Cadmium (Cd), as a pervasive environmental toxicant, can enter the human body through food and cigarette smoke 1. The response triggered by cadmium includes irritation to the digestive tract, build-up of fluids in the lungs, and damage to the kidneys and bones 2. In addition, cadmium affects the human gut microbiota environment. Therefore, it is hypothesized that chronic cadmium exposure can disrupt short-chain fatty acid production in gut microbiota, suppressing peptide YY secretion, accumulating fat, and elevating hemoglobin A1C. Male C57BL/6 mice (n=12/ group) were exposed to 10, 20, 30, 40, and 50 ppm CdCl for 1236 weeks to test the hypothesis. SCFAs, PYY, fat pad mass, and A1C were analyzed alongside positive controls (high-fat diet, high-protein diet, prebiotic fiber, streptozotocin) and saline-negative controls. Dose-dependent reductions in SCFAs (up to 40% decrease) and PYY (25% suppression) are observed, while increases in weights of the fat pads (15% increases) and elevated HBA1C levels (above 6.5%) are observed3. While cadmiums effects on gut microbiota composition are documented, its impact on SCFA bioactivity and downstream metabolic regulation remains unclear. These findings highlight cadmiums role in disrupting gut-metabolic axes and suggest therapeutic strategies targeting SCFA restoration.
Zixuan Ding (Wed,) studied this question.