Adipose tissue serves dual roles as an energy reservoir and endocrine organ. We identify YAP/TAZ, Hippo signaling pathway effectors, as key integrators of these functions. Mice with adipocyte-specific YAP/TAZ activation develop severe lipoatrophy yet maintain metabolic homeostasis through unexpectedly elevated leptin levels. Mechanistically, we demonstrate that adipocyte YAP/TAZ operates through two distinct transcriptional pathways: inhibiting PPARĪ³ target genes via a YAP/TAZ-PPARĪ³ axis, and directly upregulating leptin expression through YAP/TAZ-TEAD complex binding to a novel Lep enhancer. The physiological relevance of this mechanism is underscored by the finding that adipocyte YAP/TAZ activation correlates with and is required for regulating leptin expression during feeding-fasting cycles and high-fat diet induced obesity. Taken together, these results extend our understanding of the Hippo-YAP/TAZ pathway beyond its canonical role in organ size control, revealing a critical function in integrating adipose tissue plasticity with systemic energy homeostasis.