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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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) |
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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. |
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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 |
work_keys_str_mv |
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