Insulin enhances glucose disposal, storage and oxidation in muscles. It control the metabolites required in the muscle and is involved in maintaining glucose homeostasis. Insulin is considered to be an anabolic hormone in that it promotes the synthesis of protein and glycogen and it inhibits the degradation of these compounds in muscle tissue. Glucose normally provides energy sources for tissues of the body, its uptake by muscle requires a secretion of insulin. The initial step of glucose utilization requires the transport of glucose into the cells. The transport across certain cell membranes such as muscle is regulated by insulin. The insulin-receptor complex stimulates the cellular uptake of glucose. Insulin stimulates the uptake of amino acids into cells and simulates protein synthesis in muscle tissue. With insulin deficiency, amino acids are mobilized from muscle and transported to the liver. Physiological increase in insulin suppresses lypolysis in skeletal muscle but in supra-physiological increases this suppression of intramuscular lypolysis is inadequate, resulting in increased availability of nonestrified fatty acids which can represent a potential mechanism involved in insulin resistance in muscle. Patients with diabetes mellitus are characterized by insulin deficiency (type 1) or peripheral insulin resistance (type 2) demonstrated by decreased insulin action on glucose utilization in muscle. Muscle tissue has been considered to be a major regulator of systemic glucose homeostasis.