Blood lead levels, iron metabolism gene polymorphisms and homocysteine: a gene-environment interaction study

Kim, Kyoung Nam; Lee, Mee Ri; Lim, Youn Hee; Hong, Yun Chul

doi:10.1136/oemed-2017-104375

Cited by 16 publications

(17 citation statements)

References 43 publications

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“…All studies of this review support that Pb concentrations are correlated with high levels of Hc [9,[21][22][23][24][25][26][27][28][29][30].…”

Section: Lead (Pb)mentioning

confidence: 74%

“…Kim et al [22], in a population-based cohort, found an association between Pb and Hc concentrations in people living in South Korea. Furthermore, Kim reported, in the framework of genotypes for the target gene single-nucleotide polymorphisms analysis, that people with variant alleles in the transferrin gene showed a positive correlation with Pb and Hc increased levels.…”

Section: Lead (Pb)mentioning

confidence: 97%

“…Twelve were ruled out a subsequent review of title and abstract, and 26 studies were disqualified after review of the manuscript. In conclusion, 16 studies satisfied the inclusion criteria and were included in the systematic review [6,[21][22][23][24][25][26][27][28][29][30][31][32]. A flowchart depicting the choice of studies is revealed in Figure 1.…”

Section: Characteristics Of Eligible Studiesmentioning

confidence: 99%

“…Furthermore, Kim reported, in the framework of genotypes for the target gene single-nucleotide polymorphisms analysis, that people with variant alleles in the transferrin gene showed a positive correlation with Pb and Hc increased levels. No association with haemochromatosis protein, betaine-homocysteine S-methyltransferase, methionine synthase (MTR), and MTHFR gene alleles was found [22].…”

Section: Lead (Pb)mentioning

confidence: 99%

“…Kim and colleagues [22] underlined that blood Pb concentrations were positively associated with high Hc plasma levels and variant alleles in transferrin gene. This suggests that iron (Fe) distribution may influence the effect of lead toxicity on Hc concentration by affecting Hc metabolism.…”

Section: Lead (Pb)mentioning

confidence: 99%

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Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?

et al. 2019

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Background: Homocysteine is a sulfur amino acid whose metabolism is activated in two pathways: remethylation to methionine, which requires folate and vitamin B 12 , and transsulfuration to cystathionine, which needs pyridoxal-5'-phosphate. High homocysteine level increases the risk of developing heart disease, stroke, peripheral vascular diseases, and cognitive impairment. Some evidence showed that exposure to these metals increased plasma homocysteine levels. Methods: A systematic review was carried out to clarify the relationship between homocysteine blood levels and exposure to toxic heavy metals (Lead, Cadmium, Mercury, and Chromium). Results: The results of this systematic review indicate that exposure to Pb, Cr, Cd, and Hg is connected with nonphysiological homocysteine levels or vitamin B 12 and folate serum concentrations. Conclusions: These findings reinforce the importance of involvement in exposure to heavy metals in homocysteine metabolism. This supports the role of blood metals as potential upstream modifiable risk factors to prevent the development of other established risk factors as hyperhomocysteinemia.

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“…All studies of this review support that Pb concentrations are correlated with high levels of Hc [9,[21][22][23][24][25][26][27][28][29][30].…”

Section: Lead (Pb)mentioning

confidence: 74%

Section: Lead (Pb)mentioning

confidence: 97%

Section: Characteristics Of Eligible Studiesmentioning

confidence: 99%

Section: Lead (Pb)mentioning

confidence: 99%

Section: Lead (Pb)mentioning

confidence: 99%

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Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?

et al. 2019

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Fruit intake, genetic risk and type 2 diabetes: a population-based gene–diet interaction analysis

Luo

Dai

et al. 2021

Eur J Nutr

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Purpose Whether the association between fruit and type 2 diabetes (T2D) is modified by the genetic predisposition of T2D was yet elucidated. The current study is meant to examine the gene–dietary fruit intake interactions in the risk of T2D and related glycemic traits. Methods We performed a cross-sectional study in 11,657 participants aged ≥ 40 years from a community-based population in Shanghai, China. Fruit intake information was collected by a validated food frequency questionnaire by asking the frequency of consumption of typical food items over the previous 12 months. T2D-genetic risk score (GRS) was constructed by 34 well established T2D common variants in East Asians. The risk of T2D, fasting, 2 h-postprandial plasma glucose, and glycated hemoglobin A1c associated with T2D-GRS and each individual single nucleotide polymorphisms (SNPs) were tested. Results The risk of T2D associated with each 1-point of T2D-GRS was gradually decreased from the lower fruit intake level (< 1 times/week) [the odds ratio (OR) and 95% confidence interval (CI) was 1.10 (1.07–1.13)], to higher levels (1–3 and > 3 times/week) [the corresponding ORs and 95% CIs were 1.08 (1.05–1.10) and 1.07 (1.05–1.08); P for interaction = 0.04]. Analyses for associations with fasting, 2 h-postprandial plasma glucose and glycated hemoglobin A1c demonstrated consistent tendencies (all P for interaction ≤ 0.03). The inverse associations of fruit intake with risk of T2D and glucose traits were more prominent in the higher T2D-GRS tertile. Conclusions Fruit intakes interact with the genetic predisposition of T2D on the risk of diabetes and related glucose metabolic traits. Fruit intake alleviates the association between genetic predisposition of T2D and the risk of diabetes; the association of fruit intake with a lower risk of diabetes was more prominent in population with a stronger genetic predisposition of T2D.

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