SCN lesions in rats have been shown to abolish the daily rhythms in plasma concentrations of glucose and insulin (Yamamoto et al., 1987; la Fleur et al., 1999), and genetic disruption of clock genes in mice, such as in Clock (Rudic et al., 2004; Turek et al., 2005; Marcheva et al., 2010) and Bmal1 (Rudic et al., 2004; Marcheva et al., 2010) mutant mice, cause hyperglycemia, hypoinsulinemia, and altered adipogenesis and hepatic carbohydrate metabolism. The gene discussed is CLOCK; the disease is Hyperglycemia.