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Open AccessJournal ArticleDOI

Nonalcoholic steatohepatitis, insulin resistance, and metabolic syndrome: Further evidence for an etiologic association

TLDR
Hyperinsulinemia and insulin resistance occur frequently in patients with NASH; these conditions do not stem from a reduced hepatic insulin extraction but from an enhanced pancreatic insulin secretion compensatory to reduced insulin sensitivity.
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This article is published in Hepatology.The article was published on 2002-02-01 and is currently open access. It has received 735 citations till now. The article focuses on the topics: Insulin resistance & Metabolic syndrome.

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Citations
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Nonalcoholic fatty liver disease: From steatosis to cirrhosis

TL;DR: The present “gold standard” management of NASH is modest weight reduction, particularly correction of central obesity achieved by combining dietary measures with increased physical activity, which improves insulin resistance and reverses steatosis, hepatocellular injury, inflammation, and fibrosis.
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Nonalcoholic steatohepatitis: Summary of an AASLD Single Topic Conference

TL;DR: The research agenda for the future includes establishing the role of insulin resistance and abnormal lipoprotein metabolism in NASH, determining the pathogenesis of cellular injury, defining predisposing genetic abnormalities, identifying better noninvasive predictors of disease, and defining effective therapy.
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The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD)

TL;DR: The 'two-hit' hypothesis is now obsolete, as it is inadequate to explain the several molecular and metabolic changes that take place in NAFLD, and the "multiple hit" hypothesis considers multiple insults acting together on genetically predisposed subjects to induceNAFLD and provides a more accurate explanation of NAFLd pathogenesis.
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Nonalcoholic fatty liver disease and hepatocellular carcinoma: a weighty connection.

TL;DR: Multiple case reports and case reviews of HCC in the setting of NASH support the associations of diabetes and obesity with the risk of H CC, as well as suggest age and advanced fibrosis as significant risks.
Journal ArticleDOI

Prevalence of and risk factors for nonalcoholic fatty liver disease: The Dionysos nutrition and liver study†‡

TL;DR: NAFLD is highly prevalent in the general population, is not associated with SLD, but is associated with many features of the metabolic syndrome.
References
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Journal ArticleDOI

Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation.

TL;DR: A WHO Consultation has taken place in parallel with a report by an American Diabetes Association Expert Committee to re‐examine diagnostic criteria and classification of diabetes mellitus and is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
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Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity.

TL;DR: The outcome of cirrhosis and liver-related death is not uniform across the spectrum of nonalcoholic fatty liver, and poor outcomes are more frequent in patients in whom biopsies show ballooning degeneration and Mallory hyaline or fibrosis.
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Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR)

TL;DR: The basic premise for the de®nition is that the metabolic syndrome is a syndrome of mild anomalies which, in combination, increase cardiovascular risk and because the syndrome includes nonmetabolic features, a more appropriate name would be the `insulin resistance syndrome'.
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Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose.

TL;DR: The feasibility of the minimal model technique to determine the etiology of impaired glucose tolerance is demonstrated and it is demonstrated that subjects (regardless of weight) could be segregated into good and lower tolerance by the product of second-phase beta-cell responsivity and insulin sensitivity.
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