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

Hassan S. Dashti; Caren E. Smith; Yu Chi Lee; Laurence D. Parnell; Chao Qiang Lai; Donna K. Arnett; José M. Ordovás; Marta Garaulet

doi:10.3109/07420528.2014.886587

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

Hassan S. Dashti
, Caren E. Smith
, Yu Chi Lee
, Laurence D. Parnell
, Chao Qiang Lai
, Donna K. Arnett
, José M. Ordovás
, Marta Garaulet

Producción científica: Article › revisión exhaustiva

63 Citas (Scopus)

Resumen

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 CRY1 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 CRY1 polymorphism, rs2287161, and carbohydrate intake on insulin resistance in two independent populations: a Mediterranean (n = 728) and an European origin North American population (n = 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 CRY1 variant and dietary carbohydrates for insulin resistance in both populations (p < 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 (p = 0.011), fasting insulin (p = 0.007) and a decrease in QUICKI (p = 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 CRY1 locus in developing personalized nutrition programs aimed at reducing insulin resistance and diabetes risk.

Idioma original	English
Páginas (desde-hasta)	660-667
Número de páginas	8
Publicación	Chronobiology International
Volumen	31
N.º	5
DOI	https://doi.org/10.3109/07420528.2014.886587
Estado	Published - jun 2014

Nota bibliográfica

Funding Information:
The study sample consisted of 820 (50.5%) women (age: mean = 48.3 years, SD = 15.9 years; BMI: mean = 28.5 kg/m2, SD = 5.5 kg/m2) who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. GOLDN is part of the Program for Genetic Interactions Network and is funded by the NIH through the University of Alabama at Birmingham and in collaboration with the University of Utah, Washington University, Tufts University, University of Texas, University of Michigan, University of Minnesota and Fairview University of Minnesota Medical Center. The majority of participants were re-recruited from three-generational pedigrees from two National Heart, Lung and Blood Institute Family Heart Study field centers (Minneapolis, MN and Salt Lake City, UT) (Higgins et al., 1996). Nearly all individuals were of European descent. The details of the study are available at https:// dsgweb.wustl.edu/goldn/. The protocol was previously approved by the institutional review boards at each of the above-referenced institutions.

Funding Information:
The authors declare no conflict of interest. This study was supported by grants from Tomás Pascual and Pilar Gómez-Cuétara Foundations, Spanish Government of Science and Innovation (BFU2011-24720), Séneca Foundation from the Government of Murcia (15123/ PI/10). National Heart, Lung, and Blood Institute grants HL-54776, National Institute of Diabetes and Digestive and Kidney Diseases, Grant Number DK075030 and by contracts 53-K06-5-10 and 58-1950-9-001 from the US Department of Agriculture Research. C. Smith is supported by K08 HL112845.

Financiación

The study sample consisted of 820 (50.5%) women (age: mean = 48.3 years, SD = 15.9 years; BMI: mean = 28.5 kg/m2, SD = 5.5 kg/m2) who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. GOLDN is part of the Program for Genetic Interactions Network and is funded by the NIH through the University of Alabama at Birmingham and in collaboration with the University of Utah, Washington University, Tufts University, University of Texas, University of Michigan, University of Minnesota and Fairview University of Minnesota Medical Center. The majority of participants were re-recruited from three-generational pedigrees from two National Heart, Lung and Blood Institute Family Heart Study field centers (Minneapolis, MN and Salt Lake City, UT) (Higgins et al., 1996). Nearly all individuals were of European descent. The details of the study are available at https:// dsgweb.wustl.edu/goldn/. The protocol was previously approved by the institutional review boards at each of the above-referenced institutions. The authors declare no conflict of interest. This study was supported by grants from Tomás Pascual and Pilar Gómez-Cuétara Foundations, Spanish Government of Science and Innovation (BFU2011-24720), Séneca Foundation from the Government of Murcia (15123/ PI/10). National Heart, Lung, and Blood Institute grants HL-54776, National Institute of Diabetes and Digestive and Kidney Diseases, Grant Number DK075030 and by contracts 53-K06-5-10 and 58-1950-9-001 from the US Department of Agriculture Research. C. Smith is supported by K08 HL112845.

Financiadores	Número del financiador
Fairview University of Minnesota Medical Center
Government of Murcia	15123/ PI/10
Spanish Government of Science and Innovation	BFU2011-24720
Tomás Pascual and Pilar Gómez-Cuétara Foundations
US Department of Agriculture National Research	K08 HL112845
University of Texas, University of Michigan
National Institutes of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)	HL-54776, P50HL105185
National Institute of Diabetes and Digestive and Kidney Diseases	58-1950-9-001, DK075030, 53-K06-5-10
Minnesota State University-Mankato
University of Utah Health
Fundación Séneca
The George Washington University
Tufts University
University of Alabama, Birmingham

ODS de las Naciones Unidas

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Good health and well being

ASJC Scopus subject areas

Physiology
Physiology (medical)

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10.3109/07420528.2014.886587

