The metabolic switch from a high glycolytic metabolism to defects in the mitochondrial metabolism, through an increase of the mTOR pathway in aged T cells and a decrease in the expression of SIRT1 and FOXO1 genes in aged B cells, may contribute to ageing of the adipose tissue and result in the inflammation characteristic of obesity and metabolic disorders.2, 3. This evidence concerns the gene MTOR and Other metabolic disease.