لخّصلي

Nutrigenetics, which is a branch of nutritional genomics, focuses on the role of genetic susceptibility to diseases as well as on the link between genetic variants and response to diet [85,86].Moreover, the deleterious effect of CLOCK 3111T > C on waist circumference was only found with high saturated fatty acid intakes (>11.8%) [71].The interplay between gene variants in circadian machinery and diet demonstrated by some intervention studies described above may help to design effective, personalized nutritional strategies based on the identification of specific allele carriers.The CC carriers of CRY1 rs2287161 that ate high amounts of carbohydrates showed higher insulin resistance when compared to G carriers whose values of model assessment of insulin resistance (HOMA-IR) were independent of carbohydrate intake, remaining constant [87].The authors suggested that the additive effect of SIRT1 and CLOCK variants on resistance to weight loss could be related to the chronotype of the subject, higher plasma levels of ghrelin, and less adherence to Mediterranean diet patterns.An association between this variant combined with other SNPs in linkage disequilibrium (i.e., rs1801260, rs3736544, rs4864548 and rs3749474) and lower hyperglycemia and decreased risk of T2DM has also been reported [71,88].CRY1 rs2287161 represents an example of gene-diet interaction for insulin resistance in Mediterranean and North American populations [87].

Nutrigenetics, which is a branch of nutritional genomics, focuses on the role of genetic susceptibility to diseases as well as on the link between genetic variants and response to diet [85,86]. In the era of nutrigenetic research, the relationship between circadian system gene variants and the effectiveness of dietary intervention is noteworthy (Table 1). CRY1 rs2287161 represents an example of gene–diet interaction for insulin resistance in Mediterranean and North American populations [87]. The CC carriers of CRY1 rs2287161 that ate high amounts of carbohydrates showed higher insulin resistance when compared to G carriers whose values of model assessment of insulin resistance (HOMA-IR) were independent of carbohydrate intake, remaining constant [87]. Moreover, other gene–diet interactions associated with MetS at the CLOCK locus have been demonstrated. A protective effect of minor allele CLOCK-rs4580704 on insulin sensitivity [71] has been shown when MUFA intake was >13.2% of energy. An association between this variant combined with other SNPs in linkage disequilibrium (i.e., rs1801260, rs3736544, rs4864548 and rs3749474) and lower hyperglycemia and decreased risk of T2DM has also been reported [71,88].
Several studies suggested the association between CLOCK 3111T > C (rs1801260) and weight loss effectiveness [74,83,89] showing C carriers to be more resistant to weight loss than TT homozygotes during an energy-restricted diet [89]. In addition, the SIRT1 rs1467568 and CLOCK 3111T > C combined genotype was associated with the evening chronotype and weight loss resistance in a behavioral therapy treatment for obesity [90]. The authors suggested that the additive effect of SIRT1 and CLOCK variants on resistance to weight loss could be related to the chronotype of the subject, higher plasma levels of ghrelin, and less adherence to Mediterranean diet patterns. Moreover, the deleterious effect of CLOCK 3111T > C on waist circumference was only found with high saturated fatty acid intakes (>11.8%) [71]. Regarding the interaction between CLOCK 3111T/C and emotional eating behaviors to modulate total weight loss in overweight and obese subjects, López-Guimerà et al. [91] showed that minor C allele carriers with a high emotional score lost significantly less weight than those C carriers with a low emotional score.
These results are encouraging, since by changing our eating habits it is possible to reduce or even eliminate the deleterious effect induced by a specific allele risk. The interplay between gene variants in circadian machinery and diet demonstrated by some intervention studies described above may help to design effective, personalized nutritional strategies based on the identification of specific allele carriers. Further research is required to optimize the individual’s response to the dietary interventions.