Cadmium and lipid balance in outdoor workers exposed to urban stressor

Giammichele, Grazia; Ricci, Serafino; Pimpinella, Benedetta; Tomei, Gianfranco; Sacco, C; Suppi, A; Federica, De Marco; Donato, De Cesare Pompeo; Tomei, Francesco; Carlo, Monti

doi:10.1016/j.etap.2021.103793

Cited by 4 publications

(1 citation statement)

References 26 publications

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“…Our previous study using the same Cd exposure model (100 ppm for 30 days) showed that the Cd exposure increased Cd blood levels 38 similar to those found in occupationally Cd exposed employees, ranging between 1.2 and 50 μg/dL. 26,27,59 Kawakami et al (2010) reported that Cd is also able to accumulate in metabolic tissue, such as fat and liver after Cd exposure for 6 h (10, 20, and 30 μmol Cd/kg) or 14 days (5, 10, and 20 μmol Cd/kg) in male mice. Our results are consistent with these previous data because we demonstrated that Cd exposure increased Cd levels in the serum, parametrial, mesenteric, perirenal, retroperitoneal, and perivesical WAT, liver, pancreas, skeletal muscle, and thyroid gland.…”

Section: Discussionsupporting

confidence: 55%

Subacute cadmium exposure changes different metabolic functions, leading to type 1 and 2 diabetes mellitus features in female rats

da Costa,

de Oliveira,

Dos Santos

et al. 2024

Environmental Toxicology

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Cadmium (Cd) is a heavy metal that acts as endocrine disrupting chemical (EDC). Few studies have investigated the effects of Cd exposure on metabolic dysfunctions, such as type 1 and 2 diabetes mellitus (T1DM and T2DM). Thus, we assessed whether subacute Cd exposure at occupational levels causes abnormalities in white adipose tissue (WAT), liver, pancreas, and skeletal muscle. We administered cadmium chloride (CdCl2) (100 ppm in drinking water for 30 days) to female rats and evaluated Cd levels in serum and metabolic organs, morphophysiology, inflammation, oxidative stress, fibrosis, and gene expression. High Cd levels were found in serum, WAT, liver, pancreas, and skeletal muscle. Cd‐exposed rats showed low adiposity, dyslipidemia, insulin resistance, systemic inflammation, and oxidative stress compared to controls. Cd exposure reduced adipocyte size, hyperleptinemia, increased cholesterol levels, inflammation, apoptosis and fibrosis in WAT. Cd‐exposed rats had increased liver cholesterol levels, insulin receptor beta (IRβ) and peroxisome proliferator‐activated receptor‐gamma coactivator‐1alpha (PGC1α) expression, karyomegaly, inflammation, and fibrosis. Cd exposure reduced insulin levels and pancreatic islet size and increased inflammation and fibrosis. Cd exposure reduced skeletal muscle fiber diameter and increased IR expression and inflammation. Finally, strong positive correlations were observed between serum, tissue Cd levels, abnormal morphology, tissue inflammation and fibrosis. Thus, these data suggest that subacute Cd exposure impairs WAT, liver, pancreas and skeletal muscle function, leading to T1DM and T2DM features and other complications in female rats.

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