However, insulin did not decrease lactate production in obesity-associated cells, consistent with the fact that while the insulin-stimulated increase in glucose uptake outpaced insulin-stimulated increases in mitochondrial oxidation in all cells, excess glucose may be used for a variety of synthetic pathways (including glycogen synthesis and/or the energetic requirements of cell division) as well as lactate production. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.