Conclusions
This study demonstrates that LTA mitigates kidney and liver damage induced by long-term excess HPDs by regulating protein metabolism.
Results
Here, Sprague-Dawley rats are fed HPDs with different protein supply ratios and administered a diverse dose of LTA for 40 days. Results show that HPDs with an energy supply ratio from protein >40% impair the liver and kidneys, elevate serum ammonia and urea nitrogen, induce amino acid (AA) catabolism, and promote fatty acid (FA) synthesis via FA-binding protein 5 (Fabp5) and acetyl-CoA carboxylase 1 (ACC1). LTA intervention alleviates HPD-induced hepatic and renal injury and improves serum biochemical indices. It increases hepatic free AA content and inhibits FA synthesis by downregulating Fabp5 and ACC1. It promotes protein synthesis by acting on the mammalian target of rapamycin (mTOR) pathway, thereby alleviating HPD-induced metabolic disorders. Conclusions: This study demonstrates that LTA mitigates kidney and liver damage induced by long-term excess HPDs by regulating protein metabolism.