Unraveling the mechanisms of trans-cinnamic acid in ameliorating non-alcoholic fatty liver disease.

BACKGROUND: The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing significantly due to high amounts of fat and fructose in the diet. Phytochemicals present in herbal plants and nutrients present in food play vital roles in the management of NAFLD. One of these is trans-cinnamic acid (TCA). We are evaluate the role of TCA in NAFLD induced by a high-fat, high-fructose diet.

METHODOLOGY: Rats fed a high-fat, high-fructose (HFHF) diet for ten weeks exhibited distinct signs of NAFLD. Rats were given TCA (10 mg/kg, 20 mg/kg, and 40 mg/kg) and pioglitazone (10 mg/kg) for four weeks along with a HFHF diet. At the end, body weight, food intake, liver, lipid measurements, TNF-α, antioxidants, and histopathology were evaluated.

RESULTS: TCA significantly decreased serum glutamic-oxaloacetic transaminase and glutamic pyruvic transaminase in rats. Serum cholesterol, triglyceride, and low-density lipid levels were substantially decreased in TCA-treated rats compared to diseased controls. Superoxide dismutase, glutathione, and malondialdehyde were significantly decreased in rats treated with a high dose of TCA (40 mg/kg) compared to HFFD-fed rats. HFFD-fed rats exhibited fatty liver alterations, whereas rats treated with TCA exhibited significantly fewer morphologic changes associated with fatty liver disease. TCA at a high dose exhibited decreased TNF-α levels, thereby decreasing hepatic inflammation.

CONCLUSION: TCA proved its role in the treatment of NAFLD by substantially reducing liver enzymes, pro-inflammatory markers (TNF-α), and lipid markers. Inclusion of TCA as a therapeutic regimen alongside diet-based treatment undoubtedly has therapeutic potential in NAFLD and related diseases.