CRY1 circadian gene variant interacts with carbohydrate intake for insulin resistance in two independent populations: Mediterranean and North American. (June 2014)

• Record Type: Journal Article
• Authors: Dashti, Hassan S.; Smith, Caren E.; Lee, Yu-Chi; Parnell, Laurence D.; Lai, Chao-Qiang; Arnett, Donna K.; Ordovás, José M.; Garaulet, Marta
• Is Part Of: Chronobiology international. Volume 31:Number 5(2014)
• Page Start: 660
• Page End: 667
• Publication Date: 2014-06
• Subjects: Chronobiology -- Periodicals; Biological rhythms -- Periodicals; Circadian rhythms -- Periodicals; 571.77
• DOI: 10.3109/07420528.2014.886587
• Languages: English
• ISSNs: 0742-0528

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>Dysregulation in the circadian system induced by variants of clock genes has been associated with type 2 diabetes. Evidence for the role of cryptochromes, core components of the system, in regulating glucose homeostasis is not supported by <italic>CRY1</italic> candidate gene association studies for diabetes and insulin resistance in human, suggesting possible dietary influences. The purpose of this study was to test for interactions between a <italic>CRY1</italic> polymorphism, rs2287161, and carbohydrate intake on insulin resistance in two independent populations: a Mediterranean (<italic>n</italic> = 728) and an European origin North American population (<italic>n</italic> = 820). Linear regression interaction models were performed in two populations to test for gene–diet interactions on fasting insulin and glucose and two insulin-related traits, homeostasis model assessment of insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI). In addition, fixed effects meta-analyses for these interactions were performed. Cohort-specific interaction analyses showed significant interactions between the <italic>CRY1</italic> variant and dietary carbohydrates for insulin resistance in both populations (<italic>p</italic> < 0.05). Findings from the meta-analyses of carbohydrate–single nucleotide polymorphism interactions indicated that an increase in carbohydrate intake (% of energy intake) was associated with a significant increase in HOMA-IR (<italic>p</italic> = 0.011), fasting insulin (<italic>p</italic> = 0.007) and a decrease in QUICKI (<italic>p</italic> = 0.028), only among individuals homozygous for the minor C allele. This novel finding supports the link between the circadian system and glucose metabolism and suggests the importance this <italic>CRY1</italic> locus in developing personalized nutrition programs aimed at reducing insulin resistance and diabetes risk.</p> </abstract>