Abstract
Studies show an association between cadmium (Cd) exposure and prediabetes or type II diabetes mellitus. We have previously reported that Cd causes decreased levels of serum leptin in rats following 12 weeks of daily Cd dosing (0.6 mg/kg/b.w./day). Since leptin plays an important role in metabolism, we examined the effects of Cd on rats and db/db mice, which are deficient in leptin receptor activity. We gave rats and mice daily subcutaneous injections of saline (control) or CdCl2 at a dose of 0.6 mg/kg of Cd for 2 weeks, followed by 2 weeks of no dosing. At the end of the 4-week study, exposure to Cd resulted in a more rapid increase in blood glucose levels following an oral glucose tolerance test in db/db vs. lean mice. During the two weeks of no Cd dosing, individual rat bodyweight gain was greater (p ≤ 0.05) in Cd-treated animals. At this time point, the combined epididymal and retroperitoneal fat pad weight was significantly greater (p ≤ 0.05) in the Cd-treated lean mice compared to saline-treated controls. Although this pilot study had relatively low N values (4 per treatment group for mice and 6 for rats) the results show that clinically relevant levels of Cd exposure resulted in diabetogenic as well as obesogenic effects.
Highlights
Cadmium (Cd) is a ubiquitous environmental contaminant that is a group 1 carcinogen with toxic effects in lung, liver, testicular, kidney and bone tissues [1]
The Cd content of the renal cortex was measured because the renal cortex is considered the greatest deposition site of Cd and the most accurate measure of long-term exposure, see Table 1
Cdexposure exposure subcutaneous injection)for fortwo twoweeks weeksfollowed followed by two weeks mice and rats, resulted levels in the renal cortex
Summary
Cadmium (Cd) is a ubiquitous environmental contaminant that is a group 1 carcinogen with toxic effects in lung, liver, testicular, kidney and bone tissues [1]. The kidney is considered the primary target organ of Cd toxicity with concentrations reaching the highest levels in the renal cortex over time. Human Cd content ranges widely in the kidney cortex from approximately 25 to 84 ug/g of wet tissue weight in individuals with non-occupational exposure [2,3]. Regardless, several studies show that Cd accumulates in the overall kidney (cortex and medulla) over time and a plateauing effect with peak concentrations occurs after roughly 50 years of age; for a review, see [4]. While Cd is primarily considered a nephrotoxicant, there is a body of literature showing significant correlations between exposure to Cd and the prevalence of prediabetes and/or type II diabetes mellitus [5,6,7]. It should be noted that not all studies have found significant associations between markers of Cd exposure and diabetes mellitus [8]
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