Abstract
Background:
In the past, most researchers paid more attention to the biological activity of tea infusion and tea polyphenols; however, the prebiotic role of tea leaf powder is still unknown. Green tea leaf powder is rich in dietary fiber and is suggested to be beneficial for human health. Only limited studies have looked at the effects of tea leaf powder (which mainly contains tea dietary fiber) on gut microbiota and health.
Objective:
The purpose of our study was to determine the effects of green tea leaf powder in preventing hyperlipidemia and to understand its potential lipid-lowering mechanism.
Design:
Mice in three treatment groups were fed high-fat diets (HFDs) by administering either 0.5, 1.0, or 2.0 g/kg•d dietary fiber-enriched green tea leaf powder of low, medium, or high, respectively, for 12 weeks. Serum biochemical analyses and mRNA gene expression levels of related energy and lipid metabolism biomarkers from the liver were investigated. In addition, 16S rRNA cecal microbiota and fecal short chain fatty acids (SCFAs) were tested.
Results:
Green tea leaf powder reduced body weight and total cholesterol of HFD-fed mice in a dose-dependent manner. Green tea leaf powder also increased satiety hormone secretion and reduced systemic inflammation of HFD-fed mice. Real-time polymerase chain reaction (PCR) analyses reconfirmed that green tea leaf powder prevented dyslipidemia by enhancing hepatic mRNA expression levels of peroxisome proliferator-activated receptor alpha, cholesterol 7α-hydroxylase, and Adenosine triphosphate (ATP)-binding cassette transporter A1 and decreasing the expression of fatty acid synthase, sterol regulatory element-binding protein 1c, and liver X receptor. Green tea leaf powder promoted the growth of Blautia, Oscillibacter, Ruminiclostridium, Alloprevotella, and Butyrivibrio and inhibited the growth of Erysipelatoclostridium, Desulfovibrio, and Candidatus_Saccharimonas in the cecum of HFD-fed mice.
Conclusion:
In summary, our results indicate that green tea leaf powder improves lipid metabolism of HFD-fed mice in a dose-dependent manner. The potential mechanism involves a synergistic role in reprogramming gut microbiota, increasing satiety hormone secretion, and reducing systemic inflammation.
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