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Abstract <p>Dyslipidemia is characterized by abnormal lipid levels in the bloodstream and can be influenced by liver diseases and smoking. Nicotine exposure and liver damage are linked to lipid metabolism impairments. This study investigated the effects of nicotine on dyslipidemia in a cholestasis rat model using bile duct ligation (BDL) to establish liver fibrosis. Wistar rats received intraperitoneal nicotine at doses of 10 mg/kg (high) and 1 mg/kg (low) for three weeks. Serum levels of triglycerides (TG), cholesterol (Chol), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were quantified via a standard colorimetric kit (Pars Azmoon). Liver fibrosis confirmed through histological investigation. Additionally, the mRNA and protein expression of fatty acid synthase (FAS) were assessed using quantitative RT-PCR and immunofluorescence. Results showed that nicotine administration in healthy rats significantly increased TG, Chol, and LDL levels while decreasing HDL. In BDL rats, nicotine further reduced HDL and increased TG levels without affecting Chol and LDL. Histological analysis confirmed hepatic fibrosis, and both nicotine exposure and liver fibrosis elevated FAS expression in liver tissues. These findings indicate that BDL-induced liver fibrosis causes dyslipidemia in rats, and nicotine exposure exacerbates serum lipid profile alterations, potentially through increased FAS expression. Therefore, it is recommended that individuals with liver disease avoid nicotine to manage dyslipidemia.</p>

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Nicotine Administration Exacerbates Lipid Profile Alterations in a Wistar Rat Model of Liver Fibrosis through Fatty Acid Synthesis Modulation

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • Narges Dastmalchi,
  • Khalil Hajiasgharzadeh,
  • Hooria Amooji,
  • Mohammad Reza Alipour,
  • Behzad Mansoori,
  • Homeira Hatami Nemati,
  • Seyed Mahdi Banan Khojasteh

摘要

Abstract

Dyslipidemia is characterized by abnormal lipid levels in the bloodstream and can be influenced by liver diseases and smoking. Nicotine exposure and liver damage are linked to lipid metabolism impairments. This study investigated the effects of nicotine on dyslipidemia in a cholestasis rat model using bile duct ligation (BDL) to establish liver fibrosis. Wistar rats received intraperitoneal nicotine at doses of 10 mg/kg (high) and 1 mg/kg (low) for three weeks. Serum levels of triglycerides (TG), cholesterol (Chol), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were quantified via a standard colorimetric kit (Pars Azmoon). Liver fibrosis confirmed through histological investigation. Additionally, the mRNA and protein expression of fatty acid synthase (FAS) were assessed using quantitative RT-PCR and immunofluorescence. Results showed that nicotine administration in healthy rats significantly increased TG, Chol, and LDL levels while decreasing HDL. In BDL rats, nicotine further reduced HDL and increased TG levels without affecting Chol and LDL. Histological analysis confirmed hepatic fibrosis, and both nicotine exposure and liver fibrosis elevated FAS expression in liver tissues. These findings indicate that BDL-induced liver fibrosis causes dyslipidemia in rats, and nicotine exposure exacerbates serum lipid profile alterations, potentially through increased FAS expression. Therefore, it is recommended that individuals with liver disease avoid nicotine to manage dyslipidemia.