Since elevated Ca2+ entry via Cav1.2 L-type Ca2+ channels plays a major role in the altered detrusor contractions observed under diabetic conditions [21], we have also focused on the role of PKC-mediated extracellular Ca2+ influx through Cav1.2 Ca2+ channels to bladder dysfunction and its relationship with insulin resistance in the high-fat fed obese mice. Here, CACNA1C is linked to Insulin resistance.