Given the link between HFD-induced obesity, low-grade inflammation and insulin resistance [76], [77], one could argue that the dramatic reduction in fat mass observed with the highest P/C ratio may underlie the effects on inflammatory markers in the adipose tissue (TNFα and CD68) and the hypothalamus (TNFα), along with simultaneous changes in expression of genes involved in insulin signalling (IR, IRS-1 and GLUT4 in the adipose, IRS-1 in liver and IR in the hypothalamus), and the reduction in plasma glucose in these mice. The gene discussed is CD68; the disease is obesity disorder.