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Figure 5.3 Examples of metabolic consequences resulting from impairments of specific
circadian clocks in rodents. SCN, suprachiasmatic nuclei.
In humans, polymorphisms in some clock genes have been correlated
with metabolic risks. For instance, two Bmal1 haplotypes are linked with
type 2 diabetes and hypertension. Polymorphisms in Clock or Rev - erba
are significantly associated with high-fat mass. 120,121
Light being the most potent synchronizer for the master clock, it is not
surprising that changes in lighting conditions markedly affect circadian
timing, and possibly energy metabolism. The photoperiod (i.e., the relative
duration of the light period per 24 h) is perceived by the retina and inte-
grated by the suprachiasmatic clock. Natural fluctuations in food intake,
body mass, and adiposity occur recurrently according to seasons in
so-photoperiodic species, whose physiology is specifically regulated on a
seasonal basis. 122 In these cases, photoperiodic information is translated into
neuroendocrine changes via the nocturnal secretion of melatonin by the
pineal gland. 123 In rats, whose reproduction is not photoperiod-dependent,
free access to sucrose and imposed high-fat feeding do not have the same
obesogenic effects depending on the photoperiod. Exposure to short pho-
toperiod (shorter day and longer night) compared to long photoperiod (lon-
ger day and shorter night) stimulates spontaneous ingestion of sucrose and
promotes fat accretion, suggesting that the photoperiodic environment
can modulate metabolic responses. 124 Another important parameter of light-
ing conditions is the light intensity during the periods of wake and sleep. For
example, in spite of nondifferent levels of caloric intake and daily motor
activity, mice exposed to dim light at night consume relatively more food
 
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