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Reviews in Endocrine and Metabolic Disorders
Erschienen in: Reviews in Endocrine and Metabolic Disorders 4/2014

01.12.2014

Metabolic syndrome and the environmental pollutants from mitochondrial perspectives

Erschienen in: Reviews in Endocrine and Metabolic Disorders | Ausgabe 4/2014

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Abstract

The worldwide epidemic of diabetes and metabolic syndrome in the last few decades cannot be fully accounted for only by changes in the lifestyle factors, such as sedentary lifestyle and overeating. Besides genetic factors, there must be other causes to explain this rapid change. They could not be infectious in nature and induce insulin resistance as key biochemical abnormality. Mitochondrial dysfunction could be underlying mechanism behind the insulin resistance, thus metabolic syndrome. Then there have been increasing number of reports suggesting that chronic exposure to and accumulation of endocrine disrupting chemicals (EDCs), especially so-called the persistent organic pollutants (POPs) within the body might be associated with metabolic syndrome. Combining two concepts, we developed new “EDCs-induced mitochondrial dysfunction hypothesis of metabolic syndrome”. In this review we suggest that classifying those chemicals into 5 groups might be clinically useful considering their removal or avoidance; POPs, non-persistent organic pollutants, heavy metals, air pollutants and drugs. We will also discuss briefly how those insights could be applied to clinical medicine.
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Literatur
1.
Meigs JB. Invited commentary: insulin resistance syndrome? Syndrome X? Multiple metabolic syndrome? A syndrome at all? Factor analysis reveals patterns in the fabric of correlated metabolic risk factors. Am JEpidemiol. 2000;152:908–11.CrossRef
2.
Reaven GM. Banting lecture, Role of insulin resistance in human disease. Diabetes. 1998;37:1595–607.CrossRef
3.
Lee HK, Cho YM, Kwak SH, Lim S, Park KS, Shim EB. Mitochondrial dysfunction and metabolic syndrome-looking for environmental factors. Biochim Biophys Acta. 2010;1800(3):282–9.PubMedCrossRef
4.
Lee HK, Shim EB. Extension of Mitochondria Dysfunction Hypothesis of Metabolic Syndrome to Atherosclerosis with Emphasis on the Endocrine Disrupting Chemicals and Biophysical Laws. J Diabetes Investig. 2013;4(1):19–33.PubMedCrossRefPubMedCentral
5.
Meyer JN, Leung MC, Rooney JP, Sendoel A, Hengartner MO, Kisby GE, et al. Mitochondria as a target of environmental toxicants. Toxicol Sci. 2013;134(1):1–17.PubMedCrossRefPubMedCentral
6.
Lee DH, Porta M, Jacobs Jr DR, Vandenberg LN. Chlorinated persistent organic pollutants, obesity, and type 2 diabetes. Endocr Rev. 2014;35(4):557–601.PubMedCrossRef
7.
Lee HK, Song JH, Shin CS, Park DJ, Park KS, Lee KU, et al. Decreased mitochondrial DNA content in peripheral blood precedes the development of non-insulin-dependent diabetes mellitus. Diabetes Res Clin Pract. 1998;42:161–7.PubMedCrossRef
8.
Jucker BM, Dufour S, Ren J, Cao X, Previs SF, Underhill B, et al. Shulman GI.Assessment of mitochondrial energy coupling in vivo by 13C/31P NMR. Proc Natl Acad Sci U S A. 2000;97:6880–4.PubMedCrossRefPubMedCentral
9.
Petersen KF, Befroy D, Dufour S, Dziura J, Ariyan C, Rothman DL, et al. Mitochondrial dysfunction in the elderly: possible role in insulin resistance. Science. 2003;300:1140–2.PubMedCrossRefPubMedCentral
10.
Smith RE. Quantitative relations between liver mitochondria metabolism and total body weight in mammals. Ann NY Acad Sci. 1956;62:403–22.CrossRef
11.
Rasmussen UF, Rasmussen HN, Krustrup P, Quistorff B, Saltin B, Bangsbo J. Aerobic metabolism of human quadriceps muscle: in vivo data parallel measurements on isolated mitochondria. Am J Physiol Endocrinol Metab. 2001;280:301–7.
12.
Lee HK. Method of proof and evidences for the concept that mitochondrial genome is a thrifty genome. Diabetes Res Clin Pract. (Suppl. 2) 2001;54–63.
13.
14.
West GB, Woodruff WH, Brown JH. Allometric scaling of metabolic rate from molecules and mitochondria to cells and mammals. Proc Natl Acad Sci U S A. 2002;99 Suppl 1:2473–8.PubMedCrossRefPubMedCentral
15.
