Open AccessBerberine induces lipolysis in porcine adipocytes by activating the AMP‑activated protein kinase pathway
Author(s) -
Yongqing Yang,
Rongsheng Lu,
Fangfang Gao,
Jie Zhang,
Fenglan Liu
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.11070
Subject(s) - adipose triglyceride lipase , lipolysis , perilipin , ampk , protein kinase a , chemistry , amp activated protein kinase , medicine , phosphorylation , insulin resistance , endocrinology , insulin receptor , protein kinase b , biology , microbiology and biotechnology , adipose tissue , biochemistry , insulin
Lipolysis is closely associated with obesity and insulin resistance. Berberine (BBR), a natural alkaloid derived from Coptis chinensis, has been shown to regulate lipolysis and improve insulin resistance. However, the underlying mechanism remains unclear. The present results suggested that BBR stimulated lipolysis in porcine adipocytes in a dose‑ and time‑dependent manner, which was independent of the cAMP/protein kinase A pathway. Further experimental results indicated that BBR increased phosphorylation levels of AMP‑activated protein kinase (AMPK) and adipose triglyceride lipase (ATGL), along with downregulation of Perilipin A. The AMPK inhibitor compound C significantly reversed the effect of BBR on lipolysis, Perilipin A expression and ATGL phosphorylation. Furthermore, BBR promoted expression levels of genes related to fatty acid oxidation, such as peroxisome proliferator‑activated receptor γ coactivator‑1α, mitochondrial transcription factor A, carnitine palmitoyl‑transferase‑1 and uncoupling protein 2, which were abrogated by AMPKα1 knockdown. Moreover, it was found that BBR‑induced lipolysis did not elevate serine phosphorylation of insulin receptor substrate‑1 to block insulin signaling. Collectively, the present results suggested that BBR induced lipolysis in porcine adipocytes via a pathway that involves AMPK activation, but does not cause insulin resistance.