In this study, we demonstrated that glucose metabolism is unchanged in MffLiKO mice, which is in sharp contrast with our previous report that the disruption of mitochondrial fission in the liver protected mice from diet-induced obesity and that metabolic deterioration improved glucose metabolism in mice with targeted disruption of Drp1 in the liver [28]. Here, DNM1L is linked to obesity due to melanocortin 4 receptor deficiency.