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The digestive tract is replete with complex and diverse microbial communities that are important for the regulation of multiple pathophysiological processes in humans and animals, particularly those involved in the maintenance of intestinal homeostasis, immunity, inflammation, and tumorigenesis. The diversity of bile acids is a result of the joint efforts of host and intestinal microflora. There is a bidirectional relationship between the microbial community of the intestinal tract and bile acids in that, while the microbial flora tightly modulates the metabolism and synthesis of bile acids, the bile acid pool and composition affect the diversity and the homeostasis of the intestinal flora. Homeostatic imbalances of bile acid and intestinal flora systems may lead to the development of a variety of diseases, such as inflammatory bowel disease (IBD), colorectal cancer (CRC), hepatocellular carcinoma (HCC), type 2 diabetes (T2DM), and polycystic ovary syndrome (PCOS). The interactions between bile acids and intestinal flora may be (in)directly involved in the pathogenesis of these diseases.

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Background: Exogenous exposure to cadmium is associated with cardiovascular diseases, including atherosclerosis, but experimental evidence elucidating the molecular events involved is still unclear, hence this study. We investigated whether sub-chronic cadmium exposure alone could cause a disruption in lipid and glucose metabolisms and whether the combined effect of these dysregulations could progressively lead to atherosclerosis in ApoE (-/-) mice. Methods: Experiments were performed in male ApoE (-/-) mice (8 weeks 25 ± 3g; n=60), which were randomly placed into four (4) groups according to body weight and administered cadmium (CdCl2) 0, 50, 100 and 200 mg/L, respectively in drinking water consecutively for 4 months. After treatment, changes in body weight were evaluated and mice plasma was analyzed for LDL, HDL, TCHO, TG, insulin and glucose levels. The collected samples were sent for histological examination in the 4th month and two-way ANOVA was used for statistical analysis. Results Levels of plasma LDL increased in all treatment groups but was statistically significant in the 4th month across all treatment groups when compared both with the blank control group and the first month mice. Plasma HDL levels were lowered in all treatment groups in the 2nd and 4th months when compared with the 1st month mice. Statistically significant decreases in plasma HDL levels were also observed in the 2nd month in the group receiving CdCl2 (100mg/L and 200mg/L) when compared with the blank control. TCHO and TG levels increased but was statistically significant in the former in the 1st, 2nd and 4th month at CdCl2 (100mg/L and 200mg/L) and in the latter at the same dose only in the 4th month. Moreover, fasting plasma glucose and insulin were elevated and lowered, respectively. Histological examination of aortal root also showed a dose-dependent increase in plaque formation, being most visible in the treatment group receiving CdCl2 (200mg/L). Conclusion: In line with our hypothesis, sub-chronic oral exposure of ApoE (-/-) mice to cadmium dysregulated their glucose and lipid profiles and the combined effect of this may be a contributory molecular event in the development of atherosclerosis. Keywords: Cadmium. Atherosclerosis. Glucose dysfunction. ApoE (-/-) mice. Lipid dysfunction. Atherosclerotic plaques