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Metabolic Risk/Epidemiology
Effect of Low-Dose Persistent Organic Pollutants on Mitochondrial Function: Human and in Vitro Evidence
Se-A Kim, Hoyul Lee, Sung-Mi Park, Mi-Jin Kim, Yu-Mi Lee, Young-Ran Yoon, Hyun-Kyung Lee, Hyo-Bang Moon, In-Kyu Lee, Duk-Hee Lee
Diabetes Metab J. 2022;46(4):592-604.   Published online January 26, 2022
DOI: https://doi.org/10.4093/dmj.2021.0132
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  • 5 Web of Science
  • 7 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Chronic exposure to low-dose persistent organic pollutants (POPs) can induce mitochondrial dysfunction. This study evaluated the association between serum POP concentrations and oxygen consumption rate (OCR) as a marker of mitochondrial function in humans and in vitro cells.
Methods
Serum concentrations of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) were measured in 323 adults. The OCRs of platelets and peripheral blood mononuclear cells (PBMCs) were assessed in 20 mL of fresh blood using a Seahorse XF analyzer. Additionally, the in vitro effects of Arochlor-1254, β-hexachlorocyclohexane, and p,p´-dichlorodiphenyltrichloroethane at concentrations of 0.1 pM to 100 nM were evaluated in human platelets, human PBMCs, and Jurkat T-cells.
Results
The association between serum POP concentrations and OCR differed depending on the cell type. As serum OCP concentrations increased, basal platelet OCR levels decreased significantly; according to the OCP quintiles of summary measure, they were 8.6, 9.6, 8.2, 8.0, and 7.1 pmol/min/μg (P trend=0.005). Notably, the basal PBMC OCR levels decreased remarkably as the serum PCB concentration increased. PBMC OCR levels were 46.5, 34.3, 29.1, 16.5, and 13.1 pmol/min/μg according to the PCB quintiles of summary measure (P trend <0.001), and this inverse association was consistently observed in all subgroups stratified by age, sex, obesity, type 2 diabetes mellitus, and hypertension, respectively. In vitro experimental studies have also demonstrated that chronic exposure to low-dose POPs could decrease OCR levels.
Conclusion
The findings from human and in vitro studies suggest that chronic exposure to low-dose POPs can induce mitochondrial dysfunction by impairing oxidative phosphorylation.

Citations

Citations to this article as recorded by  
  • Persistent Organic Pollutants released from decomposed adipose tissue affect mitochondrial enzyme function in the brain and eyes other than the liver
    Dongshin Yang, Eun Ko, Hwayeon Lim, Hyojin Lee, Kitae Kim, Moonsung Choi, Sooim Shin
    Environmental Science and Pollution Research.2024; 31(7): 10648.     CrossRef
  • Can lipophilic pollutants in adipose tissue explain weight change‐related risk in type 2 diabetes mellitus?
    Duk‐Hee Lee, In‐Kyu Lee
    Journal of Diabetes Investigation.2023; 14(4): 528.     CrossRef
  • Mitochondrial and metabolic features of salugenesis and the healing cycle
    Robert K. Naviaux
    Mitochondrion.2023; 70: 131.     CrossRef
  • Obesity Paradox in Sepsis: Role of Adipose Tissue in Storing Mitochondrial Toxins
    Duk-Hee Lee
    Critical Care Medicine.2023; 51(8): e172.     CrossRef
  • Human Preadipocytes Differentiated under Hypoxia following PCB126 Exposure during Proliferation: Effects on Differentiation, Glucose Uptake and Adipokine Profile
    Zeinab El Amine, Jean-François Mauger, Pascal Imbeault
    Cells.2023; 12(18): 2326.     CrossRef
  • Is micronucleus assay in oral exfoliated cells a useful biomarker for biomonitoring populations exposed to pesticides? A systematic review with meta-analysis
    Ingra Tais Malacarne, Wilton Mitsunari Takeshita, Daniel Vitor de Souza, Barbara dos Anjos Rosario, Milena de Barros Viana, Ana Claudia Muniz Renno, Daisy Maria Favero Salvadori, Daniel Araki Ribeiro
    Environmental Science and Pollution Research.2022; 29(43): 64392.     CrossRef
  • Comment on: Obesity is Associated with Improved Postoperative Overall Survival, Independent of Skeletal Muscle Mass in Lung Adenocarcinoma by Lee et al.
    Duk‐Hee Lee
    Journal of Cachexia, Sarcopenia and Muscle.2022; 13(5): 2576.     CrossRef
Maximal Oxygen Uptake (VO2max) and Metabolic Syndrome.
Mira Kang, Ji Dong Sung, Byung Chul Yoo, Yoon Ho Choi, Sae Young Jae, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Kwang Won Kim, Moon Kyu Lee
Korean Diabetes J. 2005;29(1):65-71.   Published online January 1, 2005
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AbstractAbstract PDF
BACKGROUND
A number of studies have demonstrated an inverse relationship between cardiorespiratory fitness and metabolic syndrome. However, whether the maximal oxygen uptake (VO2max) is dependent on the number of metabolic components or on particular metabolic component remains to be assessed. METHODS: A total of 1,432 Korean subjects were studied. Each individual was assessed for the presence of metabolic syndrome using the modified NCEP-ATP III criteria. All subjects underwent a graded symptom-limited maximal exercise test to determine their VO2max, using a treadmill according to the Bruce protocol. RESULTS: The age-adjusted prevalence of metabolic syndrome in all subjects was 20.4%. The odds ratios for metabolic syndrome were higher in men, the elderly, the obese and those with a lower VO2max. The difference in the VO2max was dependent only on the presence of metabolic syndrome, not on the number of components. CONCLUSION: There were no significant differences in the VO2max according to the presence of particular metabolic components. These results suggest that the VO2max reflects the metabolic syndrome state, rather than the metabolic components, and might be a factor in determining metabolic syndrome

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