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Gender-based differences on the association between salt-sensitive genes and obesity in Korean children aged between 8 and 9 years.

Lee M, Kim MK, Kim SM, Park H, Park CG, Park HK - PLoS ONE (2015)

Bottom Line: High sodium intake is associated with the development of chronic diseases such as obesity.BP, HOMA-IR, LDLc, TG, and the girls' sodium intake significantly increased, but HDLc significantly decreased with increase in BMI.The obesity risk increased with GRK4 A486V, ACE, and SLC12A3 variants in boys, whereas it increased with GRK4 A486V and CYP11B2 variants in girls as sodium intake increased.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition, and Research Institute of Obesity Sciences, Sungshin Women's University, Seoul, Republic of Korea.

ABSTRACT

Background: High sodium intake is associated with the development of chronic diseases such as obesity. Although its role in obesity remains controversial, there may be a correlation between salt sensitivity and the early onset of chronic diseases in obese children.

Methods: In all, 2,163 Korean children (1,106 boys and 1,057 girls) aged 8-9 years were recruited from seven elementary schools in Seoul. To evaluate whether obesity risk was modulated by the salt sensitivity, 11 SNPs related to salt sensitive genes (SSG) became the target of sodium intakes in obese children.

Results: BP, HOMA-IR, LDLc, TG, and the girls' sodium intake significantly increased, but HDLc significantly decreased with increase in BMI. Regardless of sex, the obesity risk was 5.27-fold (CI; 1.320-27.560) higher in the Q2 to Q5 of sodium intake adjusted by energy (4044.9-5058.9 mg/day) than in the lowest Q1 level (2287.6 mg/day) in obese children. BP was sensitively dependent on insulin resistance and lipid accumulation in all subjects; however, sodium intake may be an independent risk factor of obesity without increasing BP in girls. GRK4 A486V mutant homozygote was highly distributed in the obese group, but other SNPs had no impact. The obesity risk increased 7.06, 16.8, and 46.09-fold more in boys with GRK4 A486V, ACE, and SLC12A3 mutants as sodium intake increased. Among girls, the obesity risk increased in GRK4 A486V heterozygote and CYP11β-2 mutant homozygote although sodium intake was relatively lower, implying that ACE, SLC12A, CYP11β-2, and GRK4 A486V polymorphisms showed gender-based differences with regard to interaction between sodium intake and obesity.

Conclusion: A high sodium intake markedly increased the obesity risk in variants of GRK4 A486V regardless of sex. The obesity risk increased with GRK4 A486V, ACE, and SLC12A3 variants in boys, whereas it increased with GRK4 A486V and CYP11B2 variants in girls as sodium intake increased. Obese children with the specific gene variants are recommended to reduce their sodium intake.

No MeSH data available.


Related in: MedlinePlus

Odds ratio (OR) for obesity risk by quintiles of residual-Na were estimated in boys (A) and girls (B).X-axis means the quintiles of sodium intakes with energy adjustments, Y-axis means OR for obesity risk and bars described. OR in each genotype of gene (lighter; wild homozygote, meddle; heterozygote, darker; mutant homozygote). In case of SLC12A3, darker block was described by combination of mutant and hetero because of few mutant frequencies. Statistically significances by p<0.05(*) were shown above bars. Means of the residual-Na in each quintile for boys are 2402.9, 3122.2, 3630.7, 4202.8 and 5194.1 mg/day. Means of residual-Na in each quintile for girls are 2190.8, 2878.4, 3378.9, 3882.5 and 4889.3 mg/day. [Abbreviation: angiotensin converting enzyme; ACE, cytochrome P450, family 11 subfamily B polypeptide 2;CYP11β-2, G protein-coupled receptor kinases type 4;GRK4 A486V, solute carrier family 12(sodium/chloride transporters)-member 3;SLC12A3.]
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pone.0120111.g002: Odds ratio (OR) for obesity risk by quintiles of residual-Na were estimated in boys (A) and girls (B).X-axis means the quintiles of sodium intakes with energy adjustments, Y-axis means OR for obesity risk and bars described. OR in each genotype of gene (lighter; wild homozygote, meddle; heterozygote, darker; mutant homozygote). In case of SLC12A3, darker block was described by combination of mutant and hetero because of few mutant frequencies. Statistically significances by p<0.05(*) were shown above bars. Means of the residual-Na in each quintile for boys are 2402.9, 3122.2, 3630.7, 4202.8 and 5194.1 mg/day. Means of residual-Na in each quintile for girls are 2190.8, 2878.4, 3378.9, 3882.5 and 4889.3 mg/day. [Abbreviation: angiotensin converting enzyme; ACE, cytochrome P450, family 11 subfamily B polypeptide 2;CYP11β-2, G protein-coupled receptor kinases type 4;GRK4 A486V, solute carrier family 12(sodium/chloride transporters)-member 3;SLC12A3.]

