While these opposing changes could counteract the metabolic effects of each endocannabinoid at an initial stage, the observed higher AEA levels at a later time point (4 months of age) may reinforce the accumulation of triglycerides in this tissue.32, 33 This could subsequently contribute to the development of impaired glucose tolerance that has been reported for this same cohort of 4-month-old OE-NPYDβH mice.20 In agreement with this finding, OE-NPYDβH mice responded to chronic CB1 blockage by AM251 with trends toward reduced fat mass and improved glucose tolerance. The gene discussed is CNR1; the disease is Impaired glucose tolerance.