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The Extraction of Liver Glycogen Molecules for Glycogen Structure Determination
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Hypoglycemic mechanism of a novel proteoglycan, extracted from Ganoderma lucidum, in hepatocytes

Zhou Yang1, Congheng Chen1, Juan Zhao1

  • 1State Key Laboratory of Molecular Engineering of Polymers, Department of Macromolecular Science, Fudan University, Shanghai 200433, PR China.

European Journal of Pharmacology
|December 14, 2017
PubMed

Insights

Ganoderma lucidum extract FYGL inhibits protein tyrosine phosphatase 1 B (PTP1B), improving insulin signaling and lowering blood glucose in type 2 diabetes models.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Metabolic Diseases

Background:

  • Protein tyrosine phosphatase 1 B (PTP1B) dephosphorylates insulin receptor substrate (IRS), disrupting insulin signaling and causing insulin resistance, a key factor in type 2 diabetes.
  • Ganoderma lucidum extract FYGL demonstrated hypoglycemic activity and PTP1B inhibition in previous studies, but its mechanism remained unclear.

Purpose of the Study:

  • To investigate the effects of FYGL on the insulin signaling pathway, targeting PTP1B in hepatocytes.
  • To elucidate the hypoglycemic mechanism of FYGL in vivo.

Main Methods:

  • Administered FYGL to ob/ob mice and HepG2 cells to assess its impact on PTP1B overexpression.
  • Analyzed the phosphorylation of IRS1, PI3K/Akt cascades, and GSK3β.
  • Evaluated insulin-stimulated glycogen synthesis in HepG2 cells and blood glucose levels in insulin resistance model mice.

Main Results:

  • FYGL inhibited PTP1B overexpression in liver tissues and HepG2 cells.
  • FYGL significantly improved IRS1 tyrosine phosphorylation and activated PI3K/Akt cascades.
  • FYGL enhanced insulin-stimulated glycogen synthesis and reduced blood glucose levels in mice.

Conclusions:

  • FYGL effectively targets PTP1B to improve insulin signaling and enhance glucose metabolism.
  • FYGL demonstrates potential as a therapeutic agent for managing type 2 diabetes.
Keywords:
GSK3βGanoderma lucidumHepatocytesPTP1B inhibitorProteoglycan

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