Hexamethonium increased the basal insulin level in both the light and dark periods indicating that under usual conditions the autonomic nervous system functions to suppress the blood insulin level. Either central or peripheral 3-5 injection causes glucopenia and energy deficiency in the brain and consequently is followed by hyperglycemia and increased food intake. Hyperglucagonemia was assumed to be a causative factor of hyperglycemia due to 2-deoxy-D-glucose (2DG). The hyperglucagonemic response was almost the same in both the light and the dark periods, indicating that hyperglucagonemia does not produce the time dependency of hyperglycemic response to 2DG. Frohman et al. suggested that the adrenal medulla plays a major role in suppressing the blood insulin level after 2DG injection. Raghu et al. presented evidence that in dogs, peripheral injections of 2DG enhanced insulin secretion via noncholinergic ganglionic neural stimulation of pancreatic B cells.