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Zahra Eslami, Yahya Mohammadnajad Panah Kandi, Alireza Norouzi, Abdorreza Eghbal Moghanlou, Mehdi Sheikh Arabi, Vahideh Kazeminejad, Seyedeh Somayeh Hosseini Alarzi, Aref Saeidi, Hamidreza Joshaghani,
Volume 16, Issue 3 (May-Jun 2022)
Abstract

Background and objectives: Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease caused by the accumulation of large amounts of fat in the hepatocytes. Given that atorvastatin is effective for treatment of NAFLD, the present study investigated effects of high-fat/fructose diet (HFFD) with atorvastatin on liver enzymes and lipid profile in a NAFLD rat model.
Methods: Thirty-two male Wistar rats were divided into four groups: 1) normal control, 2) HFFD control, 3) HFFD + atorvastatin, and 4) normal + atorvastatin. The groups received HFFD for 15 weeks to induce hepatosteatosis. Atorvastatin was administrated at the dose of 10 mg/kg/day. Lipid profile and liver enzymes were measured after eight weeks of intervention.
Results: Triglyceride, cholesterol, gamma-glutamyl transferase, and aspartate transaminase were significantly reduced in the HFFD + atorvastatin group compared with the HFFD control group. In addition, cholesterol, high-density lipoprotein, alkaline phosphatase, and gamma-glutamyl transferase were significantly increased in the normal + atorvastatin group compared with the normal control group. Low-density lipoprotein increased significantly in the HFFD + atorvastatin group and the normal + atorvastatin group compared with other groups. There was a significant difference in the alanine transaminase levels between the groups taking atorvastatin. In fact, alanine transaminase level was lowest in the normal + atorvastatin group.
Conclusion: Atorvastatin improves the lipid profile and fatty liver and controls liver enzymes. Therefore, it can be used with caution to improve the lipid profile and reduce the complications of NAFLD.
Zahra Eslami, Shayan Marhamaty, Seyyed Mehdi Jafari, Mohadese Khorasani, Mehdi Sheikh Arabi, Hamidreza Joshaghani,
Volume 19, Issue 1 (4-2025)
Abstract

background:
Bivalent minerals have an important role as cofactors which play vital roles in various metabolic pathways in the body. Zinc (Zn) has catalytic, structural, and regulatory roles. Severe Zn deficiency may cause the abnormal synthesis of nucleic acids, and proteins, impaired cellular growth, excessive cell death, and excess lipid peroxidation of the cellular membrane that is associated with shortening the RBC lifespan.
Purpose:
The aim of this study was to examine the associations between Zn status and the erythrocyte indices.
Methods and materials:
A number of 563 individuals (72.8% female) were included in this study. The level of serum Zn was measured by photometric method and blood index values were measured by using a cell counter.
Results:
The average serum Zn level is 102.8± 17.6 mg/dl. Serum Zn level is directly related with RBC (R=0.119, PV=0.005) and MCHC (R=0.086, PV=0.041) but it is inversely related with MCV (R=-0.097, PV=0.021). These results also determined that serum Zn level, as well as the levels of RBC, Hb, HCT, and MCHC, were significantly higher in men (Sig<0.01) but the level of MCV among women was higher (Sig<0.01). Moreover, in individuals with <30   serum Zn level, MCHC (Sig<0.01), and RBC (Sig<0.05) were higher whereas Hb (Sig<0.05), HCT, MCV, and MCH (Sig<0.01) were higher at >30.
Conclusion:
According to the positive relationship between Zn level and RBC, Zn deficiency affects the number of RBCs.
 

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