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Am J Gastroenterol. 2017 Jan;112(1):102-110. doi: 10.1038/ajg.2016.318. Epub 2016 Aug 16.

Clinical and Metabolic Characterization of Lean Caucasian Subjects With Non-alcoholic Fatty Liver.

Author information

1
First Department of Medicine, Paracelsus Medical University, Salzburg, Austria.
2
Obesity Research Unit, Paracelsus Medical University, Salzburg, Austria.
3
Department of Laboratory Medicine, Paracelsus Medical University Salzburg, Salzburg, Austria.
4
Department of Internal Medicine, Hospital Oberndorf, Austria.
5
Hepatology Unit, Clinic Beau-Site, Bern and Department of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
6
Department of Pharmacology and Toxicology, Paracelsus Medical University Salzburg, Salzburg, Austria.

Abstract

OBJECTIVES:

Non-alcoholic fatty liver disease (NAFLD) is closely linked to obesity; however, 5-8% of lean subjects also have evidence of NAFLD. We aimed to investigate clinical, genetic, metabolic and lifestyle characteristics in lean Caucasian subjects with NAFLD.

METHODS:

Data from 187 subjects allocated to one of the three groups according to body mass index (BMI) and hepatic steatosis on ultrasound were obtained: lean healthy (BMI≤25 kg/m2, no steatosis, N=71), lean NAFLD (BMI≤25 kg/m2, steatosis, N=55), obese NAFLD (BMI≥30 kg/m2, steatosis; N=61). All subjects received a detailed clinical and laboratory examination including oral glucose tolerance test. The serum metabolome was assessed using the Metabolomics AbsoluteIDQ p180 kit (BIOCRATES Life Sciences). Genotyping for single-nucleotide polymorphisms (SNPs) associated with NAFLD was performed.

RESULTS:

Lean NAFLD subjects had fasting insulin concentrations similar to lean healthy subjects but had markedly impaired glucose tolerance. Lean NAFLD subjects had a higher rate of the mutant PNPLA3 CG/GG variant compared to lean controls (P=0.007). Serum adiponectin concentrations were decreased in both NAFLD groups compared to controls (P<0.001 for both groups) The metabolomics study revealed a potential role for various lysophosphatidylcholines (lyso-PC C18:0, lyso-PC C17:0) and phosphatidylcholines (PCaa C36:3; false discovery rate (FDR)-corrected P-value<0.001) as well as lysine, tyrosine, and valine (FDR<0.001).

CONCLUSIONS:

Lean subjects with evidence of NAFLD have clinically relevant impaired glucose tolerance, low adiponectin concentrations and a distinct metabolite profile with an increased rate of PNPLA3 risk allele carriage.

PMID:
27527746
DOI:
10.1038/ajg.2016.318
[Indexed for MEDLINE]

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