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<p>The global prevalence of type 2 diabetes mellitus (T2DM) is rising exponentially, with alarming projections from the International Diabetes Federation estimating 589 million affected individuals in 2024 and more than 850 million in 2050. This represents an economic burden of approximately €1,015 billion worldwide. Traditional explanations such as sedentary lifestyle and overeating are insufficient to explain such a rapid expansion of the disease. Increasing attention has therefore turned toward the role of environmental endocrine disruptors (EDs), and, in particular, of persistent organic pollutants (POPs).</p><p>EDs are natural or synthetic molecules capable of altering endocrine function by interfering with biochemical pathways. They are omnipresent in daily life and have for several decades been implicated in reproductive or thyroid disorders, various hormone-dependent cancers (breast, prostate, testicular and colon cancers) and metabolic complications such as obesity.</p><p>To better understand their diabetogenic potential, numerous experimental studies have been conducted. In vitro findings showed that certain POPs increase insulin resistance in cultured adipocytes or myocytes. Bisphenol A, widely used in plastic manufacturing, induces an initial hypersecretion of insulin in pancreatic islets, followed by a later decrease in insulin sensitivity. In vivo animal studies similarly demonstrate strong diabetogenic effects.</p><p>In humans, epidemiological and longitudinal studies have revealed direct associations between exposure to POPs (e.g., organochlorine pesticides, dioxins, and polychlorinated biphenyls) and the onset of metabolic syndrome or T2DM. These effects were first observed after acute environmental exposure, such as the Seveso disaster. More recent large-scale studies confirm higher circulating levels of EDs in people living with obesity and/or T2DM, strongly demonstrating that these compounds are independent risk factors for insulin resistance.</p><p>Collectively, the evidence now supports a central role of EDs in the global rise of obesity and T2DM. Their contribution to the epidemic is no longer speculative but increasingly recognized as scientifically established.</p>

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Endocrine disruptors are contributing to type 2 diabetes mellitus

  • 期刊论文

  • 发表日期：

    2026年4月23日

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  • Sébastien Magnifico,
  • Charlotte Hinault-Boyer,
  • Nicolas Chevalier

摘要

The global prevalence of type 2 diabetes mellitus (T2DM) is rising exponentially, with alarming projections from the International Diabetes Federation estimating 589 million affected individuals in 2024 and more than 850 million in 2050. This represents an economic burden of approximately €1,015 billion worldwide. Traditional explanations such as sedentary lifestyle and overeating are insufficient to explain such a rapid expansion of the disease. Increasing attention has therefore turned toward the role of environmental endocrine disruptors (EDs), and, in particular, of persistent organic pollutants (POPs).

EDs are natural or synthetic molecules capable of altering endocrine function by interfering with biochemical pathways. They are omnipresent in daily life and have for several decades been implicated in reproductive or thyroid disorders, various hormone-dependent cancers (breast, prostate, testicular and colon cancers) and metabolic complications such as obesity.

To better understand their diabetogenic potential, numerous experimental studies have been conducted. In vitro findings showed that certain POPs increase insulin resistance in cultured adipocytes or myocytes. Bisphenol A, widely used in plastic manufacturing, induces an initial hypersecretion of insulin in pancreatic islets, followed by a later decrease in insulin sensitivity. In vivo animal studies similarly demonstrate strong diabetogenic effects.

In humans, epidemiological and longitudinal studies have revealed direct associations between exposure to POPs (e.g., organochlorine pesticides, dioxins, and polychlorinated biphenyls) and the onset of metabolic syndrome or T2DM. These effects were first observed after acute environmental exposure, such as the Seveso disaster. More recent large-scale studies confirm higher circulating levels of EDs in people living with obesity and/or T2DM, strongly demonstrating that these compounds are independent risk factors for insulin resistance.

Collectively, the evidence now supports a central role of EDs in the global rise of obesity and T2DM. Their contribution to the epidemic is no longer speculative but increasingly recognized as scientifically established.