Mentions: The interaction between SSG and sodium intake showed that the obesity risk 1.0 (reference) was given when the wild type of SSG intake Q1 residual-Na values. We found that OR significantly increased by 7.06, 16.8 and 45.09 fold in the boys with the GRK4 A486V, ACE and SLC12A3 mutant as the sodium intake was increased. (Fig. 2-A) OR increased by 45.09-fold (CI; 2.665–762.991) in boys with the highest Na intake (5194.1mg/day) with SLC12 A3 mutant plus hetero genotypes than in those with the lowest residual-Na with the wild type genotype (P-trend = 0.013). OR increased by 11.19 (CI; 1.475–23.567) and 16.68-fold (CI; 1.234–225.5) in the boys with the ACE mutant who had Q3- and Q5-Na intake and 7.06 fold (CI; 1.625–30.646) higher in the boys with GRK4 A486V mutant who had Q4-Na intake (4202.8 mg/day) compared to Q1. OR increased by 15.52-fold (CI; 1.816–131.882) and 14.61-fold (CI; 1.623–131.534) among the girls with CYP11β2 mutant although who had sodium intake about Q2 (2878.4mg/day) or Q3 (3378.9mg/day). Unlike the boys, OR increased approximately 5-fold (CI; 1.166–21.718) more in the girls with the GRK4 A486V hetero type who were in low intake of sodium between Q2 and Q3 (2878.4–3378.9mg/day). Therefore, polymorphisms of GRK4 A486V, ACE, CYP11Β-2, and SLC12A3 showed a gender-based difference in the interaction between the sodium intake and weight gain. (Fig. 2-B) However, the others of SSG were not found the interaction between sodium intake and obesity. It is important to note that confound factors should be carefully determined when screening for obesity genes or SSG.


Gender-based differences on the association between salt-sensitive genes and obesity in Korean children aged between 8 and 9 years.

Lee M, Kim MK, Kim SM, Park H, Park CG, Park HK - PLoS ONE (2015)

Odds ratio (OR) for obesity risk by quintiles of residual-Na were estimated in boys (A) and girls (B).X-axis means the quintiles of sodium intakes with energy adjustments, Y-axis means OR for obesity risk and bars described. OR in each genotype of gene (lighter; wild homozygote, meddle; heterozygote, darker; mutant homozygote). In case of SLC12A3, darker block was described by combination of mutant and hetero because of few mutant frequencies. Statistically significances by p<0.05(*) were shown above bars. Means of the residual-Na in each quintile for boys are 2402.9, 3122.2, 3630.7, 4202.8 and 5194.1 mg/day. Means of residual-Na in each quintile for girls are 2190.8, 2878.4, 3378.9, 3882.5 and 4889.3 mg/day. [Abbreviation: angiotensin converting enzyme; ACE, cytochrome P450, family 11 subfamily B polypeptide 2;CYP11β-2, G protein-coupled receptor kinases type 4;GRK4 A486V, solute carrier family 12(sodium/chloride transporters)-member 3;SLC12A3.]
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358955&req=5

