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. 2022 Mar 16:13:841463.
doi: 10.3389/fendo.2022.841463. eCollection 2022.

Association of Organochlorine Pesticides With Genetic Markers of Endoplasmic Reticulum Stress in Type 2 Diabetes Mellitus: A Case-Control Study Among the North-Indian Population

Neha Tawar  1 , Basu Dev Banerjee  1 , Sri Venkata Madhu  2 , Vivek Agrawal  3 , Sanjay Gupta  3
Affiliations

Association of Organochlorine Pesticides With Genetic Markers of Endoplasmic Reticulum Stress in Type 2 Diabetes Mellitus: A Case-Control Study Among the North-Indian Population

Neha Tawar et al. Front Endocrinol (Lausanne). .

Abstract

Background: Organochlorine pesticides (OCPs) have been long linked to type 2 diabetes mellitus (T2DM); however, this relation at the molecular level has not been explored yet. Endoplasmic reticulum (ER) stress and pro-inflammatory pathways are considered vital ones in the pathogenesis of T2DM. We aimed to investigate the existence of any association between OCPs, ER stress, and pro-inflammatory pathways in subjects with known T2DM.

Methods: Seventy subjects each with T2DM and normal glucose tolerance were recruited from the surgery department. Their visceral adipose tissue was collected intraoperatively. OCP concentration, ER stress, and pro-inflammatory markers were analyzed and compared between two study groups.

Results: We found 18 OCPs and their metabolites in visceral adipose tissue samples of study participants. The levels of δ-HCH, heptachlor, endrin, and p,p'DDT were significantly higher in the T2DM group and were also positively correlated with fasting and postprandial plasma glucose levels (p < 0.01). We observed a positive association of δ-HCH (p < 0.01), heptachlor (p < 0.05), and endrin (p < 0.05) with central adiposity and ER stress markers. However, we failed to establish the correlation of OCPs with any of the pro-inflammatory markers.

Conclusion: The existence and simultaneous complex correlation of OCPs with ER stress may explain their role in the pathogenesis of T2DM, revealing the persistence of the gene-environment interaction in the etiology of T2DM.

Keywords: ER stress; OCP; T2DM; inflammation; normal glucose tolerance; visceral adipose tissue.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Comparison of OCP levels (ng/gm) in the T2DM (N = 70) and NGT (N = 70) groups. **p ≤ 0.01; ***p ≤ 0.001.
Figure 2
Figure 2
Correlation of OCPs with plasma glucose indices. Positive correlation of fasting plasma glucose with d-HCH (A), endrin (C), heptachlor (E), and p,p’DDT (G). Positive correlation of postprandial plasma glucose with d-HCH (B), endrin (D), heptachlor (F), and p,p’DDT (H).
Figure 3
Figure 3
Relative gene expression of ER stress and pro-inflammatory genes between thetwo groups. (A) Relative change in transcriptional expression of the genes. (B) Relative change in translational expression of the genes. (C) Western blot images of the genes. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001.
See this image and copyright information in PMC

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