Ravussin E, Lillioja S, Knowler WC, Christin L, Freymond D, Abbott WG, et al. Reduced rate of energy expenditure as a risk factor for bodyweight gain. N Engl J Med. 1988;318:467–72.PubMedCrossRef
16.
Chun PW. Why does the human body maintain a constant 37-degree temperature?: thermodynamic switch controls chemical equilibrium in biological systems. Phys Scr. 2005;118:219–22.CrossRef
17.
18.
Szendroedi J, Phielix E, Roden M. The role of mitochondria in insulin resistance and type 2 diabetes mellitus. Nat Rev Endocrinol. 2012;8(2):92–103.CrossRef
19.
Pravenec M, Hyakukoku M, Houstek J, Zidek V, Landa V, Mlejnek P, et al. Direct linkage of mitochondrial genome variation to risk factors for type 2 diabetes in conplastic strains. Genome Res. 2007;17:1319–26.PubMedCrossRefPubMedCentral
20.
Fuku N, Park KS, Yamada Y, Nishigaki Y, Cho YM, Matsuo H, et al. Mitochondrial haplogroup N9a confers resistance against type 2 diabetes in Asians. Am J Hum Genet. 2007;80:407–15.PubMedCrossRefPubMedCentral
21.
Park KS, Chan JC, Chuang LM, Suzuki S, Araki E, Nanjo K, et al. A mitochondrial DNA variant at position 16189 is associated with type 2 diabetes mellitus in Asians. Diabetologia. 2008;51:602–8.PubMedCrossRef
22.
Flaquer A, Baumbach C, Kriebel J, Meitinger T, Peters A, Waldenberger M, et al. Mitochondrial Genetic Variants Identified to Be Associated with BMI in Adults. PLoS One. 2014;9(8):e105116.PubMedCrossRefPubMedCentral
23.
Hales CN, Barker DJ. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. 1992;35:595–601.PubMedCrossRef
24.
Knowler WC, Pettitt DJ, Bennett PH, Williams RC. Diabetes mellitus in the Pima Indians: genetic and evolutionary considerations. Am J Phys Anthropol. 1983;62:107–14.PubMedCrossRef
25.
Cannon B, Nedergaard J. Thermogenesis challenges the adipostat hypothesis for body-weight control. Proc Nutr Soc. 2009;68(4):401–7.PubMedCrossRef
26.
Koleva DI, Orbetzova MM, Atanassova PK. Adipose tissue hormones and appetite and body weight regulators in insulin resistance. Folia Med (Plovdiv). 2013;55(1):25–32.
27.
Krebs HA, Eggleston LV. The effect of insulin on oxidations in isolated muscle tissue. Biochem J. 1938;32(5):913913.
28.
Echave P1, Machado-da-Silva G, Arkell RS, Duchen MR, Jacobson J, Mitter R, et al. Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis. J Cell Sci. 2009;122(24):4516–22.PubMedCrossRefPubMedCentral
29.
30.
Thayer KA, Heindel JJ, Bucher JR, Gallo MA. Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review. Environ Health Perspect. 2012;120(6):779–89.PubMedCrossRefPubMedCentral
31.
Liu C, Ying Z, Harkema J, Sun Q, Rajagopalan S. Epidemiological and experimental links between air pollution and type 2 diabetes. Toxicol Pathol. 2013;41(2):361–73.PubMedCrossRefPubMedCentral
32.
Lee DH, Lee IK, Song K, Steffes M, Toscano W, Baker BA, et al. A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999–2002. Diabetes Care. 2006;29(7):1638–44.PubMedCrossRef
33.
Ruzzin J, Petersen R, Meugnier E, Madsen L, Lock EJ, Lillefosse H, et al. Persistent organic pollutant exposure leads to insulin resistance syndrome. Environ Health Perspect. 2010;118(4):465–71.PubMedCrossRefPubMedCentral
34.
Virtanen MT. Histopathological and ultrastructural changes in the gills of Poeciliareticulatus induced by an organochlorine pesticide. J Environ Pathol Toxicol Oncol. 1986;7:73–85.PubMed
35.
Shertzer HG, Genter MB, Shen D, Nebert DW, Chen Y, Dalton TP. TCDD decreases ATP levels and increases reactive oxygen production through changes in mitochondrial F (0) F (1)-ATP synthase and ubiquinone. Toxicol Appl Pharmacol. 2006;217:363–74.PubMedCrossRefPubMedCentral
36.
Nakagawa Y, Suzuki T, Ishii H, Ogata A. Biotransformation and cytotoxicity of a brominated flame retardant, tetrabromobisphenol A, and its analogues in rat hepatocytes. Xenobiotica. 2007;37:693–708.PubMedCrossRef
37.
