Mouse Clock gene was identified in 1997 [63, 64]. Recent progress in our understanding of energy homeostasis may provide further information about how the Clock genetic variations confer obesity. A recent report from Turek et al., suggests that mutated Clock mice exhibited a near total loss of selective nocturnal feeding, consuming close to 50% of their daily food intake during the light phase. These mice are hyperphagic and develop obesity. The resultant obesity is associated with increases in blood glucose, cholesterol, and triglyceride levels, as observed in obese humans with the metabolic syndrome [65]. The obese phenotype of Clock mutant mice arises from loss of circadian rhythm is an important finding. This observation is compatible with the tight coupling between circadian clock and the patterns of feeding and physical activity. Master clock-controlled rhythms have been shown for blood glucose, glucose tolerance, and plasma leptin levels. Thus, it seems possible that other metabolism-related functions are also subject to regulation by the SCN or peripheral clocks [62]. Fluctuations in body weight have been associated with changes in day length in various species
