Remarkably, the absence of both insulin and leptin receptors in ARH POMC neurons, one of the two key neuronal targets of the metabolic hormones transported by tanycytes, resulted in glucose intolerance, insulin resistance, and heightened glucose-stimulated insulin secretion from pancreatic islets [62], a phenotype similar to that observed in BoNT/BTan mice. The gene discussed is LEPR; the disease is Glucose intolerance.