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Endocrine Disruptors and Developmental Origins of Nonalcoholic Fatty Liver Disease.

Abstract Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic worldwide, particularly in countries that consume a Western diet, and can lead to life-threatening conditions such as cirrhosis and hepatocellular carcinoma. With increasing prevalence of NAFLD in both children and adults, an understanding of the factors that promote NAFLD development and progression is crucial. Environmental agents, including endocrine-disrupting chemicals (EDCs), which have been linked to other diseases, may play a role in NAFLD development. Increasing evidence supports a developmental origin of liver disease, and early-life exposure to EDCs could represent one risk factor for the development of NAFLD later in life. Rodent studies provide the strongest evidence for this link, but further studies are needed to define whether there is a causal link between early-life EDC exposure and NAFLD development in humans. Elucidating the molecular mechanisms underlying development of NAFLD in the context of developmental EDC exposures may identify biomarkers for people at risk, as well as potential intervention and/or therapeutic opportunities for the disease.
PMID
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Authors

Mayor MeshTerms

Global Health

Health Transition

Keywords
Journal Title endocrinology
Publication Year Start




PMID- 29126168
OWN - NLM
STAT- MEDLINE
DCOM- 20180221
LR  - 20180221
IS  - 1945-7170 (Electronic)
IS  - 0013-7227 (Linking)
VI  - 159
IP  - 1
DP  - 2018 Jan 1
TI  - Endocrine Disruptors and Developmental Origins of Nonalcoholic Fatty Liver
      Disease.
PG  - 20-31
LID - 10.1210/en.2017-00887 [doi]
AB  - Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic worldwide,
      particularly in countries that consume a Western diet, and can lead to
      life-threatening conditions such as cirrhosis and hepatocellular carcinoma. With 
      increasing prevalence of NAFLD in both children and adults, an understanding of
      the factors that promote NAFLD development and progression is crucial.
      Environmental agents, including endocrine-disrupting chemicals (EDCs), which have
      been linked to other diseases, may play a role in NAFLD development. Increasing
      evidence supports a developmental origin of liver disease, and early-life
      exposure to EDCs could represent one risk factor for the development of NAFLD
      later in life. Rodent studies provide the strongest evidence for this link, but
      further studies are needed to define whether there is a causal link between
      early-life EDC exposure and NAFLD development in humans. Elucidating the
      molecular mechanisms underlying development of NAFLD in the context of
      developmental EDC exposures may identify biomarkers for people at risk, as well
      as potential intervention and/or therapeutic opportunities for the disease.
CI  - Copyright (c) 2018 Endocrine Society.
FAU - Trevino, Lindsey S
AU  - Trevino LS
AD  - Center for Precision Environmental Health, Baylor College of Medicine, Houston,
      Texas.
AD  - Department of Molecular and Cellular Biology, Baylor College of Medicine,
      Houston, Texas.
FAU - Katz, Tiffany A
AU  - Katz TA
AD  - Center for Precision Environmental Health, Baylor College of Medicine, Houston,
      Texas.
AD  - Department of Molecular and Cellular Biology, Baylor College of Medicine,
      Houston, Texas.
LA  - eng
GR  - P30 ES023512/ES/NIEHS NIH HHS/United States
GR  - R01 ES023206/ES/NIEHS NIH HHS/United States
GR  - U01 ES026719/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Endocrine Disruptors)
RN  - 0 (Environmental Pollutants)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Animals
MH  - Child
MH  - Diet, Western/adverse effects
MH  - Endocrine Disruptors/*toxicity
MH  - Environmental Exposure/*adverse effects
MH  - Environmental Illness/*chemically induced/epidemiology/etiology
MH  - Environmental Pollutants/toxicity
MH  - Female
MH  - Fetal Development/drug effects
MH  - *Global Health
MH  - *Health Transition
MH  - Humans
MH  - Liver/*drug effects
MH  - Male
MH  - Non-alcoholic Fatty Liver Disease/*chemically induced/epidemiology/etiology
MH  - Pregnancy
MH  - Prevalence
PMC - PMC5761605
EDAT- 2017/11/11 06:00
MHDA- 2018/02/22 06:00
CRDT- 2017/11/11 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/10/04 00:00 [received]
PHST- 2017/11/01 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/11 06:00 [pubmed]
PHST- 2018/02/22 06:00 [medline]
PHST- 2017/11/11 06:00 [entrez]
AID - 4590243 [pii]
AID - 10.1210/en.2017-00887 [doi]
PST - ppublish
SO  - Endocrinology. 2018 Jan 1;159(1):20-31. doi: 10.1210/en.2017-00887.