Gut microbiota and serum metabolites reveal the effects of chongqing tuo tea on glucose and lipid metabolism disorders in high-fat diet-fed mice

Obesity and its associated metabolic disorders constitute a major and growing global health challenge, creating an urgent need for safe and effective dietary interventions. Chongqing Tuo Tea, a traditionally compressed tea produced from summer-autumn leaves, has a distinctive chemical profile. Although it has been found that Chongqing Tuo Tea extract (TTE) can improve glucose and lipid metabolism, the underlying mechanisms, particularly those mediated via the gut-liver axis, are not well-understood. In the present study, TTE ameliorated hepatic lipid accumulation, attenuated pancreatic damage, improved the integrity of the intestinal barrier, reduced white adipose tissue deposition and promoted its browning, enhanced glucose tolerance, alleviated insulin resistance, and alleviated lipid metabolic disorders and hepatic oxidative stress in high-fat diet (HFD)-fed mice. TTE ameliorated disorders of glucose metabolism and reduced insulin resistance by activating the hepatic AMPK and PI3K/Akt signaling pathways. It restored the gut microbiota by reversing the Firmicutes/Bacteroidetes (F/B) ratio and promoting the proliferation of beneficial bacteria such as Oscillospira and Bacteroides , thereby increasing the production of short-chain fatty acids, particularly acetic, butyric, and propionic acids. Serum metabolomics and pathway enrichment analysis revealed that TTE significantly regulated metabolism-related pathways, including caffeine metabolism; central carbon metabolism in cancer; phenylalanine metabolism; phenylalanine, tyrosine, and tryptophan biosynthesis; ABC transporters; and glycerophospholipid metabolism. Several potential biomarkers of HFD-induced metabolic dysregulation were identified, including L-histidine, uridine monophosphate, shikimate-3-phosphate, arachidonic acid, and diaminopimelic acid. These findings highlight the potential of dietary TTE supplementation as a strategy for mitigating HFD-induced weight gain and metabolic abnormalities. • TTE alleviated HFD-induced body weight gain and disorders of glucose and lipid metabolism in mice. • TTE ameliorated glucose metabolism disorders and attenuated insulin resistance by activating the hepatic AMPK and PI3K/Akt signaling pathways. • TTE reshaped gut microbiota composition in HFD-fed mice. • TTE significantly altered the serum metabolic profiles in HFD-induced obese mice.