Abstract
ObjectivePrevious studies have shown that leukocyte cell-derived chemotaxin 2 (LECT2), a recently discovered hepatokine, is associated with the inflammatory response and insulin resistance. We examined circulating plasma LECT2 levels in the subjects with non-alcoholic fatty liver disease (NAFLD) or metabolic syndrome.MethodsWe analyzed plasma LECT2 levels from the subjects of age- and sex-matched 320 adults with or without NAFLD who completed a health check-up at the Health Promotion Center of Korea University Guro Hospital.ResultsIndividuals with NAFLD showed significantly higher LECT2 levels (31.2 [20.9, 41.5] vs. 24.5[16.3, 32.7] ng/ml, P <0.001) as well as components of MetS compared to those without NAFLD. Furthermore, circulating LECT2 concentrations were greater in subjects with MetS (32.6 [17.8, 45.0] vs. 27.0 [18.7, 33.7] ng/ml, P = 0.016) and were associated with anthropometric measures of obesity, lipid profiles, high sensitivity C-reactive protein (hsCRP) and liver aminotransferase levels. However, there was no significant relationship between LECT2 levels and indicators of subclinical atherosclerosis, such as carotid intima-media thickness (CIMT) and brachial ankle pulse wave velocity (baPWV). Multivariate analysis demonstrated a progressively increasing trend of odds ratios for NAFLD according to quartiles of LECT2 levels after adjusting for risk factors, although the relationship was attenuated after further adjustment for waist circumference and lipid levels.ConclusionCirculating LECT2 concentrations were increased in individuals with NAFLD and those with MetS, but not in those with atherosclerosis. The relationship between LECT2 and both NAFLD and MetS might be mediated by its association with abdominal obesity and lipid metabolism.Trial registrationClinicaltrials.gov NCT01594710
Highlights
Non-alcoholic fatty liver disease (NAFLD) causes up to 33% of chronic liver disease worldwide, more than any other cause [1]
There was no significant relationship between Leukocyte cell-derived chemotaxin 2 (LECT2) levels and indicators of subclinical atherosclerosis, such as carotid intima-media thickness (CIMT) and brachial ankle pulse wave velocity
Multivariate analysis demonstrated a progressively increasing trend of odds ratios for NAFLD according to quartiles of LECT2 levels after adjusting for risk factors, the relationship was attenuated after further adjustment for waist circumference and lipid levels
Summary
Non-alcoholic fatty liver disease (NAFLD) causes up to 33% of chronic liver disease worldwide, more than any other cause [1]. Leukocyte cell-derived chemotaxin 2 (LECT2) is a 16-kDa secretory protein that was first isolated in 1996 from cultured supernatants of phytohemagglutinin-activated human T-cell leukemia SKW-3 cells [6] It was identified as a chemotactic factor for neutrophils [6]. Genetic deletion of LECT2 in mice increased insulin sensitivity in skeletal muscle, but treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase (JNK) in myocytes. They showed that the expression of the genes involved in mitochondria and myogenesis was up-regulated in the muscle of LECT-/- mice [10], emphasizing the pivotal role of LECT2 on the provocation of peripheral insulin resistance. There have been very limited studies to examine the clinical significance of circulating LECT2 levels in metabolic diseases including NAFLD and atherosclerosis in humans
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