Endogenous formation of trans fatty acids: Health implications and potential dietary intervention

• Published in: Journal of functional foods Vol. 25; pp. 14 - 24
• Main Authors: Hung, Wei-Lun, Sun Hwang, Lucy, Shahidi, Fereidoon, Pan, Min-Hsiung, Wang, Yu, Ho, Chi-Tang
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.08.2016; Elsevier
• Subjects: Antioxidants; Endogenous trans fatty acids; Flavonoids; Nitrogen dioxide; Thiyl radicals; Vitamins; THP-1; 2-ME; AAPH; MUFA; LUVET; Thiyl radicals; LPS; BHT; Antioxidants; NF-κB; POPC; STZ; iNOS; Endogenous trans fatty acids; GC; DOPC; AD; TFAs; PUFA; SAPC; hAPP; Vitamins; Flavonoids; TNF-α; OIR; Nitrogen dioxide; RNase A
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2016.05.006

•Trans fatty acids can be endogenously formed by free radical stress.•Thiyl radicals and nitrogen dioxide catalyse cis–trans isomerisation.•Occurrence of endogenous trans fatty acids is closely associated with some chronic diseases.•Naturally occurring antioxidants may inhibit endogenous trans fatty acid formation. Unsaturated fatty acids naturally occur as cis configuration and most dietary trans fatty acids (TFAs) originate from partially hydrogenated oils. High consumption of trans fats may cause several adverse effects on human health. However, the dietary source is not the only path by which TFAs are produced, but in vivo, they can also be formed endogenously via oxidative stress and by free radicals. Recent studies have demonstrated that thiyl radicals and nitrogen dioxide serve as the effective catalysts responsible for endogenous TFA formation through cis–trans isomerisation. Several in vivo studies have indicated that the occurrence of endogenous TFAs is closely linked with the development of some chronic diseases. Additionally, some vitamins and polyphenols exhibit inhibitory effects against the free radical-catalysed TFA formation in different in vitro experiments. Therefore, we postulate that dietary supplementation of antioxidants may serve as an effective strategy against endogenous TFA formation during pathogenesis of chronic diseases.