Early-life exposure to sibling modifies the relationship betweenCD14polymorphisms and allergic sensitization

Abstract Early life exposure to famine was associated with adulthood metabolic syndrome and nonalcoholic fatty liver disease (NAFLD), and NAFLD was also affected by cardiometabolic traits. However, the role of cardiometabolic traits in the associations from famine exposure to NAFLD was largely unknown. This study aimed to investigate whether the relationship between early life famine exposure and adulthood NAFLD risk was mediated by cardiometabolic traits. Overall, 7,578 subjects aged 56.0 ± 3.7 years in the Dongfeng-Tongji cohort were included and classified into late-exposed (1952-1954), middle-exposed (1954-1956), early-childhood-exposed (1956-1958), fetal-exposed (1959-1961), and nonexposed (1962-1966, reference) group according to the birth year. NAFLD was diagnosed by experienced physicians via abdominal B-type ultrasound inspection. Mediation analysis was used to evaluate the mediating effects of cardiometabolic traits. Compared with those nonexposed, after multivariable adjustment, participants in fetal-exposed group (OR: 1.37; 95% CI: 1.08-1.73) had 37% higher risk to develop NAFLD, and the overall childhood-exposed group had marginally significant association with NAFLD (OR: 1.39; 95% CI: 0.99-1.94). Stratification analysis found the famine-NAFLD associations more evident in women and those born in areas severely affected by famine. Mediation analysis showed that cardiometabolic traits such as TC, TyG index, γ-GT, ALP, and ALT mediated 6.7%-22.2% of the relation from famine exposure to higher NAFLD risk. Early life exposure to famine was related to increased adulthood NAFLD risk, and this relationship was partly mediated by cardiometabolic traits.

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Chemically Contaminated Eel Fed to Pregnant and Lactating Mouse Dams Causes Hyperactivity in Their Offspring

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000288 ◽

2016 ◽

Vol 86 (1-2) ◽

pp. 36-47 ◽

Cited By ~ 2

Author(s):

Imen Dridi ◽

Nidhal Soualeh ◽

Torsten Bohn ◽

Rachid Soulimani ◽

Jaouad Bouayed

Keyword(s):

Open Field ◽

Early Life ◽

Home Cage ◽

Anguilla Anguilla ◽

Acetylcholinesterase Activity ◽

Female Offspring ◽

Significant Inhibition ◽

Standard Diet ◽

Early Life Exposure ◽

Cage Test

Abstract.This study examined whether perinatal exposure to polluted eels (Anguilla anguilla L.) induces changes in the locomotor activity of offspring mice across lifespan (post-natal days (PNDs) 47 – 329), using the open field and the home cage activity tests. Dams were exposed during gestation and lactation, through diets enriched in eels naturally contaminated with pollutants including PCBs. Analysis of the eel muscle focused on the six non-dioxin-like (NDL) indicator PCBs (Σ6 NDL-PCBs: 28, 52, 101, 138, 153 and 180). Four groups of dams (n = 10 per group) received either a standard diet without eels or eels (0.8 mg/kg/day) containing 85, 216, or 400 ng/kg/day of ϵ6 NDL-PCBs. The open field test showed that early-life exposure to polluted eels increased locomotion in female offspring of exposed dams but not in males, compared to controls. This hyperlocomotion appeared later in life, at PNDs 195 and 329 (up to 32 % increase, p < 0.05). In addition, overactivity was observed in the home cage test at PND 305: exposed offspring females showed a faster overall locomotion speed (3.6 – 4.2 cm/s) than controls (2.9 cm/s, p <0.05); again, males remained unaffected. Covered distances in the home cage test were only elevated significantly in offspring females exposed to highest PCB concentrations (3411 ± 590 cm vs. 1377 ± 114 cm, p < 0.001). These results suggest that early-life exposure to polluted eels containing dietary contaminants including PCBs caused late, persistent and gender-dependent neurobehavioral hyperactive effects in offspring mice. Furthermore, female hyperactivity was associated with a significant inhibition of acetylcholinesterase activity in the hippocampus and the prefrontal cortex.

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