To address the hypothesis that deletion of PAR2 might ameliorate age-related obesity and impaired glucose homeostasis, we assessed body composition and insulin action in 18-month-old male PAR2 knockout (PAR2KO-AG), age-matched (AG) and young C57BL6 (YG, 6-month-old) mice. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.