Diagnosis of non-alcoholic fatty liver disease (NAFLD)

Yki‐Järvinen, Hannele

doi:10.1007/s00125-016-3944-1

Cited by 89 publications

(66 citation statements)

References 56 publications

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“…Several risk scores for NAFLD based on serum biomarkers, transient elastography and genetic analyses may help to improve diagnostic efficacy. In her review in this symposium series, Hannele Yki-Järvinen proposes a new pathogenic classification of NAFLD: the obese/metabolic, the genetic, and the 'double/triple trouble' forms, which would require different screening and follow-up procedures [6]. Indeed, the new EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease propose a step-wise diagnostic algorithm, which requires joint work-up by diabetologists and hepatologists [5].…”

Section: Nafld and Diabetes Mellitusmentioning

confidence: 99%

The liver in focus

Roden

2016

Diabetologia

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Section: Nafld and Diabetes Mellitusmentioning

confidence: 99%

The liver in focus

Roden

2016

Diabetologia

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“…Nonalcoholic fatty liver disease (NAFLD) is the most frequent chronic liver disease in developed countries and its increased prevalence parallels the rise in obesity, type 2 diabetes and metabolic syndrome in recent decades (Tuyama & Chang 2012, Yki-Jarvinen 2016. NAFLD encompasses hepatic steatosis driven by factors other than excessive alcohol consumption and is estimated to affect 25% of the global population (Zhu et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Hepatic lipid accumulation: cause and consequence of dysregulated glucoregulatory hormones

Geisler

Renquist

2017

Journal of Endocrinology

153

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Fatty liver can be diet, endocrine, drug, virus or genetically induced. Independent of cause, hepatic lipid accumulation promotes systemic metabolic dysfunction. By acting as peroxisome proliferator-activated receptor (PPAR) ligands, hepatic non-esterified fatty acids upregulate expression of gluconeogenic, beta-oxidative, lipogenic and ketogenic genes, promoting hyperglycemia, hyperlipidemia and ketosis. The typical hormonal environment in fatty liver disease consists of hyperinsulinemia, hyperglucagonemia, hypercortisolemia, growth hormone deficiency and elevated sympathetic tone. These endocrine and metabolic changes further encourage hepatic steatosis by regulating adipose tissue lipolysis, liver lipid uptake, de novo lipogenesis (DNL), beta-oxidation, ketogenesis and lipid export. Hepatic lipid accumulation may be induced by 4 separate mechanisms: (1) increased hepatic uptake of circulating fatty acids, (2) increased hepatic de novo fatty acid synthesis, (3) decreased hepatic beta-oxidation and (4) decreased hepatic lipid export. This review will discuss the hormonal regulation of each mechanism comparing multiple physiological models of hepatic lipid accumulation. Nonalcoholic fatty liver disease (NAFLD) is typified by increased hepatic lipid uptake, synthesis, oxidation and export. Chronic hepatic lipid signaling through PPARgamma results in gene expression changes that allow concurrent activity of DNL and beta-oxidation. The importance of hepatic steatosis in driving systemic metabolic dysfunction is highlighted by the common endocrine and metabolic disturbances across many conditions that result in fatty liver. Understanding the mechanisms underlying the metabolic dysfunction that develops as a consequence of hepatic lipid accumulation is critical to identifying points of intervention in this increasingly prevalent disease state.

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“…Non-alcoholic fatty liver disease is considered a benign disease, mostly related to the different clinical expression of IR, which ranges from altered lipid metabolism to MS and/or T2DM [8]. While simple steatosis can safely be considered a non-evolutive condition, steatohepatitis (NASH) should not be considered a benign disease because it may evolve into liver cirrhosis and/or HCC [2,16,19].…”

Section: Discussionmentioning

confidence: 99%

Liver biopsy in Type 2 Diabetes Mellitus: Steatohepatitis represents the sole feature of liver damage

Masarone

Rosato

Aglitti

et al. 2016

Digestive and Liver Disease

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Recent studies report a prevalence of non-alcoholic fatty liver disease (NAFLD) of between 70% and 80% in patients with metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Nevertheless, it is not possible to differentiate between simple steatosis and nonalcoholic steatohepatitis (NASH) with non-invasive tests. The aim of this study was to differentiate between simple steatosis and NASH by liver biopsy in patients with hypertransaminasemia and MS or T2DM. Two hundred and fifteen patients with increased ALT levels and MS, and 136 patients at their first diagnosis of T2DM regardless of ALT values were consecutively admitted to a tertiary hepatology center between January 2004 and November 2014. Exclusion criteria were other causes of liver disease/ALT increase. Each patient underwent a clinical, laboratory and ultrasound evaluation, and a liver biopsy. Gender distribution, age, and body mass index were similar in the two groups of patients, whereas cholesterol levels, glycemia and blood pressure were significantly different between the two groups. The prevalence of NAFLD was 94.82% in MS patients and 100% in T2DM patients. NASH was present in 58.52% of MS patients and 96.82% of T2DM. Consequently, this study reveals that, by using liver biopsy, almost all patients with T2DM or MS have NAFLD, which in patients with T2DM means NASH. Importantly, it suggests that NASH may be one of the early complications of T2DM due to its pathophysiological correlation with insulin resistance.

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Diagnosis of non-alcoholic fatty liver disease (NAFLD)

Abstract: Non-alcoholic fatty liver disease (NAFLD) in-

Cited by 89 publications

References 56 publications

The liver in focus

The liver in focus

Hepatic lipid accumulation: cause and consequence of dysregulated glucoregulatory hormones

Liver biopsy in Type 2 Diabetes Mellitus: Steatohepatitis represents the sole feature of liver damage

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