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Obesity is increasing rapidly across the globe. It is widely accepted that natural products with a long safety background may modulate obesity. The current work aimed to investigate the effect of Nigella sativa, atorvastatin, or L-Carnitine on high-fat diet-induced obesity in white male albino rats. A regular basal diet was fed to 7 rats, and a high-fat diet (HFD) was fed to 24 rats throughout the study for 12 weeks. The HFD group was split equally into four subgroups, each containing six rats. The first group fed on HFD with no medication, the second group received HFD+ Nigella sativa, the third group received HFD+ atorvastatin, and the fourth group received HFD+L-carnitine. At the beginning of the seventh week (the start of the treatment regimen), Nigella sativa, atorvastatin, or L-Carnitine were administered for six weeks. Glucose, body weight, serum atherogenic index (AI), ALT, and AST activities were analyzed. The pathological alterations in the hepatic tissues were examined microscopically and scored. The results revealed that the HFD diet significantly increased the final body weight, serum AI, and serum levels of liver enzymes. Treatment with L-carnitine or Nigella sativa significantly normalized the lipid profile and decreased the final body weight, serum AI, and Serum ALT. Histopathological examination of the liver of HFD received rats showed features of steatosis, which were mitigated by the administration of Nigella sativa or L-Carnitine, while atorvastatin had no significant effect on the improvement of hepatic lesions. Collectively, study findings showed that Nigella sativa or L-Carnitine has mitigated effects on metabolic and histopathological changes in the liver tissues of rats fed with HFD.

Background: There is a mutual effect between central obesity and low total serum testosterone. Moreover, oxidative stress acts as a bridge between obesity and its complications. Taken together, we aimed to evaluate whether atorvastatin (AS), a cholesterol-lowering drug, has protective potential against high fat diet (HFD)-induced low fertility, which was exemplified in serum testosterone determination. Moreover, we aimed to deduce a putative mechanism of action through evaluation of the testicular oxidant/antioxidant system. Methods: Adult male albino Wistar rats (Rattus norvegicus albinus) were divided into three groups: 1) normal control group, rats were fed a normal diet for four weeks; 2) HFD group, rats were fed an HFD for four weeks; and 3) AS group, rats were fed an HFD and 5 mg/kg/day atorvastatin for the last two weeks of the experiment. Serum atherogenic index, testosterone, and thyroid stimulating hormone were estimated. Moreover, testicular reduced glutathione and malondialdehyde contents, as well as glutathione-S-transferase, superoxide dismutase, and glutathione reductase activities were also determined. The statistical differences were analyzed using analysis of variance (ANOVA). Results: AS ameliorated the increased level of serum atherogenic index induced by an HFD, as well as testicular malonaldehyde and reduced glutathione levels. On the other hand, AS increased the depleted level and activity of serum testosterone and testicular glutathione reductase, respectively, induced by HFD. Conclusion: The ameliorative effect of AS on the deteriorated level of total serum testosterone induced by HFD might partially be due to oxidant/antioxidant disturbance. Further studies should be carried out to evaluate mTOR pathway contribution, which could enable researchers to deduce drugs targeting members of the oxidant/antioxidant system and/or mTOR pathway to ameliorate putative HFD-induced low fertility.