Replacing C16:0 with 30% cis-9, C18:1 reduced the risk of subcutaneous fat obesity, adipose tissue and systemic low-grade inflammation by accelerating FA oxidative utilization, improving colonization of anti-inflammatory bacteria Akkermansia, reducing intestinal barrier damage, and down-regulating NF-κB activation. This evidence concerns the gene NFKB1 and obesity due to melanocortin 4 receptor deficiency.