Theabrownin isolated from Pu‐erh tea regulates Bacteroidetes to improve metabolic syndrome of rats induced by high‐fat, high‐sugar and high‐salt diet

Abstract

BACKGROUND Theabrownin (TB), a high macromolecular compound and a characteristic component of Pu‐erh tea, is able to markedly regulate blood lipid and glucose metabolism. We hypothesized that TB could ameliorate metabolic syndrome induced by high‐fat, high‐sugar and high‐salt diet (HFSSD). RESULTS To test these hypotheses, we fed rats with HFSSD and administered a gavage of TB. HFSSD successfully induced metabolic syndrome in rats. TB significantly improved serum lipid status, prevented obesity and fasting blood glucose (FBG) and glycosylated hemoglobin (GHbAIc) in rats. After TB intervention, Firmicutes/Bacteroides (F/B) ratio was greatly reduced and showed a dose‐effect relationship. TB promoted the reproduction of Bacteroidetes such as prevotella_sp._CAG:1031, prevotella_sp._MGM2 and Bacteroides_sartorii, and inhibited the reproduction of Firmicutes such as roseburia_sp._1XD42‐69 and roseburia_sp._831b. CONCLUSION In HFSSD mode, prevotella_sp._CAG:1031 was one of the main dominant characteristic bacteria of TB targeting regulation, while roseburia_sp._1XD42‐69 mainly inhibitory intestinal bacteria, which help to reduce body weight, TG and blood sugar levels of HFSSD rats. Glycerophospholipid metabolism, arachidonic acid metabolism, glycolysis/gluconeogenesis and insulin resistance were the critical pathway. TB has a high application potential in reducing the risk of metabolic diseases. © 2022 Society of Chemical Industry.

Pu-erh tea partly improved liver cholesterol metabolism disorders in colitis mice via the gut-liver axis

“…Theabrownin may reduce intracellular lipid synthesis and accumulation by promoting the levels of adenosine triphosphate-binding transporter A1 and cholesterol 7α-hydroxylase in HepG2 cells [30][31] . Gavage of theabrownin in the high glucose model rats significantly reduced the extent of liver and pancreatic lesions and improved insulin resistance [32] . And recently, theabrownin was shown to be the main active component of Pu-erh tea in lowering cholesterol [18] , which balanced liver lipid homeostasis in mice by regulating gut microbes as well as bile acid metabolism.…”

An Ilex latifolia‐containing compound tea regulates glucose–lipid metabolism and modulates gut microbiota in high‐fat diet‐fed mice

“…After supplementation with CKT, the composition and structure of the gut microbiota changed, and the changes were reflected in the increase in Bacteroidota and the decrease in Firmicutes . Bacteroidota and Firmicutes are the main components of the gut microbiota, accounting for more than 90% of the gut microbiome in humans and mice (Stojanov et al., 2020; Yue et al., 2022). The Firmicutes/Bacteroidetes (F/B) ratio is widely accepted to have an important influence in maintaining normal intestinal homeostasis.…”

Theabrownin from Fu Brick tea ameliorates high-fat induced insulin resistance, hepatic steatosis, and inflammation in mice by altering the composition and metabolites of gut microbiota

“…In addition, the serum levels of adiponectin, leptin, and glucokinase are elevated after the TB intervention. 14,15,18 TB reduces hepatic triglyceride and cholesterol levels to greatly reduce fat deposition and prevent the formation of fatty liver. 16 TB also influences the activity of fatty acid oxidation-related enzymes in hepatocytes, increasing the activity of hormone-sensitive lipase (HSL) and carnitine palmitoyltransferases I and II (CPT I and CPT II), as well as inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA).…”

“…17 TB from Pu-erh tea also affects inflammation-related gut microbiota, such as reducing the increase in the ratio of Firmicutes / Bacteroidetes induced by a HFD. 18 Wang et al found that TB from Fu Brick tea increased the content of short chain fatty acids, especially butyrate, activating AMP activated protein kinase-peroxisome proliferator activated receptors-γ Co activating factor-1 α (AMPK-PGC1 α). The signaling pathway enhanced fat browning and upregulated the expression of heat producing genes uncoupling protein 1 (UCP-1) and PR domain protein 16 (PRDM16) closely related to lipolysis in adipose tissue.…”