Berberine is a potential therapeutic agent for metabolic syndrome via brown adipose tissue activation and metabolism regulation

Xiaofei Hu, Yaqi Zhang, Yuan Xue, Zhuoli Zhang, Jian Wang*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations

Abstract

Berberine (BBR), an isoquinoline alkaloid that derived from the Chinese medicinal plant Coptis chinensis, has been identified with multiple pharmacological activities, including regulating glucose and cholesterol levels, anti-obesity effects and anti-diabetic effects. Due to its multiple activities, BBR and its metabolites have drawn great attention in biomedical research and clinical practices. After the recent re-discovery of brown adipose tissue (BAT) in adult humans, stimulating energy-dissipating via BAT activation and white-to-brown adipose tissue conversion have been regarded as potential therapeutic strategies for obesity and diabetes. Recent studies have demonstrated the activities of BBR in the activation of BAT and white-to-brown adipose tissue conversion, showing significant effectiveness in the treatment of diabetes. This review has summarized current studies that focused on the effect of BBR in the treatment of metabolic syndrome, especially in regulating BAT activities. Besides, the potential and molecular mechanisms of BBR in treating other risk factors of metabolic syndrome, including insulin resistance and dyslipidemia, are also reviewed, showing the great potential of BBR in treating the metabolic syndrome systematically.

Original languageEnglish (US)
Article numberAJTR0076780
Pages (from-to)3322-3329
Number of pages8
JournalAmerican Journal of Translational Research
Volume10
Issue number11
StatePublished - 2018

Keywords

  • Berberine
  • Brown adipose tissue
  • Metabolic syndrome
  • Obesity

ASJC Scopus subject areas

  • Molecular Medicine
  • Clinical Biochemistry
  • Cancer Research

Fingerprint

Dive into the research topics of 'Berberine is a potential therapeutic agent for metabolic syndrome via brown adipose tissue activation and metabolism regulation'. Together they form a unique fingerprint.

Cite this