Testosterone with Silymarin Improves Diabetes-obesity Comorbidity Complications by Modulating Inflammatory Responses and CYP7A1/ACC Gene Expressions in Rats


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Abstract

Background::The co-morbidity of DMOB has become increasingly problematic among the world's population because of a high-calorie diet and sedentary lifestyle. DMOB is associated with lower testosterone (TN) levels, the male sex hormone. The phytochemical compound silymarin (SN) exerts antidiabetic activity by modifying β-cells and anti-obesity activity by inhibiting adipogenesis by methylxanthine.

Aim::The goal of this study was to find out how well testosterone (TN) with silymarin (SN) protects against oxidative stress and inflammation in the liver of the experimental rats with type 2 diabetes (T2D) and obesity (DMOB).

Objectives::The present study evaluates the efficacy of TN and SN combination (TNSN) on the levels of the potential parameters, such as body mass, serum marker enzymes, fasting glucose levels, HbA1c levels, lipid profile, enzymatic and non-enzymatic antioxidants, proinflammatory cytokines, gene expression pathways, and histopathology in a DMOB comorbidity rat model.

Methods::Male Sprague-Dawley (SD) rats were fed a high-fat diet (HFD) for 20 weeks with an administration of a single dose of streptozotocin (STZ) i.p. injection (30 mg/kg) on the 9th week of the study. The procedure was to develop the DMOB co-morbidity model in the experimental animals. Co-treatment of TN and SN administration were followed throughout the experiment. Rats were sacrificed after overnight fasting to collect serum and liver tissue samples. Samples were analyzed using a clinical chemistry automated analyzer, spectrophotometry, and quantitative real-time PCR (qPCR) methods and protocols.

Results::Analyses of body mass changes, serum marker enzymes, fasting glucose levels, HbA1c levels, lipid profiles, enzymatic and non-enzymatic antioxidants, TNF-α, IL-6, adiponectin, CYP7A1, ACC expression pathways, and histopathology showed significant abnormal levels (P ≤ 0.05) in the pathological group. These were efficiently treated to normal by the administration of TNSN.

Conclusion::These results concluded that TNSN exerted protective efficacy against the liver abnormalities in the co-morbidity of the DMOB rat model.

About the authors

Dongli Zhu

Department of Endocrinology,, Daqing Oilfield General Hospital

Email: info@benthamscience.net

Yuanyuan Du

Department of Endocrinology, Daqing Oilfields General Hospital

Email: info@benthamscience.net

Lili Zhu

Department of Endocrinology, Yantai Penglai People's Hospital

Email: info@benthamscience.net

Tahani Alahmadi

Department of Pediatrics, College of Medicine and King Khalid University Hospital, King Saud University

Email: info@benthamscience.net

Samer Hasan Hussein-Al-Ali

Department of Chemistry, Faculty of Science, Isra University

Email: info@benthamscience.net

Qinhu Wang

Department of Endocrinology, The Third People's Hospital of Gansu Province, Lanzhou, Gansu Province, 730000, China

Author for correspondence.
Email: info@benthamscience.net

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