Abstract
Introduction
Obesity is a chronic metabolic disorder that results in excessive energy accumulated in adipose tissue causing dysfunction of adipocytes, inflammation, and oxidative stress. Diosgenin (DG), a steroidal saponin produced by several plants, has been reported to have antioxidant activity. This study aimed to evaluate the effects of diosgenin on oxidative stress and inflammation in mice fed with a high-fat diet (HFD).
Methods
Thirty adult male mice were divided into three groups including the control group, mice fed with a normal diet; the HFD group, mice fed with a high-fat diet for 6 weeks; and the HFD+DG group, mice fed with a high-fat diet and diosgenin daily for 6 weeks. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), and total antioxidant capacity (TAC) activities were evaluated. Histopathological changes in the adipose tissues have been investigated.
Results
Data showed that diosgenin increased TAC activities with a concomitant decrease in MDA levels. As well, DG reduces the TNF and IL-6 levels. The histopathological changes in the adipose tissues due to high-fat consumption were restored upon DG supplementation.
Conclusion
Our results suggested that diosgenin is a promising agent for regulating obesity by increasing the levels of antioxidants, modifying oxidative stress and pro-inflammatory cytokines, which might prevent the onset of many diseases.
Ethical Statement
The study was conducted according to the guidelines of the Declaration of Helsinki and approved by the National Hepatology and Tropical Medicine Research Institute Office for IRB, Egypt. The work complied with relevant guidelines for animal handling and welfare (Approval no: 14-2015, Dated: 5 July 2018).
Acknowledgments
The authors greatly thank and acknowledge Taif University, for its support. This research has been supported by Taif University Research Supporting Project number (TURSP-2020/104) Taif University, Taif, Saudi Arabia.
Disclosure
The authors report no conflicts of interest in this work.