These relationships led us to the hypothesis that HE3286 decreased HbA1c in patients with higher obesity (BMI), in conjunction with improved pancreatic beta cell function and decreased fasting glucose, that, for placebo patients, HbA1c change and Hb CV were related to inflammation status (MCP-1), and that weight loss in placebos might be related to inflammation effects on malnutrition. The gene discussed is CCL2; the disease is obesity due to melanocortin 4 receptor deficiency.