G allele at RAGE SNP82 is associated with proinflammatory markers in obese subjects

Oh Yoen Kim, Seog Hyun Jo, Yangsoo Jang, Jey Sook Chae, Ji Young Kim, Yae Jung Hyun, Jong Ho Lee

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Abstract

Obesity is closely associated with low-grade inflammation. The Gly82Ser (G82S) polymorphism in the receptor for the advanced glycation end products (RAGE) gene related to RAGE expression is also involved in inflammatory response. We examined the association between RAGEG82S and obesity on soluble RAGE (sRAGE) and inflammatory markers in Korean men. The following were measured: anthropometric and biochemical parameters, RAGEG82S polymorphism, sRAGE, advanced glycation end products (AGEs), and inflammatory markers in men (n = 1252; range, 30-70 years; body mass index [BMI], ≥18.5 kg/m2). Allele frequencies satisfied Hardy-Weinberg Equilibrium (G/G: 72.2%, G/S: 25.5%, S/S: 2.3%). RAGEG82S (β-coefficient = -0.384, P < .001) and BMI (β-coefficient = -0.168, P = .001) were major factors affecting sRAGE concentrations. In all subjects, those with 'S/S' homozygotes showed the lowest levels of sRAGE (G/G: 1036.3 ± 40.3, G/S: 807.0 ± 49.6, S/S: 443.0 ± 47.8 pg/mL) before (P < .001) and after adjusted for age, BMI, cigarette smoking, and alcohol drinking (P < .001). When subdivided according to BMI of 25 kg/m2 (Asian Pacific guideline), obese subjects (BMI ≥25 kg/m2) had significantly lower levels of sRAGE (831.7 ± 36.7 vs 1022.7 ± 47.8 pg/mL, P = .009) and higher levels of high sensitivity C-reactive protein (hs-CRP) (1.10 ± 0.07 vs 0.72 ± 0.05 mg/dL, P < .001) compared with nonobese subjects (BMI <25 kg/m2). Particularly in obese subjects, S/S carriers showed significantly higher concentrations of AGEs (P = .012) and hs-CRP (P = .006) than G allele carriers, whereas nonobese people had no significant RAGEG82S-related differences in AGEs (P = .743) and hs-CRP (P = .436). In conclusion, G allele at RAGEG82S may be more associated with inflammatory markers under obese status than nonobese conditions. In this case, it may help to suggest proper dietary modification for controlling obesity to people with genetic variants.

Original languageEnglish
Pages (from-to)106-113
Number of pages8
JournalNutrition Research
Volume29
Issue number2
DOIs
Publication statusPublished - 2009 Feb 1

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Body Mass Index
Alleles
C-Reactive Protein
Obesity
Diet Therapy
Advanced Glycosylation End Products
Homozygote
Gene Frequency
Alcohol Drinking
Advanced Glycosylation End Product-Specific Receptor
Smoking
Guidelines
Inflammation
Genes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

Cite this

Kim, Oh Yoen ; Jo, Seog Hyun ; Jang, Yangsoo ; Chae, Jey Sook ; Kim, Ji Young ; Hyun, Yae Jung ; Lee, Jong Ho. / G allele at RAGE SNP82 is associated with proinflammatory markers in obese subjects. In: Nutrition Research. 2009 ; Vol. 29, No. 2. pp. 106-113.
@article{e467dcecb30c4179a38d235ab8138be2,
title = "G allele at RAGE SNP82 is associated with proinflammatory markers in obese subjects",
abstract = "Obesity is closely associated with low-grade inflammation. The Gly82Ser (G82S) polymorphism in the receptor for the advanced glycation end products (RAGE) gene related to RAGE expression is also involved in inflammatory response. We examined the association between RAGEG82S and obesity on soluble RAGE (sRAGE) and inflammatory markers in Korean men. The following were measured: anthropometric and biochemical parameters, RAGEG82S polymorphism, sRAGE, advanced glycation end products (AGEs), and inflammatory markers in men (n = 1252; range, 30-70 years; body mass index [BMI], ≥18.5 kg/m2). Allele frequencies satisfied Hardy-Weinberg Equilibrium (G/G: 72.2{\%}, G/S: 25.5{\%}, S/S: 2.3{\%}). RAGEG82S (β-coefficient = -0.384, P < .001) and BMI (β-coefficient = -0.168, P = .001) were major factors affecting sRAGE concentrations. In all subjects, those with 'S/S' homozygotes showed the lowest levels of sRAGE (G/G: 1036.3 ± 40.3, G/S: 807.0 ± 49.6, S/S: 443.0 ± 47.8 pg/mL) before (P < .001) and after adjusted for age, BMI, cigarette smoking, and alcohol drinking (P < .001). When subdivided according to BMI of 25 kg/m2 (Asian Pacific guideline), obese subjects (BMI ≥25 kg/m2) had significantly lower levels of sRAGE (831.7 ± 36.7 vs 1022.7 ± 47.8 pg/mL, P = .009) and higher levels of high sensitivity C-reactive protein (hs-CRP) (1.10 ± 0.07 vs 0.72 ± 0.05 mg/dL, P < .001) compared with nonobese subjects (BMI <25 kg/m2). Particularly in obese subjects, S/S carriers showed significantly higher concentrations of AGEs (P = .012) and hs-CRP (P = .006) than G allele carriers, whereas nonobese people had no significant RAGEG82S-related differences in AGEs (P = .743) and hs-CRP (P = .436). In conclusion, G allele at RAGEG82S may be more associated with inflammatory markers under obese status than nonobese conditions. In this case, it may help to suggest proper dietary modification for controlling obesity to people with genetic variants.",
author = "Kim, {Oh Yoen} and Jo, {Seog Hyun} and Yangsoo Jang and Chae, {Jey Sook} and Kim, {Ji Young} and Hyun, {Yae Jung} and Lee, {Jong Ho}",
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G allele at RAGE SNP82 is associated with proinflammatory markers in obese subjects. / Kim, Oh Yoen; Jo, Seog Hyun; Jang, Yangsoo; Chae, Jey Sook; Kim, Ji Young; Hyun, Yae Jung; Lee, Jong Ho.

