Thus, its perhaps not surprising that in studies of maternal protein restriction, stress and dexamethasone treatment, the expression of the glucocorticoid receptor (Gr) and the enzyme involved in converting inactive cortisone to cortisol (11βHsd1), are increased in the liver (as well as adipose and skeletal muscle) of adult offspring in association with both enhanced inflammatory state and impaired glucose tolerance [88, 92, 93, 130, 135, 138]. This evidence concerns the gene NR3C1 and Impaired glucose tolerance.