Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • A few animal and cell culture

    2021-09-27

    A few animal and cell culture studies have been reported that the reason of HCV-related hepatic steatosis in CHC infection is mainly HCV core protein (Chang et al., 2007; Perlemuter et al., 2002; Ferré, 2004). HCV core protein inhibits activities of microsomal triglyceride transfer protein (MTP) and peroxisome proliferator activating receptor alpha (PPAR-α), which are a crucial players in lipid metabolism (Perlemuter et al., 2002; Dharancy et al., 2005). MTP is a lipid transfer protein expressed in the liver, intestine and heart, and that is consist of a 97-kDa and a 58-kDa subunits, and its pivotal role is to transfer of triglycerides from hepatocytes to apolipoprotein B (ApoB). Moreover, MTP provides correctly assembly and secretion of very low-density lipoprotein (VLDL) together with ApoB (Namikawa et al., 2004; García-García et al., 2005). Karpe et al. (1998) have identified –493G/T (rs1800591) polymorphism in the promoter region of MTP gene, and this polymorphism is associated with HCV-related hepatic steatosis and different diseases in a few studies (Mirandola et al., 2006; Zampino et al., 2008; Mirandola et al., 2009; Bernard et al., 2000; García-García et al., 2005; Namikawa et al., 2004). The SSR 69071 studies reported that while the -493T allele is related to an increased MTP expression in healthy individuals, the -493G allele leads to decreased MTP transcription (Karpe et al., 1998; Namikawa et al., 2004). However, this polymorphism's influence on HCV-related hepatic steatosis is controversial (Mirandola et al., 2008; Petit et al., 2006; Magri et al., 2017; Mirandola et al., 2010). Further, only one study investigated the association of MTP gene –493G/T polymorphism with the 93 patients infected with HCV genotype-1 (Siqueira et al., 2012). Therefore, the –493G/T variant was selected as a candidate polymorphism in patients with HCV genotype 1 for the elucidation of its role in hepatic steatosis. The aim of this study, for the first time, was to analyze the effect of MTP gene –493G/T polymorphism on HCV genotype 1-related hepatic steatosis in the Turkish population. MTP gene –493G/T polymorphism was investigated in 144 patients with HCV genotype 1 using real time polymerase chain reaction (RT-PCR) assay in Turkish population.
    Methods
    Results The clinical and demographic characteristics of the patients were shown in Table 1. All patients were Turkish and Caucasian in the present study. The most of the patients were female (64.6%). The patients' steatosis grades were as follows: grade 0, n = 39 (27.1%); grade 1, n = 66 (45.8%); grade 2, n = 27 (18.8%); grade 3, n = 12 (8.3%). 39 patients with grade 0 (27.1%) were classified as the group of non-steatosis, and 105 patients with grade 1–3 (72.9%) were classified as the group with steatosis. Fibrosis stages of the patients were as follows: F0, n = 2 (1.4%); F1, n = 20 (13.9%); F2, n = 18 (12.5%); F3, n = 75 (52.1%); F4, n = 29 (20.1%). Fibrosis stages were categorized into two groups (F0–2, n = 40 (27.8%); F3–4, n = 104 (72.2%)) to provide adequate statistical power. No significant correlation was found between the stages of fibrosis and grades of steatosis. Additionally, there was no significant difference between the non-steatosis group and the group with steatosis in terms of gender. There were statistically significant differences in the biochemical parameters including triglyceride, total cholesterol, LDL, VLDL levels between the two groups (Table 1). The patients with steatosis had higher triglyceride, total cholesterol, LDL and VLDL levels than the patients with non-steatosis (median values: 112.5 vs 78.5; 168.5 vs 143; 98 vs 80; 22.5 vs 16.3, respectively). Moreover, there was a significant association between these two groups for BMI. The patients with steatosis had higher BMI than the patients with non-steatosis (Table 1). We, also, evaluated the clinical and demographic characteristics of the patients according to MTP genotypes. MTP genotypes were categorized into two groups (GG wild type genotype versus combined TG + TT genotypes as mutant allele carrying genotypes) to provide adequate statistical power. MTP genotypes (GG vs. TG + TT) were not associated with BMI, fibrosis stages and the levels of biochemical parameters (Table 4).