Tetradecylthioacetic Acid (TTA)


Tetradecylthioacetic Acid (TTA)

Tetradecylthioacetic Acid, otherwise known as TTA, is a PPAR-alpha activator. Although similar in structure to an omega-3 fatty acid, it cannot be utilized for energy and thus has no relevant caloric value to humans. PPAR-alpha is a transcription factor and a major regulator of lipid metabolism in the liver. PPAR-alpha is activated under conditions of energy deprivation and is necessary for the process of ketogenesis, a key adaptive response to prolonged fasting.
Activation of PPAR-alpha promotes uptake, utilization, and catabolism of fatty acids by upregulation of genes involved in fatty acid transport, fatty acid binding, and activation, and peroxisomal and mitochondrial fatty acid. β-oxidation. The clearing of fat from the blood causes a drop in lipoproteins and a lowering of LDL cholesterol. TTA has also been shown to decrease blood pressure and exert a mild antioxidant effect.


Dietary supplementation of tetradecylthioacetic acid increases feed intake but reduces body weight gain and dipose depot sizes in rats fed on high-fat diets.
Despite higher feed intake during the final 2 weeks of the study, rats fed on TTA gained less body weight than lard-fed rats and had markedly decreased subcutaneous, epididymal, perirenal and mesenteric adipose depots. The effects of TTA feeding with reduced body weight gain and energy efficiency (weight gain/feed intake) started between day 10 and 13. Body contents of fat, protein, and water were reduced after feeding lard plus TTA, with a stronger decrease in fat relative to protein. Plasma lipids, including Non-Esterified Fatty Acids (NEFA), were significantly reduced, whereas fatty acid β-oxidation in liver and heart was enhanced in lard plus TTA-fed rats. Hepatic UCP3 was expressed ectopically both at protein and mRNA level (>1900-fold), whereas Ucp1 mRNA was increased 30-fold in epididymal and 90-fold in mesenteric fat after lard plus TTA feeding.
Conclusion: Our data support the hypothesis that TTA feeding may increase hepatic fatty acid β-oxidation, and thereby reduce the size of adipose tissues. The functional importance of ectopic hepatic UCP3 is unknown but might be associated with enhanced energy expenditure and thus the reduced feed efficiency.

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