At this time, the ADGRL1-deficient mice and their control group had similar body weights and insulin sensitivity (ADGRL1-deficient mice vs control group: body weight, 26.5 ±1 vs 25.1 ±0.6 g; AUC of blood glucose levels obtained during insulin tolerance test, 966 ± 83.34 vs 884.2 ± 71.48 mmol/l × min, n=11 and 14, respectively), indicating that the fasting hyperinsulinaemia and glucose-stimulated hypersecretion of insulin were consequences of ADGRL1 deficiency and not secondary to obesity or insulin resistance. This evidence concerns the gene ADGRL1 and obesity disorder.