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IGF-1 treatment of Th17 cells decreases mitochondrial membrane potential and mROS production in an IGF-1R and IR dependent manner To determine if these IGF-1-mediated changes on Th17 cell mitochondrial membrane potential and mROS require signaling by IR, IGF-1R, or both, we differentiated Th17 cells in vitro from IGF-1R cKO mice or IR cKO mice, and littermate controls

The gradual increase gives the body time to adapt to the stronger receptor activation

and implications for interpreting clinical data from weight management RCTs

Research Highlights Metabolic Regulation and Anti-Obesity Effects: Potent inhibition of nicotinamide N-methyltransferase (NNMT) increases cellular NAD and S-adenosylmethionine (SAM) levels, enhances polyamine flux, boosts energy expenditure, and suppresses lipogenesis