Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.

There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30. Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mit...

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Autores principales: Soo Lim, Sun Young Ahn, In Chan Song, Myung Hee Chung, Hak Chul Jang, Kyong Soo Park, Ki-Up Lee, Youngmi Kim Pak, Hong Kyu Lee
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Publicado: Public Library of Science (PLoS) 2009
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Acceso en línea:https://doaj.org/article/bdfd7ce2665d430bb4e3536df016bad3
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spelling oai:doaj.org-article:bdfd7ce2665d430bb4e3536df016bad32021-11-25T06:16:10ZChronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.1932-620310.1371/journal.pone.0005186https://doaj.org/article/bdfd7ce2665d430bb4e3536df016bad32009-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19365547/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30. Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mitochondria, we investigated whether chronic exposure to low concentrations of ATZ might cause obesity or insulin resistance by damaging mitochondrial function. Sprague-Dawley rats (n = 48) were treated for 5 months with low concentrations (30 or 300 microg kg(-1) day(-1)) of ATZ provided in drinking water. One group of animals was fed a regular diet for the entire period, and another group of animals was fed a high-fat diet (40% fat) for 2 months after 3 months of regular diet. Various parameters of insulin resistance were measured. Morphology and functional activities of mitochondria were evaluated in tissues of ATZ-exposed animals and in isolated mitochondria. Chronic administration of ATZ decreased basal metabolic rate, and increased body weight, intra-abdominal fat and insulin resistance without changing food intake or physical activity level. A high-fat diet further exacerbated insulin resistance and obesity. Mitochondria in skeletal muscle and liver of ATZ-treated rats were swollen with disrupted cristae. ATZ blocked the activities of oxidative phosphorylation complexes I and III, resulting in decreased oxygen consumption. It also suppressed the insulin-mediated phosphorylation of Akt. These results suggest that long-term exposure to the herbicide ATZ might contribute to the development of insulin resistance and obesity, particularly where a high-fat diet is prevalent.Soo LimSun Young AhnIn Chan SongMyung Hee ChungHak Chul JangKyong Soo ParkKi-Up LeeYoungmi Kim PakHong Kyu LeePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 4, p e5186 (2009)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Soo Lim
Sun Young Ahn
In Chan Song
Myung Hee Chung
Hak Chul Jang
Kyong Soo Park
Ki-Up Lee
Youngmi Kim Pak
Hong Kyu Lee
Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
description There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30. Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mitochondria, we investigated whether chronic exposure to low concentrations of ATZ might cause obesity or insulin resistance by damaging mitochondrial function. Sprague-Dawley rats (n = 48) were treated for 5 months with low concentrations (30 or 300 microg kg(-1) day(-1)) of ATZ provided in drinking water. One group of animals was fed a regular diet for the entire period, and another group of animals was fed a high-fat diet (40% fat) for 2 months after 3 months of regular diet. Various parameters of insulin resistance were measured. Morphology and functional activities of mitochondria were evaluated in tissues of ATZ-exposed animals and in isolated mitochondria. Chronic administration of ATZ decreased basal metabolic rate, and increased body weight, intra-abdominal fat and insulin resistance without changing food intake or physical activity level. A high-fat diet further exacerbated insulin resistance and obesity. Mitochondria in skeletal muscle and liver of ATZ-treated rats were swollen with disrupted cristae. ATZ blocked the activities of oxidative phosphorylation complexes I and III, resulting in decreased oxygen consumption. It also suppressed the insulin-mediated phosphorylation of Akt. These results suggest that long-term exposure to the herbicide ATZ might contribute to the development of insulin resistance and obesity, particularly where a high-fat diet is prevalent.
format article
author Soo Lim
Sun Young Ahn
In Chan Song
Myung Hee Chung
Hak Chul Jang
Kyong Soo Park
Ki-Up Lee
Youngmi Kim Pak
Hong Kyu Lee
author_facet Soo Lim
Sun Young Ahn
In Chan Song
Myung Hee Chung
Hak Chul Jang
Kyong Soo Park
Ki-Up Lee
Youngmi Kim Pak
Hong Kyu Lee
author_sort Soo Lim
title Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
title_short Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
title_full Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
title_fullStr Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
title_full_unstemmed Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
title_sort chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance.
publisher Public Library of Science (PLoS)
publishDate 2009
url https://doaj.org/article/bdfd7ce2665d430bb4e3536df016bad3
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