PUBLICATION

Polysiphonia japonica Extract Attenuates Palmitate-Induced Toxicity and Enhances Insulin Secretion in Pancreatic Beta-Cells

Authors
Cha, S.H., Kim, H.S., Hwang, Y., Jeon, Y.J., Jun, H.S.
ID
ZDB-PUB-181205-5
Date
2018
Source
Oxidative medicine and cellular longevity   2018: 4973851 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Cell Survival
  • Cells, Cultured
  • Glucose/metabolism
  • Insulin Secretion/drug effects*
  • Insulin-Secreting Cells/drug effects
  • Insulin-Secreting Cells/metabolism*
  • Insulin-Secreting Cells/pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Palmitates/toxicity*
  • Plant Extracts/pharmacology*
  • Rats
  • Rhodophyta/chemistry*
  • Zebrafish
PubMed
30510621 Full text @ Oxid Med Cell Longev
Abstract
Beta-cell loss is a major cause of the pathogenesis of diabetes. Elevated levels of free fatty acids may contribute to the loss of β-cells. Using a transgenic zebrafish, we screened ~50 seaweed crude extracts to identify materials that protect β-cells from free fatty acid damage. We found that an extract of the red seaweed Polysiphonia japonica (PJE) had a β-cell protective effect. We examined the protective effect of PJE on palmitate-induced damage in β-cells. PJE was found to preserve cell viability and glucose-induced insulin secretion in a pancreatic β-cell line, Ins-1, treated with palmitate. Additionally, PJE prevented palmitate-induced insulin secretion dysfunction in zebrafish embryos and mouse primary islets and improved insulin secretion in β-cells against palmitate treatment. These findings suggest that PJE protects pancreatic β-cells from palmitate-induced damage. PJE may be a potential therapeutic functional food for diabetes.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping