Arsenic Exposure Decreases Adiposity During High-Fat Feeding.

Objective: Arsenic is an endocrine-disrupting chemical associated with diabetes risk. Increased adiposity is a significant risk factor for diabetes and its comorbidities. Here, the impact of chronic arsenic exposure on adiposity and metabolic health was assessed in mice.

Developmental exposure to the endocrine disruptor tolylfluanid induces sex-specific later-life metabolic dysfunction.

Endocrine-disrupting chemicals (EDCs) are implicated in the developmental mis-programming of energy metabolism. This study examined the impact of combined gestational and lactational exposure to the fungicide tolylfluanid (TF) on metabolic physiology in adult offspring. C57BL/6 J dams received standard rodent chow or the same diet containing 67 mg/kg TF.

Arsenic modifies serotonin metabolism through glucuronidation in pancreatic β-cells.

In arsenic-endemic regions of the world, arsenic exposure correlates with diabetes mellitus. Multiple animal models of inorganic arsenic (iAs, as As) exposure have revealed that iAs-induced glucose intolerance manifests as a result of pancreatic β-cell dysfunction. To define the mechanisms responsible for this β-cell defect, the MIN6-K8 mouse β-cell line was exposed to environmentally relevant doses of iAs.

Diet-dependence of metabolic perturbations mediated by the endocrine disruptor tolylfluanid.

Emerging evidence implicates environmental endocrine-disrupting chemicals (EDCs) in the pathogenesis of metabolic diseases such as obesity and diabetes; however, the interactions between EDCs and traditional risk factors in disease pathogenesis remain incompletely characterized. The present study interrogates the interaction of the EDC tolylfluanid (TF) and traditional dietary stressors in the promotion of metabolic dysfunction. Eight-week-old male C57BL/6 mice were fed a high-fat, high-sucrose diet (HFHSD) or a high-sucrose diet (HSD), with or without TF supplementation at 100 μg/g, for 12 weeks.

Arsenic exposure induces glucose intolerance and alters global energy metabolism.

Environmental pollutants acting as endocrine-disrupting chemicals (EDCs) are recognized as potential contributors to metabolic disease pathogenesis. One such pollutant, arsenic, contaminates the drinking water of ~100 million people globally and has been associated with insulin resistance and diabetes in epidemiological studies. Despite these observations, the precise metabolic derangements induced by arsenic remain incompletely characterized.

Dietary exposure to the endocrine disruptor tolylfluanid promotes global metabolic dysfunction in male mice.

Environmental endocrine disruptors are implicated as putative contributors to the burgeoning metabolic disease epidemic. Tolylfluanid (TF) is a commonly detected fungicide in Europe, and previous in vitro and ex vivo work has identified it as a potent endocrine disruptor with the capacity to promote adipocyte differentiation and induce adipocytic insulin resistance, effects likely resulting from activation of glucocorticoid receptor signaling. The present study extends these findings to an in vivo mouse model of dietary TF exposure.

Environmental endocrine disruption of energy metabolism and cardiovascular risk.

Rates of metabolic diseases have increased at an astounding rate in recent decades. Even though poor diet and physical inactivity are central drivers, these lifestyle changes alone fail to fully account for the magnitude and rapidity of the epidemic. Thus, attention has turned to identifying novel risk factors, including the contribution of environmental endocrine disrupting chemicals.