Together with previous molecular and cellular analyses on glucose uptake, glucose metabolism, and calcium responses in pancreatic islets, these data establish that the insulin secretory process is normal in p-KO mice and that impaired insulin response in vivo and glucose intolerance in the absence of insulin resistance are unlikely to be caused by intrinsic β-cell secretory defects or altered islet distribution. The gene discussed is INS; the disease is Glucose intolerance.