As reported previously, transgenic mice overexpressing human FFAR1 (hFFAR1) in pancreatic β cells exhibit improved glucose excursion and increased insulin secretion during the oral glucose tolerance test (OGTT) and develop resistance to high-fat diet-induced glucose intolerance [3], whereas FFAR1-deficient mice show impaired or unaffected GSIS [4], [5] and absence of insulin and incretin secretion in response to FFAs [6]. Here, INS is linked to Glucose intolerance.