Thus, the hypermetabolic state (manifested by complete β-oxidation in skeletal muscle, increased brown adipogenesis in brown and white adipose depots, and increased sympathetic tone to adipose tissue), appears to offset the negative effect of hyperphagia in young Cc2−/− males and maintain them insulin-sensitive until 8–9 months of age when they become hypometabolic exhibiting lower spontaneous physical activity than their wild-type counterparts and developing systemic insulin resistance [14,16]. The gene discussed is INS; the disease is Insulin resistance.