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A common polymorphism near the interleukin-6 gene modifies the association between dietary fat intake and insulin sensitivity.

Cuda C, Garcia-Bailo B, Karmali M, El-Sohemy A, Badawi A - J Inflamm Res (2012)

Bottom Line: The single nucleotide polymorphism was not associated with any of the measures of insulin sensitivity.There was an inverse relationship between total fat intake and HOMA-IR in individuals who were homozygous for the A allele (β = -0.012 ± 0.006, P = 0.047).These findings suggest that dietary fat influences insulin sensitivity differently depending on genotype.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.

ABSTRACT

Background: Increasing evidence suggests a role for inflammation in the development of type 2 diabetes. Elevated levels of inflammatory cytokines, including interleukin-6, have been associated with insulin resistance, and dietary lipids can increase cytokine production. The objective of this study was to determine whether a single nucleotide polymorphism near the IL6 gene (rs7801406) modifies the relationship between dietary fat and markers of insulin sensitivity.

Methods: Subjects were healthy men and women aged 20-29 years from the Toronto Nutrigenomics and Health Study. Dietary intake was estimated using a one-month semiquantitative food frequency questionnaire. Fasting blood samples were taken for genotyping and biomarker measurement.

Results: The single nucleotide polymorphism was not associated with any of the measures of insulin sensitivity. However, it modified the relationship between total dietary fat and the homeostasis model assessment of insulin resistance (P = 0.053 for interaction). Total fat intake was positively related to HOMA-IR in individuals homozygous for the G allele (β = 0.005 ± 0.002, P = 0.03), but not among heterozygotes. There was an inverse relationship between total fat intake and HOMA-IR in individuals who were homozygous for the A allele (β = -0.012 ± 0.006, P = 0.047).

Conclusion: These findings suggest that dietary fat influences insulin sensitivity differently depending on genotype.

No MeSH data available.


Related in: MedlinePlus

Interaction between dietary fat, the rs7801406 polymorphism, and HOMAIR levels.Notes: Values are means ± standard error of the mean adjusted for total: HDL cholesterol ratio, plasma triglycerides, waist circumference, and ethnocultural group. Dietary fat was inversely related to HOMA-IR in A/A carriers (β = −0.012 ± 0.006, P = 0.047) and positively among G/G homozygotes (β = 0.005 ± 0.002, P = 0.03). This relationship (in the G/G carriers) was significantly different from the A/A homozygotes (P = 0.02).Abbreviations: HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment of insulin resistance.
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f1-jir-5-001: Interaction between dietary fat, the rs7801406 polymorphism, and HOMAIR levels.Notes: Values are means ± standard error of the mean adjusted for total: HDL cholesterol ratio, plasma triglycerides, waist circumference, and ethnocultural group. Dietary fat was inversely related to HOMA-IR in A/A carriers (β = −0.012 ± 0.006, P = 0.047) and positively among G/G homozygotes (β = 0.005 ± 0.002, P = 0.03). This relationship (in the G/G carriers) was significantly different from the A/A homozygotes (P = 0.02).Abbreviations: HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment of insulin resistance.

Mentions: We evaluated whether the rs7801406 polymorphism modifies the association between dietary fat and biomarkers of insulin sensitivity (HOMA-IR and serum insulin levels). A significant interaction was found between the genotypes and total dietary fat on serum insulin (P = 0.02, adjusted for waist circumference, triglycerides, ethnicity, and serum glucose) and HOMA-IR (P = 0.053, adjusted for waist circumference, ethnicity, triglycerides, and total cholesterol:HDL-cholesterol). Dietary fat intake was inversely related to HOMA-IR in individuals homozygous for the A allele (β = −0.012 ± 0.006, P = 0.047); however, a positive relationship was found among G/G homozygotes (β = 0.005 ± 0.002, P = 0.03, Figure 1). The association between dietary fat and HOMA-IR in the G/G homozygotes was significantly different from the A/A homozygotes (P = 0.02), but not the heterozygotes (P = 0.78). However, the relationship in A/A homozygotes differed significantly from that in the heterozygotes (P = 0.03). Furthermore, the relationship between dietary total fat intake and HOMA-IR was not significant among heterozygotes (β = 0.005 ± 0.093, P = 0.51) and the slope of this relationship did not differ significantly from the other genotype groups. No interactions were observed with any of the other covariates in the model.


