Ginsenoside Rk1 Reduces Cell Stress and Prevents Cell Death in Diabetic Pancreas

Jenn Hoskins
28th May, 2024

Ginsenoside Rk1 Reduces Cell Stress and Prevents Cell Death in Diabetic Pancreas

Image Source: Natural Science News, 2024

Key Findings

  • The University of Macau study explored the effects of Ginsenoside Rk1 on pancreatic β-cells under ER stress and high-fat diet-induced diabetes
  • Ginsenoside Rk1 reduced ER stress-induced apoptosis in pancreatic β-cells by activating the IGF-1R pathway
  • In diabetic mice, Ginsenoside Rk1 decreased pancreas weights and increased pancreatic insulin content, suggesting protection against high-fat diet effects
Type 2 Diabetes Mellitus (T2DM) is a chronic condition characterized by high blood glucose levels due to insulin resistance and relative insulin deficiency caused by β-cell failure. One of the key factors contributing to β-cell dysfunction is endoplasmic reticulum (ER) stress, which can lead to cell apoptosis (programmed cell death)[2]. The University of Macau recently conducted a study to explore the effects of Ginsenoside Rk1, a compound derived from Ginseng, on ER stress-induced apoptosis in pancreatic β-cells and its potential as a treatment for T2DM[1]. The study aimed to investigate how Ginsenoside Rk1 affects ER stress in pancreatic β-cells and whether it can protect against β-cell apoptosis in a high-fat diet (HFD)-induced diabetic pancreas. Previous research has shown that various ginsenosides from Ginseng possess anti-diabetic properties, including the ability to improve insulin resistance and protect islet cells[3]. However, the specific effects of Ginsenoside Rk1 on pancreatic cells in the context of T2DM had not been studied until now. The researchers used a pancreatic β-cell line known as MIN6 and an HFD-induced diabetic mouse model to conduct their experiments. They discovered that Ginsenoside Rk1 alleviated ER stress-induced apoptosis in MIN6 cells by targeting and activating the insulin-like growth factor 1 receptor (IGF-1R). This activation triggered a cascade of events involving the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/B-cell lymphoma-2 (Bcl-2)-associated agonist of cell death (Bad)-Bcl-2 pathway. Essentially, this pathway helps cells survive under stress conditions by preventing apoptosis. To confirm the role of IGF-1R in mediating the anti-apoptotic effects of Ginsenoside Rk1, the researchers used an IGF-1R inhibitor called PQ401. The use of this inhibitor abolished the protective effects of Ginsenoside Rk1, thereby confirming that IGF-1R plays a crucial role in this process. In addition to the cellular experiments, the researchers also observed the effects of Ginsenoside Rk1 in an HFD-induced diabetic mouse model. They found that Ginsenoside Rk1 reduced pancreas weights and increased pancreatic insulin contents, suggesting that it could protect the pancreas from the detrimental effects of a high-fat diet, which is known to impair glucose metabolism and lead to insulin resistance[4]. This study ties together previous findings on the role of ER stress in β-cell dysfunction[2] and the anti-diabetic properties of various ginsenosides[3]. By demonstrating that Ginsenoside Rk1 can activate the IGF-1R pathway and protect β-cells from ER stress-induced apoptosis, the researchers have provided new insights into potential therapeutic strategies for T2DM. This is particularly significant given the complex nature of T2DM and the limited effectiveness of current treatments in addressing β-cell dysfunction. In summary, the University of Macau's study highlights the novel protective effects of Ginsenoside Rk1 on pancreatic β-cells under conditions of ER stress and high-fat diet-induced diabetes. By targeting IGF-1R and activating the PI3K/Akt/Bad-Bcl-2 pathway, Ginsenoside Rk1 shows promise as a potential drug for the treatment of T2DM, offering a new avenue for therapeutic intervention.

MedicineHealthBiochem

References

Main Study

1) Ginsenoside Rk1 Ameliorates ER Stress-Induced Apoptosis through Directly Activating IGF-1R in Mouse Pancreatic [Formula: see text]-Cells and Diabetic Pancreas.

Published 27th May, 2024

https://doi.org/10.1142/S0192415X24500484

Related Studies

2) Endoplasmic reticulum stress in the β-cell pathogenesis of type 2 diabetes.

https://doi.org/10.1155/2012/618396

3) Therapeutic Potential of Ginsenosides as an Adjuvant Treatment for Diabetes.

https://doi.org/10.3389/fphar.2018.00423

4) GLP-2 as Beneficial Factor in the Glucose Homeostasis in Mice Fed a High Fat Diet.

https://doi.org/10.1002/jcp.25039


Related Articles

An unhandled error has occurred. Reload 🗙