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Polychlorinated biphenyls (PCB) are persistent environmental chemicals that are known thyroid hormone disrupters. Frequently the disruption of one endocrine axis and the timing of the disruption have an impact on other interdependent hormonal responses. Although the mechanisms for the interdependency of thyroid hormones and leptin have not been fully characterized, both are linked to development and regulation of metabolism. Furthermore, PCB accumulation in depot fat could potentially alter leptin production. In the present study 15-and 30-day-old Sprague-Dawley rats were exposed gestationally and lactationally to 1.25 ppm of Aroclor 1254®, a mixture of 52 PCB congeners, via maternal diet, to determine the effect on leptin and thyroid hormones. Additionally, young adult female rats were fed 1.25 PCB for 21 days and the same hormones were assessed. Serum leptin concentrations were determined by a sensitive murine leptin ELISA (DSL, Inc., Webster, TX). Serum thyroid hormone levels were determined by RIA kits (MP Biomedicals, Carson, CA). Leptin concentrations were significantly depressed in 15-day-old animals exposed to PCB when compared to same-aged control animals, while thyroid hormones were similar in control and experimental animals. Thirty-day-old PCB treated rats displayed significantly elevated leptin levels and depressed triiodothyronine concentrations. Young adult rats exposed to PCB for 21 days displayed significantly depressed leptin concentrations, however PCB had no effect on thyroid hormones in this group. In summary, exposure to dietary PCB, at relatively low concentrations, is leading to measurable alterations in serum leptin levels. We speculate that the accumulation of fat-soluble PCB in adipocytes may be sufficient to cause these alterations. Further investigation into the mechanism causing leptin alteration and long-term effects of such alterations is warranted.