The downregulation of SLC2A4 may consequently be linked to the reduced DNL capacity of adipose tissue in obesity [7,8,21], which interferes with the inter-organ crosstalk to regulate systemic insulin sensitivity through adipose-tissue-derived lipokines [9] and promotes the development of insulin resistance in obese individuals. This evidence concerns the gene SLC2A4 and obesity due to melanocortin 4 receptor deficiency.