Therefore, AdipoR stimulation can be suggested as the replacement therapy of adiponectin against the NIDDM because an adiponectin-like therapeutic agent, AdipoRon (2-(4-benzoylphenoxy)-N-[1-(phenylmethyl)-4-piperidinyl]acetamide) (Fig. 1a), an orally active synthetic small-molecule AdipoR agonist, showed in vivo evidence that impaired glucose tolerance and insulin resistance in db/db mice with reduced high-fat diet-induced adiponectin secretion was improved by AdipoRon (50 mg/kg)7. This evidence concerns the gene ADIPOQ and Impaired glucose tolerance.