Being skewed toward a proinflammatory state, alterations in adipocyte-intrinsic cellular metabolism impacts adipocyte-immune cell crosstalk via changes in adiponectin, leptin, and IL-6, as well as other pro-inflammatory mediators (e.g., TNF, IL-1, type I IFNs, etc.)is dysregulated during obesity. This evidence concerns the gene IL1B and obesity due to melanocortin 4 receptor deficiency.