In: Nutrition Research, Vol. 29, No. 2, 01.02.2009, p. 106-113.

Research output: Contribution to journalArticle

TY - JOUR

T1 - G allele at RAGE SNP82 is associated with proinflammatory markers in obese subjects

AU - Kim, Oh Yoen

AU - Jo, Seog Hyun

AU - Jang, Yangsoo

AU - Chae, Jey Sook

AU - Kim, Ji Young

AU - Hyun, Yae Jung

AU - Lee, Jong Ho

PY - 2009/2/1

Y1 - 2009/2/1

N2 - Obesity is closely associated with low-grade inflammation. The Gly82Ser (G82S) polymorphism in the receptor for the advanced glycation end products (RAGE) gene related to RAGE expression is also involved in inflammatory response. We examined the association between RAGEG82S and obesity on soluble RAGE (sRAGE) and inflammatory markers in Korean men. The following were measured: anthropometric and biochemical parameters, RAGEG82S polymorphism, sRAGE, advanced glycation end products (AGEs), and inflammatory markers in men (n = 1252; range, 30-70 years; body mass index [BMI], ≥18.5 kg/m2). Allele frequencies satisfied Hardy-Weinberg Equilibrium (G/G: 72.2%, G/S: 25.5%, S/S: 2.3%). RAGEG82S (β-coefficient = -0.384, P < .001) and BMI (β-coefficient = -0.168, P = .001) were major factors affecting sRAGE concentrations. In all subjects, those with 'S/S' homozygotes showed the lowest levels of sRAGE (G/G: 1036.3 ± 40.3, G/S: 807.0 ± 49.6, S/S: 443.0 ± 47.8 pg/mL) before (P < .001) and after adjusted for age, BMI, cigarette smoking, and alcohol drinking (P < .001). When subdivided according to BMI of 25 kg/m2 (Asian Pacific guideline), obese subjects (BMI ≥25 kg/m2) had significantly lower levels of sRAGE (831.7 ± 36.7 vs 1022.7 ± 47.8 pg/mL, P = .009) and higher levels of high sensitivity C-reactive protein (hs-CRP) (1.10 ± 0.07 vs 0.72 ± 0.05 mg/dL, P < .001) compared with nonobese subjects (BMI <25 kg/m2). Particularly in obese subjects, S/S carriers showed significantly higher concentrations of AGEs (P = .012) and hs-CRP (P = .006) than G allele carriers, whereas nonobese people had no significant RAGEG82S-related differences in AGEs (P = .743) and hs-CRP (P = .436). In conclusion, G allele at RAGEG82S may be more associated with inflammatory markers under obese status than nonobese conditions. In this case, it may help to suggest proper dietary modification for controlling obesity to people with genetic variants.

AB - Obesity is closely associated with low-grade inflammation. The Gly82Ser (G82S) polymorphism in the receptor for the advanced glycation end products (RAGE) gene related to RAGE expression is also involved in inflammatory response. We examined the association between RAGEG82S and obesity on soluble RAGE (sRAGE) and inflammatory markers in Korean men. The following were measured: anthropometric and biochemical parameters, RAGEG82S polymorphism, sRAGE, advanced glycation end products (AGEs), and inflammatory markers in men (n = 1252; range, 30-70 years; body mass index [BMI], ≥18.5 kg/m2). Allele frequencies satisfied Hardy-Weinberg Equilibrium (G/G: 72.2%, G/S: 25.5%, S/S: 2.3%). RAGEG82S (β-coefficient = -0.384, P < .001) and BMI (β-coefficient = -0.168, P = .001) were major factors affecting sRAGE concentrations. In all subjects, those with 'S/S' homozygotes showed the lowest levels of sRAGE (G/G: 1036.3 ± 40.3, G/S: 807.0 ± 49.6, S/S: 443.0 ± 47.8 pg/mL) before (P < .001) and after adjusted for age, BMI, cigarette smoking, and alcohol drinking (P < .001). When subdivided according to BMI of 25 kg/m2 (Asian Pacific guideline), obese subjects (BMI ≥25 kg/m2) had significantly lower levels of sRAGE (831.7 ± 36.7 vs 1022.7 ± 47.8 pg/mL, P = .009) and higher levels of high sensitivity C-reactive protein (hs-CRP) (1.10 ± 0.07 vs 0.72 ± 0.05 mg/dL, P < .001) compared with nonobese subjects (BMI <25 kg/m2). Particularly in obese subjects, S/S carriers showed significantly higher concentrations of AGEs (P = .012) and hs-CRP (P = .006) than G allele carriers, whereas nonobese people had no significant RAGEG82S-related differences in AGEs (P = .743) and hs-CRP (P = .436). In conclusion, G allele at RAGEG82S may be more associated with inflammatory markers under obese status than nonobese conditions. In this case, it may help to suggest proper dietary modification for controlling obesity to people with genetic variants.

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