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Persistent organic pollutants, mitochondrial dysfunction, and metabolic syndrome
Author(s) -
Lim Soo,
Cho Young Min,
Park Kyong Soo,
Lee Hong Kyu
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05622.x
Subject(s) - insulin resistance , metabolic syndrome , mitochondrial dna , diabetes mellitus , mitochondrion , mechanism (biology) , bioinformatics , type 2 diabetes , medicine , biology , etiology , insulin , endocrinology , genetics , gene , philosophy , epistemology
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.