2nd Edition of International Obesity and Metabolism Conference 2026

Abstract

Kidney Yang Deficiency Syndrome (KDS-Yang), one of the primary concepts in traditional Chinese medicine (TCM), shares similar clinical signs of the glucocorticoid withdrawal syndrome. Studies have shown that patients with KDS-Yang are more prone to cognitive impairment, however, the mechanism remains elusive. Electrophysiological, Golgi Cox staining, Western blot, and transmission electron microscopy analyses revealed that hippocampal synaptic structure and long-term potentiation (LTP) damaged in hydrocortisone-induced KDS-Yang rats, accompanied by significantly increased expression of total and phosphorylated Tau protein. Tau protein solubility analysis showed that the phosphorylation levels of soluble (SDS) and insoluble (70% formic acid) Tau proteins increased in KDS-Yang rats, which may be related to an imbalance of kinase esterase. In addition, the ubiquitination of Tau fragments and proteasome activity declined in KDS-Yang rats, leading to aggregation of Tau. While, there was no significant difference in Mapt mRNA expression, suggested that the degradation of Tau protein may be reduced in KDS-Yang. We conclude that KDS-Yang stimulate accumulation of Tau proteins and Tau hyperphosphorylation, which might be the biological basis for “kidney essence deficiency leads to insufficient intelligence”.