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Investigating Susceptibility to Diabetes Using Features of the Adipose Tissue in Response to In Utero Polycyclic Aromatic Hydrocarbons Exposure (Diabetes Metab J 2016;40:494-508)

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D I A B E T E S & M E T A B O L I S M J O U R N A L

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Copyright © 2016 Korean Diabetes Association http://e-dmj.org

Investigating Susceptibility to Diabetes Using Features of the Adipose Tissue in Response to In Utero

Polycyclic Aromatic Hydrocarbons Exposure (Diabetes Metab J 2016;40:494-508)

Myoung Jin Ji, Sung Hee Choi

Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea

Corresponding author: Sung Hee Choi http://orcid.org/0000-0003-0740-8116 Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 82 Gumi-ro 173beon-gil, Bundang-gu, Seongnam 13620, Korea

E-mail: [email protected]

Polycyclic aromatic hydrocarbons (PAHs) is known as an envi- ronmental contaminant (there are more than 200 PAHs), which has multiple aromatic rings. PAH can be found in vari- ous environments including the situation of imperfect com- bustion of oil and coal. The toxicity of PAH occurs by binding to its receptor for arylhydrocarbons in humans [1,2]. Recent studies showed that PAH in the air was associated with insulin resistance and the development of type 2 diabetes mellitus [3- 5]. In addition, PAH exposure was related to higher prevalence of diabetes in American adults [6]. But the causality between PAH and metabolic diseases is still unknown.

In this article, Gato et al. [7] reported the influence of 2AA exposure to the fetus, with special focus on the changes of adi- pose tissue. They analyzed pups and pregnant dams from con- trol to high dose of 2AA exposure (0 to 100 mg/kg) in regular diet group and in moderate to high fat diet group. Serum glu- cose level was increased with increasing doses of 2AA in ani- mals. The mean sizes of adipocytes were larger in treated and combined 2AA and high fat diet group. Even if 2AA had influ- ences on insulin resistance and glucose metabolism, the results of exposure of 2AA in pregnant animals and direct effects on fetus are rare and interesting. We have several questions for your work [7].

First question is about weight changes in the animals. Al- though there is no significant differences, the high dose 2AA

group showed the lowest weight gain, which was even lower than control group in this experiment. The same phenomenon was shown regarding the accumulation of CD68 in adipocyte, which showed lowest expression in the high-dose of 2AA ex- posure. Considering that obesity and adipocyte inflammation are important factors in developing insulin resistance and dia- betes, this needs more explanation. Is chronic, low-dose expo- sure of PAH is more important than acute or high-dose expo- sure of PAH?

Second question is, were the size of adipocytes, serum glu- cose level, and the amount of adiponectin expression different according to differences in age of pregnant animals? For con- sidering the alteration of glucose metabolism and insulin resis- tance was significantly related to the higher age of the pregnant women [8-10].

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was re- ported.

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7. Gato WE, Hunter DA, Whitby SL, Mays CA, Yau W. Investi- gating susceptibility to diabetes using features of the adipose tissue in response to in utero polycyclic aromatic hydrocarbons exposure. Diabetes Metab J 2016;40:494-508.

8. Copeland KC, Colletti RB, Devlin JT, McAuliffe TL. The rela- tionship between insulin-like growth factor-I, adiposity, and aging. Metabolism 1990;39:584-7.

9. Solomon CG, Willett WC, Carey VJ, Rich-Edwards J, Hunter DJ, Colditz GA, Stampfer MJ, Speizer FE, Spiegelman D, Man- son JE. A prospective study of pregravid determinants of gesta- tional diabetes mellitus. JAMA 1997;278:1078-83.

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