Adrenal insufficiency is a rare disorder of adrenal glands that are unable to produce enough cortisol (glucocorticoid) from the adrenal cortex. Cholesterol is converting into cortisol during the adrenal steroidogenesis process. Deficiency or lack of enzymes required to synthesize the cortisol leads to adrenal insufficiency and its main cause is congenital adrenal hyperplasia. Transgenic, knockout mice and rat models like (targeted disruption of the mouse gene encoding StAR protein provides insights into congenital lipoid adrenal hyperplasia, Cyp11b1 Null Mouse, a Model of Congenital Adrenal Hyperplasia, inducing Congenital Lipoidal Adrenal Hyperplasia by Inhibition of cholesterol side chain cleavage, inhibition of 3 β-Hydroxysteroid dehydrogenase by Estradiol-17 β and inducing congenital adrenocortical hyperplasia in rats, Chronic stress induces adrenal hyperplasia and hypertrophy in rats and constitutive β-catenin activation induces adrenal hyperplasia) are expensive. This study focused on inducing the adrenal insufficiency in the Wistar rats by metyrapone, which blocks the enzyme 11β- hydroxylase essential for cortisol synthesis. Metyrapone at three different doses were selected (100, 150, 200 mg/kg) and administered for 28 days and assessed the cortisol and locomotor scores on day 0, 7, 14, 21 and 28 respectively. Results indicates decreased cortisol and reduced locomotor scores. Results indicates adrenal insufficiency was developed in Wistar albino rats. Hence it is simple and cost effective model to induce adrenal insufficiency for day to day screening of animal activity.