Extract of Kuding tea prevents high-fat diet-induced metabolic disorders in C57BL/6 mice via liver X receptor (LXR) β antagonism

PLoS One. 2012;7(12):e51007. doi: 10.1371/journal.pone.0051007. Epub 2012 Dec 4.

Abstract

Objective: To investigate the effects of ilex kudingcha C. J. Tseng (kuding tea), a traditional beverage in China, on the metabolic disorders in C57BL/6 mice induced by high-fat diets.

Design: For the preventive experiment, the female C57BL/6 mice were fed with a standard diet (Chow), high-fat diet (HF), and high-fat diet mixed with 0.05% ethanol extract of kuding tea (EK) for 5 weeks. For the therapeutic experiment, the C57BL/6 mice were fed high-fat diet for 3 months, and then mice were split and EK was given with oral gavages for 2 weeks at 50 mg/day/kg. Body weight and daily food intake amounts were measured. At the end of treatment, the adipocyte images were assayed with a scanning electron microscope, and the fasting blood glucose, glucose tolerance test, serum lipid profile and lipids in the livers were analyzed. A reporter gene assay system was used to test the whether EK could act on nuclear receptor transcription factors, and the gene expression analysis was performed with a quantitative PCR assay.

Results: In the preventive treatment, EK blocked the body weight gain, reduced the size of the adipocytes, lowered serum triglyceride, cholesterol, LDL-cholesterol, fasting blood glucose levels and glucose tolerance in high-fat diet-fed C57BL/6 mice. In the therapeutic treatment, EK reduced the size of the white adipocytes, serum TG and fasting blood glucose levels in obese mice. With the reporter assay, EK inhibited LXRβ transactivity and mRNA expression of LXRβ target genes.

Conclusion: We observed that EK has both preventive and therapeutic roles in metabolic disorders in mice induced with high-fat diets. The effects appear to be mediated through the antagonism of LXRβ transactivity. Our data indicate that kuding tea is a useful dietary therapy and a potential source for the development of novel anti-obesity and lipid lowering drugs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / cytology
  • Adipocytes / drug effects
  • Animals
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics
  • Culture Media / pharmacology
  • Diet, High-Fat
  • Ethanol
  • Female
  • Gene Expression Regulation / drug effects
  • Hyperlipidemias / complications
  • Hyperlipidemias / drug therapy
  • Hyperlipidemias / pathology
  • Hyperlipidemias / prevention & control
  • Ligands
  • Lipogenesis / drug effects
  • Lipogenesis / genetics
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Liver X Receptors
  • Metabolic Diseases / drug therapy*
  • Metabolic Diseases / genetics
  • Metabolic Diseases / pathology
  • Metabolic Diseases / prevention & control*
  • Mice
  • Mice, Inbred C57BL
  • Obesity / complications
  • Obesity / drug therapy
  • Obesity / pathology
  • Obesity / prevention & control
  • Orphan Nuclear Receptors / antagonists & inhibitors*
  • Orphan Nuclear Receptors / metabolism
  • Phytotherapy
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use*
  • Tea / chemistry*

Substances

  • Culture Media
  • Ligands
  • Liver X Receptors
  • Orphan Nuclear Receptors
  • Plant Extracts
  • Tea
  • Ethanol

Grants and funding

This work was supported by National Natural Science Foundation of China (no. 30873260), the Talents Scheme from the Science and Technology Commission of Shanghai Municipality (no. 09XD1403800), the Supporting Project for Elitists in the New Century from The Ministry of Education (no. NCET-07563), the Shanghai Leading Academic Discipline Project (no. J50305 and E3008), and the XinLin Scholar and Outstanding Team Training Plan of Shanghai University of Traditional Chinese Medicine. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.