The Lipid-Redox Axis in Sarcopenic Obesity: Crosstalk, Mechanisms, and Therapeutic Opportunities
Smita Milind Chatrabhuji1 and Vaidehi Vinay Raole2*
1,2*Department of Kriya Sharir, Parul Institute of Ayurved, Parul University, Vadodara - 391760 (India) *Corresponding Author Email ID: vaidehi.raole@paruluniversity.ac.in
ABSTRACT
Sarcopenic obesity (SO), the specific co-occurrence of skeletal muscle atrophy and excess adiposity, represents a unique and escalating health challenge. This review elucidates the intricate mechanistic “crosstalk” between dysfunctional adipose tissue and skeletal muscle, identifying mitochondrial redox signaling as the central integrator. We critically examine how the “Lipid-Redox Axis” drives muscle wasting. We detail how adipocyte-derived inflammatory cytokines (TNFalpha, IL-6) and lipotoxic intermediates (ceramides) synergistically amplify mitochondrial reactive oxygen species (ROS) production in myocytes. This oxidative surge triggers a pathogenic cascade: (1) suppression of the NRF2/Keap1 antioxidant defense system; (2) oxidative modification of Drp1 (S-nitrosylation) promoting mitochondrial fission; and (3) activation of the NLRP3 inflammasome. SO is a disease of organelle dysfunction. Therapeutic strategies targeting mitochondrial quality control—including mitochondriatargeted antioxidants and molecularly valid traditional phytomedicines (Rasayanas)—offer the most promising avenue. Future protocols must integrate these interventions with precision, accounting for potential pharmacokinetic interactions.