pone.0120111.g002: Odds ratio (OR) for obesity risk by quintiles of residual-Na were estimated in boys (A) and girls (B).X-axis means the quintiles of sodium intakes with energy adjustments, Y-axis means OR for obesity risk and bars described. OR in each genotype of gene (lighter; wild homozygote, meddle; heterozygote, darker; mutant homozygote). In case of SLC12A3, darker block was described by combination of mutant and hetero because of few mutant frequencies. Statistically significances by p<0.05(*) were shown above bars. Means of the residual-Na in each quintile for boys are 2402.9, 3122.2, 3630.7, 4202.8 and 5194.1 mg/day. Means of residual-Na in each quintile for girls are 2190.8, 2878.4, 3378.9, 3882.5 and 4889.3 mg/day. [Abbreviation: angiotensin converting enzyme; ACE, cytochrome P450, family 11 subfamily B polypeptide 2;CYP11β-2, G protein-coupled receptor kinases type 4;GRK4 A486V, solute carrier family 12(sodium/chloride transporters)-member 3;SLC12A3.]
Mentions: The interaction between SSG and sodium intake showed that the obesity risk 1.0 (reference) was given when the wild type of SSG intake Q1 residual-Na values. We found that OR significantly increased by 7.06, 16.8 and 45.09 fold in the boys with the GRK4 A486V, ACE and SLC12A3 mutant as the sodium intake was increased. (Fig. 2-A) OR increased by 45.09-fold (CI; 2.665–762.991) in boys with the highest Na intake (5194.1mg/day) with SLC12 A3 mutant plus hetero genotypes than in those with the lowest residual-Na with the wild type genotype (P-trend = 0.013). OR increased by 11.19 (CI; 1.475–23.567) and 16.68-fold (CI; 1.234–225.5) in the boys with the ACE mutant who had Q3- and Q5-Na intake and 7.06 fold (CI; 1.625–30.646) higher in the boys with GRK4 A486V mutant who had Q4-Na intake (4202.8 mg/day) compared to Q1. OR increased by 15.52-fold (CI; 1.816–131.882) and 14.61-fold (CI; 1.623–131.534) among the girls with CYP11β2 mutant although who had sodium intake about Q2 (2878.4mg/day) or Q3 (3378.9mg/day). Unlike the boys, OR increased approximately 5-fold (CI; 1.166–21.718) more in the girls with the GRK4 A486V hetero type who were in low intake of sodium between Q2 and Q3 (2878.4–3378.9mg/day). Therefore, polymorphisms of GRK4 A486V, ACE, CYP11Β-2, and SLC12A3 showed a gender-based difference in the interaction between the sodium intake and weight gain. (Fig. 2-B) However, the others of SSG were not found the interaction between sodium intake and obesity. It is important to note that confound factors should be carefully determined when screening for obesity genes or SSG.

Bottom Line: High sodium intake is associated with the development of chronic diseases such as obesity.BP, HOMA-IR, LDLc, TG, and the girls' sodium intake significantly increased, but HDLc significantly decreased with increase in BMI.The obesity risk increased with GRK4 A486V, ACE, and SLC12A3 variants in boys, whereas it increased with GRK4 A486V and CYP11B2 variants in girls as sodium intake increased.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition, and Research Institute of Obesity Sciences, Sungshin Women's University, Seoul, Republic of Korea.

ABSTRACT

Background: High sodium intake is associated with the development of chronic diseases such as obesity. Although its role in obesity remains controversial, there may be a correlation between salt sensitivity and the early onset of chronic diseases in obese children.

Methods: In all, 2,163 Korean children (1,106 boys and 1,057 girls) aged 8-9 years were recruited from seven elementary schools in Seoul. To evaluate whether obesity risk was modulated by the salt sensitivity, 11 SNPs related to salt sensitive genes (SSG) became the target of sodium intakes in obese children.

Results: BP, HOMA-IR, LDLc, TG, and the girls' sodium intake significantly increased, but HDLc significantly decreased with increase in BMI. Regardless of sex, the obesity risk was 5.27-fold (CI; 1.320-27.560) higher in the Q2 to Q5 of sodium intake adjusted by energy (4044.9-5058.9 mg/day) than in the lowest Q1 level (2287.6 mg/day) in obese children. BP was sensitively dependent on insulin resistance and lipid accumulation in all subjects; however, sodium intake may be an independent risk factor of obesity without increasing BP in girls. GRK4 A486V mutant homozygote was highly distributed in the obese group, but other SNPs had no impact. The obesity risk increased 7.06, 16.8, and 46.09-fold more in boys with GRK4 A486V, ACE, and SLC12A3 mutants as sodium intake increased. Among girls, the obesity risk increased in GRK4 A486V heterozygote and CYP11β-2 mutant homozygote although sodium intake was relatively lower, implying that ACE, SLC12A, CYP11β-2, and GRK4 A486V polymorphisms showed gender-based differences with regard to interaction between sodium intake and obesity.

Conclusion: A high sodium intake markedly increased the obesity risk in variants of GRK4 A486V regardless of sex. The obesity risk increased with GRK4 A486V, ACE, and SLC12A3 variants in boys, whereas it increased with GRK4 A486V and CYP11B2 variants in girls as sodium intake increased. Obese children with the specific gene variants are recommended to reduce their sodium intake.

No MeSH data available.


Related in: MedlinePlus