Lind L, Zethelius B, Salihovic S, van Bavel B, Lind PM. Circulating levels of perfluoroalkyl substances and prevalent diabetes in the elderly. Diabetologia. 2014;57(3):473–9.PubMedCrossRef
38.
Esposti MD, Ngo A, Myers MA. Inhibition of mitochondrial complex I may account for IDDM induced by intoxication with the rodenticide Vacor. Diabetes. 1996;45:1531–4.PubMedCrossRef
39.
Rahimi R, Abdollahi MA. review on the mechanism involved in hyperglycaemia induced by organophosphorus pesticides. Pestic Biochem Physiol. 2007;88:115–21.CrossRef
40.
Karami-Mohajeri S, Hadian MR, Fouladdel S, Azizi E, Ghahramani MH, Hosseini R, et al. Mechanisms of muscular electrophysiological and mitochondrial dysfunction following exposure tomalathion, an organophosphorus pesticide. Hum ExpToxicol. 2014;33(3):251–63.CrossRef
41.
McKinlay R, Plant JA, Bell JNB, Voulvoulis N. Endocrine disrupting pesticides: implications for risk assessment. Environ Int. 2008;34:168–83.PubMedCrossRef
42.
Jeong SH, Kim BY, Kang HG, Ku HK, Cho JH. Effect of chlorpyrifos-methyl on steroid and thyroid hormones in rat F0− andF1-generations. Toxicology. 2006;220:189–202.PubMedCrossRef
43.
Soloman KR, Baker DB, Richards RP, Dixon KR, Klaine SJ. Ecological risk assessment of atrazine in North American surface waters. Environ Toxicol Chem. 1996;15:31–76.CrossRef
44.
Lim S, Ahn SY, Song IC, Chung MH, Jang HC, Park KS, et al. Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance. PLoS One. 2009;4(4):e5186.PubMedCrossRefPubMedCentral
45.
Nicodemo D, Maioli MA, Medeiros HC, Guelfi M, Balieira KV, De Jong D, et al. Fipronil and imidacloprid reduce honeybee mitochondrial activity. Environ Toxicol Chem. 2014;33(9):2070–5.PubMedCrossRef
46.
Lind PM, Zethelius B. Circulating levels of phthalate metabolites are associated with prevalent diabetes in the elderly. Diabetes Care. 2012;35(7):1519–24.PubMedCrossRefPubMedCentral
47.
Hurst CH, Waxman DJ. Activation of PPARalpha and PPARgamma by environmental phthalate monoesters. Toxicol Sci. 2003;74:297–308.PubMedCrossRef
48.
Bility MT, Thompson JT, McKee RH, David RM, Butala JH, VandenHeuvel JP. Activation of mouse and human peroxisome proliferator-activated receptors (PPARs) by phthalate monoesters. Toxicol Sci. 2004;82:170.182.PubMed
49.
Posnack NG, Swift LM, Kay MW, Lee NH, Sarvazyan N. Phthalate exposure changes the metabolic profile of cardiac muscle cells. Environ Health Perspect. 2012;120(9):1243–51.PubMedCrossRefPubMedCentral
50.
Ishido M, Suzuki J. Classification of phthalates based on an in vitro neurosphere assay using rat mesencephalic neural stem cells. J Toxicol Sci. 2014;39(1):25–32.PubMedCrossRef
51.
Goodman M, Lakind JS, Mattison DR. Do phthalates act as obesogens in humans? A systematic review of the epidemiological literature. Crit Rev Toxicol. 2014;44(2):151–75.PubMedCrossRef
52.
Polyzos SA, Kountouras J, Deretzi G, Zavos C, Mantzoros CS. The emerging role of endocrine disruptors in pathogenesis of insulin resistance: a concept implicating nonalcoholic fatty liver disease. Curr Mol Med. 2012;12(1):68–82.PubMedCrossRef
53.
Alonso-Magdalena P, Quesada I, Nadal A. Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat Rev Endocrinol. 2011;7(6):346–53.PubMedCrossRef
54.
Moon MK, Kim MJ, Jung IK, Koo YD, Ann HY, Lee KJ, et al. Bisphenol A impairs mitochondrial function in the liver at doses below the no observed adverse effect level. J Korean Med Sci. 2012;27(6):644–552.PubMedCrossRefPubMedCentral
55.
Kaur K, Chauhan V, Gu F, Chauhan A. Bisphenol A induces oxidative stress and mitochondrial dysfunction in lymphoblasts from children with autism and unaffected siblings. Free Radic Biol Med. 2014;76C:25–33.PubMedCrossRef
56.
Chen YW, Yang CY, Huang CF, Hung DZ, Leung YM, Liu SH. Heavy metals and islet function and diabetes development. Islets. 2009;1:169–76.PubMedCrossRef
57.
58.
