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Significance Excess energy intake and physical inactivity are two major factors causing obesity, but the underlying mechanisms have not been fully understood. Both excess energy intake and physical inactivity increase cellular energy status that is monitored by the energy-sensing AMP-activated protein kinase (AMPK). We demonstrate that the AMPK–tre-2/USP6, BUB2, cdc16 domain family member 1 (the TBC domain is the GTPase activating protein domain) (TBC1D1) signaling nexus regulates insulin-like growth factor 1 (IGF1) secretion. Disruption of this AMPK–TBC1D1 signaling nexus in mice enhances lipogenic gene expression via promoting IGF1 secretion, causes obesity, and eventually leads to development of metabolic syndrome. These findings reveal a novel regulatory mechanism that links energy status to development of obesity via control of IGF1 secretion.

Disruption of the AMPK–TBC1D1 nexus increases lipogenic gene expression and causes obesity in mice via promoting IGF1 secretion