Importantly, Nnat gene deletion in pancreatic β cells was shown to disrupt glucose-stimulated insulin secretion in β-cell-specific knockout mice [74], which reported that these animals exhibited glucose intolerance in a nutrient-rich environment, despite normal food intake and body weight, which suggests that Nnat serves a critical role in β-cell physiology, rather than in systemic energy balance [74]. This evidence concerns the gene INS and Glucose intolerance.