Jomova K, Jenisova Z, Feszterova M, Baros S, Liska J, Hudecova D, et al. Arsenic: toxicity, oxidative stress and human disease. J Appl Toxicol. 2011;31(2):95–107.PubMed
59.
Liu C, Ying Z, Harkema J, Sun Q, Rajagopalan S. Epidemiological and experimental links between air pollution and type 2 diabetes. Toxicol Pathol. 2013;41(2):361–73.PubMedCrossRefPubMedCentral
60.
Andersen ZJ, Raaschou-Nielsen O, Ketzel M, Jensen SS, Hvidberg M, Loft S, et al. Diabetes incidence and long-term exposure to air pollution: a cohort study. Diabetes Care. 2012;35(1):92–8.PubMedCrossRefPubMedCentral
61.
Coogan PF, White LF, Jerrett M, Brook RD, Su JG, Seto E, et al. Air pollution and incidence of hypertension and diabetes mellitus in black women living in Los Angeles. Circulation. 2012;125(6):767–72.PubMedCrossRefPubMedCentral
62.
Liu C, Bai Y, Xu X, Sun L, Wang A, Wang TY, et al. Exaggerated effects of particulate matter air pollution in genetic type II diabetes mellitus. Part Fibre Toxicol. 2014; 11:27.
63.
Adar SD, Filigrana PA, Clements N, Peel JL. Ambient Coarse Particulate Matter and Human Health: A Systematic Review and Meta-Analysis. Curr Environ Health Rep. 2014;8(1):258–74.
64.
Lewis W, Day BJ, Copeland WC. Mitochondrial toxicity of NRTI antiviral drugs: an integrated cellular perspective. Nat Rev Drug Discov. 2003;2:812–22.PubMedCrossRef
65.
Gerschenson M, Kim C, Berzins B, Taiwo B, Libutti DE J, Choi J, et al. Mitochondrial function, morphology and metabolic parameters improve after switching from stavudine to a tenofovir-containing regimen. J Antimicrob Chemother. 2009;63:1244–50.PubMedCrossRef
66.
Boelsterli UA, Lim PL. Mitochondrial abnormalities-a link to idiosyncratic drug hepatotoxicity? Toxicol Appl Pharmacol. 2007;220:92–107.PubMedCrossRef
67.
Amacher DE. Drug-associated mitochondrial toxicity and its detection. Curr Med Chem. 2005;12(16):1829–39.PubMedCrossRef
68.
Hectors TL, Vanparys C, Van Gaal LF, Jorens PG, Covaci A, Blust R. Insulin resistance and environmental pollutants: experimental evidence and future perspectives. Environ Health Perspect. 2013;121(11–12):1273–81.PubMedPubMedCentral
69.
Park WH, Jun DW, Kim JT, Jeong JH, Park H, Chang YS, et al. Novel cell-based assay reveals associations of circulating serum AhR-ligands with metabolic syndrome and mitochondrial dysfunction. Biofactors. 2013;39(4):494–504.PubMedCrossRef
70.
Shanle EK, Xu W. Endocrine disrupting chemicals targeting estrogen receptor signaling: identification and mechanisms of action. Chem Res Toxicol. 2011;24(1):6–19.PubMedCrossRefPubMedCentral
71.
Shizu R, Benoki S, Numakura Y, Kodama S, Miyata M, Yamazoe Y, et al. Xenobiotic-induced hepatocyte proliferation associated with constitutive active/androstane receptor (CAR) or peroxisome proliferator-activated receptor α (PPARα) is enhanced by pregnane X receptor (PXR) activation in mice. PLoS One. 2013;8(4):e61802.PubMedCrossRefPubMedCentral
72.
73.
Pereira-Fernandes A, Demaegdt H, Vandermeiren K, Hectors TL, Jorens PG, Blust R, et al. Evaluation of screening system for obesogenic compounds: screening of endocrinedisrupting compounds and evaluation of the PPAR dependency of the effect. PLoS One. 2013;8(10):e77481.PubMedCrossRefPubMedCentral
74.
75.
Kim JT, Kim SS, Jun DW, Hwang YH, Park WH, Pak YK, et al. Serum arylhydrocarbon receptor transactivating activity is elevated in type 2 diabetic patients with diabetic nephropathy. J Diabetes Investig. 2013;4(5):483–91.PubMedCrossRefPubMedCentral
Metadaten
Titel
Metabolic syndrome and the environmental pollutants from mitochondrial perspectives
Publikationsdatum
01.12.2014
Erschienen in
Reviews in Endocrine and Metabolic Disorders / Ausgabe 4/2014
Print ISSN: 1389-9155
Elektronische ISSN: 1573-2606
DOI
https://doi.org/10.1007/s11154-014-9297-5

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