While the purpose of our current study is not to develop novel antidiabetic drugs, GPR92 in IMs could potentially be targeted to transactivate β cell function as a proficient therapeutic strategy to avert the damage caused by islet inflammation — which is caused by diet-induced obesity — and to regulate β cell-mediated insulin secretion in patients with T2D. Here, LPAR5 is linked to obesity due to melanocortin 4 receptor deficiency.