Consistent with the idea of divergent outputs for leptin signaling in POMC neurons and with the differences between prenatal and adult-specific suppression of leptin signaling, knockdown of Cacna1e only in arcuate POMC neurons did not alter food intake, leptin suppression of feeding, or body weight but caused defective regulation of HGP and insulin resistance in adult mice. This evidence concerns the gene POMC and Insulin resistance.