Chronic pesticide exposure may increase the risk for obesity by suppressing diet-induced thermogenesis

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Abstract

Dear Editor,

The unregulated and injudicious use, or rather overuse, of pesticides in Pakistan is alarming. Pesticides are predominantly used in the agricultural industry, and Pakistan, being an agricultural country, is one of the largest consumers of pesticides in South Asia. The use of pesticides has increased by 1169% in the past two decades (more than 10 sprays per crop), raising great concerns and posing a grave threat to the ecosystem(1). According to the pre-existing literature, the urinary levels of biomarkers for chlorpyrifos (an organophosphate pesticide) and diazinon are high in workers of the pesticide industry, and general residents of areas around these industries, due to the pesticide loading onto dust. Thus pesticides engender significant health risks to occupational workers such as farmers and pesticide industry workers and  residential populations (2). Apart from the well-recognized dermatological, gastrointestinal, respiratory, carcinogenic, neurological and endocrine effects of pesticide exposure (3), a novel consequence in recent studies is the reduction of diet-induced thermogenesis in those chronically exposed to pesticides. Some of the most commonly used pesticides, such as chlorpyrifos, may thus be the yet-neglected precursors of obesity in the developing world. A recent ground-breaking study has hypothesized (with sufficient evidence) that the pesticide chlorpyrifos promotes obesity by suppressing diet-induced thermogenesis in brown adipose tissue. Obesity is responsible for multiple pathological conditions, including insulin resistance, high blood pressure, non-alcoholic fatty liver disease (NAFLD) and dyslipidaemias. The study has thus sparked major concerns.

So, the question arises: What is the specific mechanism that would likely explain the possible role of pesticides in obesity?

Uncoupling protein 1 (UCP1) is a well-documented protein that has a vital role in adaptive thermogenesis. Its role has been validated by prior studies involving the experimental removal of the UCP 1 gene in mice and the resulting obesity, insulin resistance, and NAFLD observed on administration of a high- fat diet and thermoneutral environment [5]. During the study under discussion, analysis of food contaminants at concentrations as low as 1 pM revealed the gene repression of UCP1 by chlorpyrifos. It does this by a twofold mechanism, namely the reduction of UCP1 promoter activity and mRNA expression, ultimately suppressing UCP1 protein. In addition, chronic exposure to even small quantities disrupted brown adipose tissue mitochondrial functions such as fatty acid oxidation regulation and cytochrome c oxidase assembly factor.

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https://doi.org/10.47391/JPMA.5456