GIP receptor agonists are not used as single-target drugs to treat patients with diabetes, because after GIPR is activated, in addition to the lipogenic effect of insulin, GIP can recruit chylomicrons, enhance the activity of lipoprotein lipase, promote the hydrolysis of dietary triglycerides and the release of free fatty acids, and promote lipid storage, thus leading to obesity [7]. Here, INS is linked to obesity due to melanocortin 4 receptor deficiency.