Catechins prevent obesity-induced kidney damage by modulating PPARγ/CD36 pathway and gut-kidney axis in rats

Obesity is an epidemic and a growing public health concern worldwide. It is one of the significant risk factors for developing chronic kidney disease. In the present study, we evaluated the preventive effect of green tea catechins (GTC) against obesity-induced kidney damage and revealed the underlying molecular mechanism of action. Various green tea catechins were quantified in the catechins-rich fraction using HPLC. In vitro, the palmitic and oleic acid-treated NRK-52E cells showed reduced fat accumulation and modulated expressions of PPAR gamma, CD36, and TGF beta after GTC treatment. In vivo, rats were fed with a high-fat diet (HFD), and the effect of GTC was assessed at 150 and 300 mg/kg body weight doses. HFD-fed rats showed a significant reduction in weight gain and improved serum creatinine, urea, and urine microalbumin levels after GTC treatment. The improved adi-pokines and insulin levels in GTC treated groups indicated the insulin-sensitizing effect. Histopathology revealed reduced degenerative changes, fibrous tissue deposition, and mesangial matrix proliferation in GTC treated groups. GTC treatment also downregulated the gene expressions of lipogenic and inflammatory factors and improved the altered expressions of CD36 and PPAR gamma in the kidney tissue. Further, GTC prevented gut dysbiosis in rats by promoting healthy microbes like Akkermansia muciniphila and Lactobacillus reuteri. Faecal metabolome revealed reduced saturated fatty acids, and improved amino acid levels in the GTC treated groups, which help to maintain gut health and metabolism. Overall, GTC prevented obesity-induced kidney damage by modulating PPAR gamma/CD36 signaling and maintaining gut health in rats.

Automated summary

Obesity is a global epidemic and a major risk factor for chronic kidney disease. This study investigated the preventive effect of green tea catechins (GTC) on obesity-induced kidney damage and identified the molecular mechanism involved. In vitro experiments demonstrated that GTC treatment reduced fat accumulation and modulated the expressions of key molecules in fat metabolism in cultured kidney cells. In vivo experiments in rats fed a high-fat diet showed that GTC treatment significantly reduced weight gain and improved markers of kidney function. GTC also improved insulin sensitivity and reduced kidney tissue damage. Furthermore, GTC treatment promoted the growth of beneficial gut bacteria and improved gut health and metabolism. Overall, GTC prevented obesity-induced kidney damage by modulating specific signaling pathways and maintaining gut health.