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Tytuł pozycji:

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress.

Tytuł:
Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress.
Autorzy:
Li H; School of Public Health, Beihua University, Jilin, 132013, China.
Li J; School of Public Health, Beihua University, Jilin, 132013, China.
Qu Z; Jilin Combine Traditional Chinese and Western Hospital, Jilin, 132012, China.
Qian H; School of Public Health, Beihua University, Jilin, 132013, China.
Zhang J; School of Public Health, Beihua University, Jilin, 132013, China.
Wang H; School of Public Health, Beihua University, Jilin, 132013, China.
Xu X; School of Public Health, Beihua University, Jilin, 132013, China.
Liu S; Shenzhen Nanshan Center for Chronic Disease Control, Shenzhen, 518054, China. .
Źródło:
Scientific reports [Sci Rep] 2020 Oct 01; Vol. 10 (1), pp. 16360. Date of Electronic Publication: 2020 Oct 01.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: London : Nature Publishing Group, copyright 2011-
MeSH Terms:
Dibutyl Phthalate/*administration & dosage
Endocrine Disruptors/*administration & dosage
Endoplasmic Reticulum Stress/*drug effects
Obesity/*chemically induced
Prenatal Exposure Delayed Effects/*chemically induced
Uncoupling Protein 1/*metabolism
Animals ; Apoptosis/drug effects ; Body Composition/drug effects ; Dibutyl Phthalate/adverse effects ; Endocrine Disruptors/adverse effects ; Energy Metabolism/drug effects ; Female ; Mice ; Obesity/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism
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Substance Nomenclature:
0 (Endocrine Disruptors)
0 (Uncoupling Protein 1)
2286E5R2KE (Dibutyl Phthalate)
Entry Date(s):
Date Created: 20201002 Date Completed: 20210101 Latest Revision: 20211001
Update Code:
20240105
PubMed Central ID:
PMC7529907
DOI:
10.1038/s41598-020-73477-3
PMID:
33004990
Czasopismo naukowe
Dibutyl phthalate (DBP) is recognized as an environmental endocrine disruptor that has been detected in fetal and postnatal samples. Recent evidence found that in utero DBP exposure was associated with an increase of adipose tissue weight and serum lipids in offspring, but the precise mechanism is unknown. Here we aimed to study the effects of in utero DBP exposure on obesity in offspring and examine possible mechanisms. SPF C57BL/6J pregnant mice were gavaged with either DBP (5 mg /kg/day) or corn oil, from gestational day 12 until postnatal day 7. After the offspring were weaned, the mice were fed a standard diet for 21 weeks, and in the last 2 weeks 20 mice were selected for TUDCA treatment. Intrauterine exposure to low-dose DBP promoted obesity in offspring, with evidence of glucose and lipid metabolic disorders and a decreased metabolic rate. Compared to controls, the DBP exposed mice had lower expression of UCP1 and significantly higher expression of Bip and Chop, known markers of endoplasmic reticulum (ER) stress. However, TUDCA treatment of DBP exposed mice returned these parameters nearly to the levels of the controls, with increased expression of UCP1, lower expression of Bip and Chop and ameliorated obesity. Intrauterine exposure of mice to low-dose DBP appears to promote obesity in offspring by inhibiting UCP1 via ER stress, a process that was largely reversed by treatment with TUDCA.
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