Slc16a1 haploinsufficient mice are resistant to diet-induced obesity and associated metabolic perturbations40, vice versa Slc16a1 overexpression would rather result in a detrimental metabolic phenotype, supported by the finding of exercise-induced hyperinsulinemia in human patients with promotor-activating mutations in SLC16A141,42 and in a transgenic mouse line with beta cell-specific Slc16a1 overexpression43. Here, SLC16A1 is linked to obesity disorder.