Cellular metabolism and energetics have emerged as central regulators of biological processes, spanning development, disease, and evolution. Notably, molecular factors governing these processes are implicated in lifestyle disorders (e.g., diabetes, obesity), aging, and age-related pathologies (e.g., cancer, neurodegeneration). Perturbed feed-fast cycles and disrupted circadian rhythms are well-established drivers of metabolic dysfunction and are increasingly linked to accelerated aging and loss of physiological resilience.

Our research employs a multi-scale systems approach to unravel the molecular mechanisms that couple metabolic inputs to cellular and organismal physiology. Using diverse model systems viz. from Drosophila to mammals and integrative methodologies, we have uncovered novel non-cell-autonomous mechanisms that coordinate metabolic homeostasis across tissues. Our work has demonstrated how mitochondrial-nuclear crosstalk and endocrine signals synchronize metabolic responses to optimize organismal fitness under varying nutrient conditions.

A key focus of lab is deciphering how mitochondrial energetics, nuclear-mitochondrial communication, epigenetic regulation, and circadian metabolic cycles converge to mediate state reversals (e.g., fasting/feeding) and physiological transitions. By combining real-time metabolic/physiological analyses, omics-scale datasets, and mathematical modeling, we have revealed how dynamic molecular oscillations and anticipatory responses are integrated across time to maintain homeostasis. Our findings highlight the plasticity of metabolic networks in adapting to stress, aging, and environmental challenges, offering new avenues for therapeutic interventions.