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@article{b4bb823c2a0e4da5b7b563ab2aa37cff,

title = "CRY1 circadian gene variant interacts with carbohydrate intake for insulin resistance in two independent populations: Mediterranean and North American",

abstract = "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 CRY1 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 CRY1 polymorphism, rs2287161, and carbohydrate intake on insulin resistance in two independent populations: a Mediterranean (n = 728) and an European origin North American population (n = 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 CRY1 variant and dietary carbohydrates for insulin resistance in both populations (p < 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 (p = 0.011), fasting insulin (p = 0.007) and a decrease in QUICKI (p = 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 CRY1 locus in developing personalized nutrition programs aimed at reducing insulin resistance and diabetes risk.",

keywords = "CRY1, Carbohydrate intake, Diabetes, Gene-diet interaction, Genetic epidemiology",

author = "Dashti, \{Hassan S.\} and Smith, \{Caren E.\} and Lee, \{Yu Chi\} and Parnell, \{Laurence D.\} and Lai, \{Chao Qiang\} and Arnett, \{Donna K.\} and Ordov{\'a}s, \{Jos{\'e} M.\} and Marta Garaulet",

note = "Funding Information: The study sample consisted of 820 (50.5\%) women (age: mean = 48.3 years, SD = 15.9 years; BMI: mean = 28.5 kg/m2, SD = 5.5 kg/m2) who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. GOLDN is part of the Program for Genetic Interactions Network and is funded by the NIH through the University of Alabama at Birmingham and in collaboration with the University of Utah, Washington University, Tufts University, University of Texas, University of Michigan, University of Minnesota and Fairview University of Minnesota Medical Center. The majority of participants were re-recruited from three-generational pedigrees from two National Heart, Lung and Blood Institute Family Heart Study field centers (Minneapolis, MN and Salt Lake City, UT) (Higgins et al., 1996). Nearly all individuals were of European descent. The details of the study are available at https:// dsgweb.wustl.edu/goldn/. The protocol was previously approved by the institutional review boards at each of the above-referenced institutions. Funding Information: The authors declare no conflict of interest. This study was supported by grants from Tom{\'a}s Pascual and Pilar G{\'o}mez-Cu{\'e}tara Foundations, Spanish Government of Science and Innovation (BFU2011-24720), S{\'e}neca Foundation from the Government of Murcia (15123/ PI/10). National Heart, Lung, and Blood Institute grants HL-54776, National Institute of Diabetes and Digestive and Kidney Diseases, Grant Number DK075030 and by contracts 53-K06-5-10 and 58-1950-9-001 from the US Department of Agriculture Research. C. Smith is supported by K08 HL112845.",

year = "2014",

month = jun,

doi = "10.3109/07420528.2014.886587",

language = "English",

volume = "31",

pages = "660--667",

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}

TY - JOUR

T1 - CRY1 circadian gene variant interacts with carbohydrate intake for insulin resistance in two independent populations

T2 - Mediterranean and North American

AU - Dashti, Hassan S.

AU - Smith, Caren E.

AU - Lee, Yu Chi

AU - Parnell, Laurence D.

AU - Lai, Chao Qiang

AU - Arnett, Donna K.

AU - Ordovás, José M.

AU - Garaulet, Marta

N1 - Funding Information: The study sample consisted of 820 (50.5%) women (age: mean = 48.3 years, SD = 15.9 years; BMI: mean = 28.5 kg/m2, SD = 5.5 kg/m2) who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. GOLDN is part of the Program for Genetic Interactions Network and is funded by the NIH through the University of Alabama at Birmingham and in collaboration with the University of Utah, Washington University, Tufts University, University of Texas, University of Michigan, University of Minnesota and Fairview University of Minnesota Medical Center. The majority of participants were re-recruited from three-generational pedigrees from two National Heart, Lung and Blood Institute Family Heart Study field centers (Minneapolis, MN and Salt Lake City, UT) (Higgins et al., 1996). Nearly all individuals were of European descent. The details of the study are available at https:// dsgweb.wustl.edu/goldn/. The protocol was previously approved by the institutional review boards at each of the above-referenced institutions. Funding Information: The authors declare no conflict of interest. This study was supported by grants from Tomás Pascual and Pilar Gómez-Cuétara Foundations, Spanish Government of Science and Innovation (BFU2011-24720), Séneca Foundation from the Government of Murcia (15123/ PI/10). National Heart, Lung, and Blood Institute grants HL-54776, National Institute of Diabetes and Digestive and Kidney Diseases, Grant Number DK075030 and by contracts 53-K06-5-10 and 58-1950-9-001 from the US Department of Agriculture Research. C. Smith is supported by K08 HL112845.

PY - 2014/6

Y1 - 2014/6

N2 - 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 CRY1 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 CRY1 polymorphism, rs2287161, and carbohydrate intake on insulin resistance in two independent populations: a Mediterranean (n = 728) and an European origin North American population (n = 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 CRY1 variant and dietary carbohydrates for insulin resistance in both populations (p < 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 (p = 0.011), fasting insulin (p = 0.007) and a decrease in QUICKI (p = 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 CRY1 locus in developing personalized nutrition programs aimed at reducing insulin resistance and diabetes risk.

AB - 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 CRY1 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 CRY1 polymorphism, rs2287161, and carbohydrate intake on insulin resistance in two independent populations: a Mediterranean (n = 728) and an European origin North American population (n = 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 CRY1 variant and dietary carbohydrates for insulin resistance in both populations (p < 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 (p = 0.011), fasting insulin (p = 0.007) and a decrease in QUICKI (p = 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 CRY1 locus in developing personalized nutrition programs aimed at reducing insulin resistance and diabetes risk.

KW - CRY1

KW - Carbohydrate intake

KW - Diabetes

KW - Gene-diet interaction

KW - Genetic epidemiology

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UR - https://www.scopus.com/pages/publications/84901946805#tab=citedBy

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DO - 10.3109/07420528.2014.886587

M3 - Article

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AN - SCOPUS:84901946805

SN - 0742-0528

VL - 31

SP - 660

EP - 667

JO - Chronobiology International

JF - Chronobiology International

IS - 5

ER -

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

Resumen

Nota bibliográfica

Financiación

ODS de las Naciones Unidas

ASJC Scopus subject areas

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