Dysregulation in Plasma ω3 Fatty Acids Concentration and Serum Zinc in Heavy Alcohol-Drinking HCV Patients.

IF 1.1 Q4 VIROLOGY
Advances in Virology Pub Date : 2020-06-09 eCollection Date: 2020-01-01 DOI:10.1155/2020/7835875
Vatsalya Vatsalya, Ruchita Agrawal, Jane Frimodig, Shweta Srivastava, Melanie L Schwandt
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引用次数: 3

Abstract

Alcohol use disorder (AUD) patients comorbid with hepatitis C virus (HCV) infection (HCV + AUD) could have progressively severe clinical sequels of liver injury and inflammation. Serum zinc and several polyunsaturated fatty acids (PUFAs) get dysregulated in AUD as well as HCV. However, the extent of dysregulation of PUFAs and zinc deficiency and their interaction in HCV + AUD as a comorbid pathology has not been studied. We examined the role of dysregulation of FAs and low zinc in HCV + AUD patients. 138 male and female participants aged 21-67 years were grouped as HCV-only (Gr. 1; n = 13), HCV + AUD (Gr. 2; n = 25), AUD without liver injury (Gr. 3; n = 37), AUD with liver injury (Gr. 4; n = 51), and healthy volunteers (Gr. 5 or HV; n = 12). Drinking history, individual demographic measures, fasting fatty acids, liver function, and zinc were measured and analyzed. HCV + AUD patients showed the highest ALT level compared to the rest of the groups. Serum zinc concentrations were the lowest, and the proinflammatory shift was the highest (characterized by ω6 : ω3 ratio) in the HCV + AUD patients. Total ω3, eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) were the lowest in HCV + AUD patients. Total ω3, α-linoleic acid (α-LA) along with covariable number of drinking days past 90 days (NDD90), eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA5,3) independently showed significant association with low zinc in the HCV + AUD patients. Heavy drinking pattern showed that NDD90 has a significant mediating role in the representation of the relationship between candidate ω3 PUFAs and zinc uniquely in the HCV + AUD patients. Low serum zinc showed a distinctively stronger association with total and candidate ω3s in the HCV + AUD patients compared to the patients with HCV or AUD alone, supporting dual mechanism involved in the exacerbation of the proinflammatory response in this comorbid cohort. This trial is registered with NCT#00001673.

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重度饮酒HCV患者血浆ω3脂肪酸浓度和血清锌的失调。
酒精使用障碍(AUD)合并丙型肝炎病毒(HCV)感染(HCV + AUD)的患者可能会出现逐渐严重的肝损伤和炎症的临床后遗症。血清锌和几种多不饱和脂肪酸(PUFAs)在AUD和HCV中失调。然而,PUFAs和锌缺乏症的失调程度及其在HCV + AUD中作为共病病理的相互作用尚未得到研究。我们研究了FAs失调和低锌在HCV + AUD患者中的作用。138名年龄在21-67岁的男性和女性参与者被分为仅hcv组(Gr. 1;n = 13), HCV + AUD (Gr. 2;n = 25),无肝损伤的AUD (Gr. 3;n = 37), AUD伴肝损伤(Gr. 4;n = 51),健康志愿者(Gr. 5或HV;n = 12)。测量并分析了饮酒史、个人人口统计指标、空腹脂肪酸、肝功能和锌。与其他组相比,HCV + AUD患者的ALT水平最高。HCV + AUD患者血清锌浓度最低,促炎转移最高(ω6: ω3比值)。总ω3、二十碳五烯酸(EPA)和二十碳五烯酸(DPA5、3)在HCV + AUD患者中最低。总ω3、α-亚油酸(α-LA)和协变量90天以上饮酒天数(NDD90)、二十碳五烯酸(EPA)、二十碳五烯酸(dpa5,3)分别与HCV + AUD患者的低锌水平显著相关。重度饮酒模式表明NDD90在HCV + AUD患者候选ω3 PUFAs与锌之间的关系中具有显著的中介作用。与单纯HCV或AUD患者相比,低血清锌与HCV + AUD患者的总ω3s和候选ω3s的相关性明显更强,支持在该合并症队列中参与促炎反应加剧的双重机制。本试验注册编号为NCT#00001673。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.30
自引率
0.00%
发文量
23
审稿时长
22 weeks
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