A common polymorphism near the interleukin-6 gene modifies the association between dietary fat intake and insulin sensitivity.

Cuda C, Garcia-Bailo B, Karmali M, El-Sohemy A, Badawi A - J Inflamm Res (2012)

Interaction between dietary fat, the rs7801406 polymorphism, and HOMAIR levels.Notes: Values are means ± standard error of the mean adjusted for total: HDL cholesterol ratio, plasma triglycerides, waist circumference, and ethnocultural group. Dietary fat was inversely related to HOMA-IR in A/A carriers (β = −0.012 ± 0.006, P = 0.047) and positively among G/G homozygotes (β = 0.005 ± 0.002, P = 0.03). This relationship (in the G/G carriers) was significantly different from the A/A homozygotes (P = 0.02).Abbreviations: HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment of insulin resistance.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3278256&req=5

f1-jir-5-001: Interaction between dietary fat, the rs7801406 polymorphism, and HOMAIR levels.Notes: Values are means ± standard error of the mean adjusted for total: HDL cholesterol ratio, plasma triglycerides, waist circumference, and ethnocultural group. Dietary fat was inversely related to HOMA-IR in A/A carriers (β = −0.012 ± 0.006, P = 0.047) and positively among G/G homozygotes (β = 0.005 ± 0.002, P = 0.03). This relationship (in the G/G carriers) was significantly different from the A/A homozygotes (P = 0.02).Abbreviations: HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment of insulin resistance.
Mentions: We evaluated whether the rs7801406 polymorphism modifies the association between dietary fat and biomarkers of insulin sensitivity (HOMA-IR and serum insulin levels). A significant interaction was found between the genotypes and total dietary fat on serum insulin (P = 0.02, adjusted for waist circumference, triglycerides, ethnicity, and serum glucose) and HOMA-IR (P = 0.053, adjusted for waist circumference, ethnicity, triglycerides, and total cholesterol:HDL-cholesterol). Dietary fat intake was inversely related to HOMA-IR in individuals homozygous for the A allele (β = −0.012 ± 0.006, P = 0.047); however, a positive relationship was found among G/G homozygotes (β = 0.005 ± 0.002, P = 0.03, Figure 1). The association between dietary fat and HOMA-IR in the G/G homozygotes was significantly different from the A/A homozygotes (P = 0.02), but not the heterozygotes (P = 0.78). However, the relationship in A/A homozygotes differed significantly from that in the heterozygotes (P = 0.03). Furthermore, the relationship between dietary total fat intake and HOMA-IR was not significant among heterozygotes (β = 0.005 ± 0.093, P = 0.51) and the slope of this relationship did not differ significantly from the other genotype groups. No interactions were observed with any of the other covariates in the model.

Bottom Line: The single nucleotide polymorphism was not associated with any of the measures of insulin sensitivity.There was an inverse relationship between total fat intake and HOMA-IR in individuals who were homozygous for the A allele (β = -0.012 ± 0.006, P = 0.047).These findings suggest that dietary fat influences insulin sensitivity differently depending on genotype.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.

ABSTRACT

Background: Increasing evidence suggests a role for inflammation in the development of type 2 diabetes. Elevated levels of inflammatory cytokines, including interleukin-6, have been associated with insulin resistance, and dietary lipids can increase cytokine production. The objective of this study was to determine whether a single nucleotide polymorphism near the IL6 gene (rs7801406) modifies the relationship between dietary fat and markers of insulin sensitivity.

Methods: Subjects were healthy men and women aged 20-29 years from the Toronto Nutrigenomics and Health Study. Dietary intake was estimated using a one-month semiquantitative food frequency questionnaire. Fasting blood samples were taken for genotyping and biomarker measurement.

Results: The single nucleotide polymorphism was not associated with any of the measures of insulin sensitivity. However, it modified the relationship between total dietary fat and the homeostasis model assessment of insulin resistance (P = 0.053 for interaction). Total fat intake was positively related to HOMA-IR in individuals homozygous for the G allele (β = 0.005 ± 0.002, P = 0.03), but not among heterozygotes. There was an inverse relationship between total fat intake and HOMA-IR in individuals who were homozygous for the A allele (β = -0.012 ± 0.006, P = 0.047).

Conclusion: These findings suggest that dietary fat influences insulin sensitivity differently depending on genotype.

No MeSH data available.


Related in: MedlinePlus