Selenium deficiency is associated with insulin resistance in patients with hepatitis C virus-related chronic liver disease

Department of Integrated Medicine, Kagawa University School of Medicine, Kagawa, Japan.
Nutrition research (Impact Factor: 2.47). 11/2011; 31(11):829-35. DOI: 10.1016/j.nutres.2011.09.021
Source: PubMed


The relationship between selenium (Se) deficiency and insulin resistance has not much been established in persistent hepatitis C virus (HCV) infection, although Se deficiency is often observed in patients with liver cirrhosis. We hypothesized that the decreased serum Se levels were associated with the severity of hepatic fibrosis or insulin resistance in patients with HCV-related chronic liver disease (CLD). To test the hypothesis, 52 patients with HCV-related CLD including chronic hepatitis and liver cirrhosis were enrolled in this study. The severity of hepatic fibrosis was divided into 4 categories (F(1) through F(4)) according to the new Inuyama classification. Insulin resistance was defined by the homeostasis model for assessment of insulin resistance value. Serum Se levels significantly declined in proportion to the severity of hepatic fibrosis and were positively correlated with serum albumin (r = 0.372, P = .0065) and zinc (r = 0.403, P = .0081) concentrations. Serum Se levels were also linked to glutathione peroxidase activities in the sera of the enrolled patients (r = 0.374, P = .0148). By contrast, serum Se levels were inversely correlated with the homeostasis model for assessment of insulin resistance values (r = -0.304, P = .0338). However, serum Se levels were independent of HCV genotype and loads of HCV-RNA. These findings suggest that Se deficiency was associated with the severity of hepatic fibrosis in patients with HCV-related CLD and that Se deficiency was likely to be one of the factors contributing to insulin resistance in those patients.

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    • "Exposure to an excess amount of selenium is toxic and can cause health problems such as gastrointestinal upsets, hair loss, white blotchy nails, garlic breathe odour and nerve damage. Selenium deficiency on the other hand, has been linked to cancer, heart diseases, muscular dystrophy , multiple sclerosis, immune system, osteoarthopathy, reproductive disorder in humans and white muscle disease in animals [2]. The World Health Organization has set a limit of 10 μg L −1 selenium concentration in drinking water [3]. "
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    ABSTRACT: This work presents a simple and cheaper method of detecting selenium in water using an electrochemical sensor based on gold nanoparticle (AuNP) modified glassy carbon electrode. AuNPs were electrochemically deposited on a glassy carbon electrode (GCE) using cyclic voltammetry within the potential range of - 0.4 mV to 1.1 mV for 10 cycles. The modification of GCE with AuNPs resulted in an increase in the electroactive surface area of the electrode which led to the enhancement of the redox current peaks of [Fe (CN)6]3 -/4 - and [Ru (NH3)6]2 +/3 + in comparison to the bare GCE. Square wave anodic stripping voltammetry was used to detect Se (IV) in water (in 0.1 M H2SO4 as supporting electrolyte) at the following optimum conditions: pH 1, deposition potential of - 100 mV, pre-concentration time of 60 s. The GCE-AuNP sensor was able to detect Se (IV) to the limit of 0.64 μg L- 1 and was not susceptible to many interfering cations except Cu (II) and Cd (II). This method involves a simple one step electrode modification. The sensor was used to detect Se (IV) in a real sample. This method was validated by its good correlation with the result obtained from inductively coupled plasma method.
    Full-text · Article · Dec 2015 · Journal of electroanalytical chemistry
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    • "Impairment of insulin receptor substrate-1 (IRS-1) by HCV core protein directly or through a variety of cytokines and trace elements may account for insulin resistance in those patients [11]. We previously revealed that zinc and selenium deficiency resulted in impaired insulin signaling in patients with HCV-related chronic liver disease (CLD-C) [12,13]. "
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    ABSTRACT: CD36, a class B scavenger receptor, participates in the pathogenesis of metabolic dysregulation such as insulin resistance, hepatic steatosis, and atherosclerosis. Persistent hepatitis C virus (HCV) infection often evokes these metabolic abnormalities. The primary purpose of this study was to investigate the role of CD36 in the pathogenesis of insulin resistance and hepatic steatosis caused by chronic HCV infection. Forty-five patients with HCV-related chronic liver disease (CLD-C) were enrolled in this study. CD36 expression in the liver specimen was examined by an immunohistochemical procedure. The concentrations of circulating soluble form of CD36 (sCD36) and oxLDL were determined by the enzyme-linked innunosorbent assay. Insulin resistance was estimated by the values of HOMA-IR. Moderate to extensive hepatic CD36 expression was observed in the sinusoids of all enrolled CLD-C patients. CD36-positive sinusoids appeared to be identical to Kupffer cells. The severity of CD36 expression in the hepatic sinusoids was significantly correlated with the sCD36 level in sera of patients with CLD-C. The serum sCD36 levels were significantly correlated with body mass index and serum oxLDL levels in those patients. However, the serum sCD36 concentrations were independent of the values of HOMA-IR and the severity of hepatic steatosis. These data suggest that the serum sCD36 levels reflect the severity of CD36 expression on the Kupffer cells in patients with CLD-C, and that the serum sCD36 levels were associated with obesity, although the levels were independent of insulin resistance and hepatic steatosis in those patients.
    Full-text · Article · Sep 2013 · Diabetology and Metabolic Syndrome
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    • "Several authors have reported that serum selenium levels are correlated with the activity of GP. The results of these studies suggested that selenium deficiency is associated with the development of hepatic fibrosis in patients and that a lack of selenium is one of the potential factors contributing to insulin resistance (Himoto et al. 2011). Additionally , GP has been found to be one of the real-time markers of selenium status (Xun et al. 2011), along with other selenoproteins (Schomburg 2011). "
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    ABSTRACT: Selenium supplementation and its effects on Northerners have been little studied. The aim of our study was to assess the selenium levels of the inhabitants of North European Russia, the seasonal aspects of selenium supplementation, and the interrelationships between selenium levels and the levels of thyroid gland hormones. To study the particular features of selenium metabolism in Northerners over the course of 1 year, 19 healthy male Caucasian volunteers (18-21 years old) were recruited for the present study. The subjects were military guards in a Northern European region of Russia (Syktyvkar, Russia, 62°N latitude) who spent 6-10-h outdoors daily. The study was conducted over a 12-month period. Selenium levels, glutathione peroxidase (GP) activity, as well as total triiodothyronine (T3), total thyroxin (T4), free thyroxin, free triiodothyronine, and thyrotropin (TSH) levels, were determined in the blood serum. The study subjects showed low levels of plasma selenium throughout the year. We observed a noticeable decrease in plasma selenium levels during the period from May to August, with the lowest levels in July. Selenium levels in the military guards correlated with the levels of selenium-dependent GP enzyme activity throughout the year. Additionally, we demonstrated a significant correlation between selenium and pituitary-thyroid axis hormones (total T3, free T4, and TSH) in periods in which plasma selenium levels were lower than the established normal ranges. Over the course of 1 year, low levels of plasma selenium affect GP activity and thyroid hormone levels in humans living in North European Russia.
    Full-text · Article · Jul 2013 · International Archives of Occupational and Environmental Health
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