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Adipose tissue modulates energy homeostasis by secreting leptin, but little is known about the factors governing leptin production. We show that succinate, long perceived as a mediator of immune response and lipolysis, controls leptin expression via its receptor SUCNR1. Adipocyte-specific deletion of Sucnr1 influences metabolic health according to nutritional status. Adipocyte Sucnr1 deficiency impairs leptin response to feeding, whereas oral succinate mimics nutrient-related leptin dynamics via SUCNR1. SUCNR1 activation controls leptin expression via the circadian clock in an AMPK/JNK-C/EBPα-dependent manner. Although the anti-lipolytic role of SUCNR1 prevails in obesity, its function as a regulator of leptin signaling contributes to the metabolically favorable phenotype in adipocyte-specific Sucnr1 knockout mice under standard dietary conditions. Obesity-associated hyperleptinemia in humans is linked to SUCNR1 overexpression in adipocytes, which emerges as the major predictor of adipose tissue leptin expression. Our study establishes the succinate/SUCNR1 axis as a metabolite-sensing pathway mediating nutrient-related leptin dynamics to control whole-body homeostasis. [Display omitted] • Extracellular succinate in adipocytes controls circadian clock and leptin via SUCNR1 • SUCNR1 modulates leptin via AMPK/JNK-BMAL1-C/EBPα-dependent signaling • The metabolic impact of SUCNR1 deficiency in adipocytes is dependent on nutritional status • Hyperleptinemia in human obesity is related to overactive succinate/SUCNR1 signaling Villanueva-Carmona et al. describe a new function for the succinate/SUCNR1 axis in controlling leptin expression in adipocytes via a mechanism involving the circadian clock. This system is overactivated in obesity, which might contribute to obesity-related hyperleptinemia. [ABSTRACT FROM AUTHOR]