PMID- 20649553
OWN - NLM
STAT- MEDLINE
DCOM- 20100809
LR  - 20171116
IS  - 1749-6632 (Electronic)
IS  - 0077-8923 (Linking)
VI  - 1201
DP  - 2010 Jul
TI  - Persistent organic pollutants, mitochondrial dysfunction, and metabolic syndrome.
PG  - 166-76
LID - 10.1111/j.1749-6632.2010.05622.x [doi]
AB  - The number of individuals with metabolic syndrome is increasing worldwide, 
      constituting a major social problem in many countries. Recently, epidemiological 
      and experimental studies have associated insulin resistance or type 2 diabetes 
      with elevated body burdens of persistent organic pollutants (POPs). It has been 
      proposed that mitochondrial dysfunction plays a key role in this association. 
      Mitochondrial DNA abnormalities are known to cause pancreas beta cell damage, 
      insulin resistance, and diabetes mellitus. Recently, much evidence has emerged 
      showing that environmental toxins, including POPs, affect mitochondrial function 
      and subsequently induce insulin resistance. In this review, we present a novel 
      concept in which metabolic syndrome is the result of mitochondrial dysfunction, 
      which in turn is caused by exposure to POPs. The potential mechanism including 
      POPs for mitochondrial dysfunction on metabolic syndrome is also discussed. We 
      propose that the mitochondrial paradigm for the etiology of metabolic syndrome 
      will facilitate the prevention and treatment of this major health problem.
FAU - Lim, Soo
AU  - Lim S
AD  - Department of Internal Medicine, Seoul National University College of Medicine, 
      Seoul, Korea.
FAU - Cho, Young Min
AU  - Cho YM
FAU - Park, Kyong Soo
AU  - Park KS
FAU - Lee, Hong Kyu
AU  - Lee HK
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Adiponectin)
RN  - 0 (DNA, Mitochondrial)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Organic Chemicals)
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Adiponectin/metabolism
MH  - Animals
MH  - DNA, Mitochondrial/metabolism
MH  - Endoplasmic Reticulum/metabolism
MH  - Environmental Pollutants/*toxicity
MH  - Humans
MH  - Inflammation
MH  - Insulin Resistance
MH  - Metabolic Syndrome/metabolism/*pathology
MH  - Mitochondria/*metabolism
MH  - Mitochondrial Diseases/metabolism/*pathology
MH  - Models, Biological
MH  - Organic Chemicals/*toxicity
MH  - Oxidative Stress
MH  - Reactive Oxygen Species
RF  - 89
EDAT- 2010/07/24 06:00
MHDA- 2010/08/10 06:00
CRDT- 2010/07/24 06:00
PHST- 2010/07/24 06:00 [entrez]
PHST- 2010/07/24 06:00 [pubmed]
PHST- 2010/08/10 06:00 [medline]
AID - NYAS5622 [pii]
AID - 10.1111/j.1749-6632.2010.05622.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2010 Jul;1201:166-76. doi: 10.1111/j.1749-6632.2010.05622.x.