolment criteria, in all NAFLD and HCV cases. Overall HOMA-IR correlated with BMI and GGT (P<0.01). FHBL and healthy groups had similar HOMA-IR and GGT values, whereas higher levels were observed in HCV and NAFLD. HCV3a and FHBL patients were hypolipidemic. HOMA-IR was similar in FHBL patients and controls and lower than in HCV and NAFLD. FHBL patients had a high extent of steatosis, similar to that observed in HCV3a, but lower grading and staging than NAFLD and HCV. At multivariate analysis, steatosis and GGT predicted HOMA-IR.

CONCLUSIONS:

Data suggest that not all hepatic fat associates with IR. FHBL patients, for some aspects, resemble HCV3a infection, possibly suggesting a shared steatogenic mechanism. Among steatotic patients serum GGT levels is the independent predictor of IR.

PMID:
16168516
[PubMed - indexed for MEDLINE]
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