![]() ![]() The inactivation of Cry genes has no effect on average GH levels (p 0.20 and p 0.15 for control versus Cry / mice in males and females, respectively, Mann-Whitney U test). B, the total amount of GH was quantified from whole pituitary glands of Cry / (open circles) and control (solid circles) males and females. **, p 0.01 between wild type and Cry / males (Dunn's multiple comparison test). The median values of the four groups are significantly different (p 0.05, Kruskal-Wallis test). Individual values outside 90% of the population distributions are plotted as black circles. A, box plots of circulating GH levels measured in trunk blood randomly collected between ZT2 and ZT8 from wild type (WT, solid boxes with median in white, n 30 males and 30 females) and Cry / mice (open boxes with median in black, n 20 males and 30 females) of each sex. We thus conclude that circadian timing, sex dimorphism, and liver metabolism are finely interconnected.Ĭirculating GH levels are altered in Cry / males. Altogether, our observations suggest that the 24-h clock paces the dimorphic ultradian pulsatility of GH that is responsible for sex-dependent liver activity. It is noteworthy that hormonal injections able to mimic male GH pulses reversed the feminized gene expression profile in the liver of Cry1(-/-) Cry2(-/-) males. In addition, body growth of Cry-deficient mice is impaired, also in a sex-biased manner, and this phenotype goes along with an altered pattern of circulating growth hormone (GH) in mutant males, specifically. Indeed, double mutant Cry1(-/-) Cry2(-/-) male mice that lack a functional circadian clock express a number of sex-specific liver products, including several cytochrome P450 enzymes, at levels close to those measured in females. Here we show that dimorphic liver metabolism is altered when the circadian regulators Cryptochromes, Cry1 and Cry2, are inactivated. However, whether the circadian clock itself contributes to sex-biased metabolism has remained unknown, although several daily output parameters differ between sexes in a number of species, including humans. A major example of such sex dimorphism in mouse involves hepatic drug metabolism, which is also a noticeable target of circadian timekeeping. In mammals, males and females exhibit anatomical, hormonal, and metabolic differences.
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