Related Experiment Video

Updated: Aug 8, 2025

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

444

Sulfated fuco-manno-glucuronogalactan alleviates pancreatic beta cell senescence via PI3K/AKT/FoxO1 pathway

Wenjing Zhang1, Nan Wu1, Hong Wang1

  • 1Department of Endocrinology and Metabolism, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.

International Journal of Biological Macromolecules
|March 2, 2023
PubMed

Insights

A novel compound, sulfated fuco-manno-glucuronogalactan (SFGG), effectively reverses beta cell senescence and dysfunction. This discovery offers a promising new avenue for treating type 2 diabetes (T2D) and preventing disease progression.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Cellular senescence in pancreatic beta cells is a key driver of type 2 diabetes (T2D) onset.
  • Senescent beta cells exhibit impaired insulin synthesis and secretion, contributing to hyperglycemia.
  • Identifying therapeutic targets to combat beta cell senescence is crucial for T2D management.

Purpose of the Study:

  • To investigate the therapeutic potential of a sulfated fuco-manno-glucuronogalactan (SFGG) in alleviating beta cell senescence and dysfunction.
  • To elucidate the underlying molecular mechanisms by which SFGG impacts senescent beta cells.
  • To evaluate SFGG's efficacy in preclinical models of T2D.

Main Methods:

  • Structural analysis of SFGG to determine its composition and linkages.
  • In vitro and in vivo assessment of SFGG's effects on senescence markers (e.g., cell cycle arrest, SA-β-gal activity, DNA damage, SASP).
  • Evaluation of SFGG's impact on beta cell function, including insulin synthesis and glucose-stimulated insulin secretion.
  • Investigation of SFGG's mechanism of action, focusing on the PI3K/AKT/FoxO1 signaling pathway.

Main Results:

  • SFGG demonstrated significant alleviation of senescence-related phenotypes in beta cells, both in vitro and in vivo.
  • SFGG treatment improved key indicators of beta cell function, including insulin synthesis and glucose-stimulated insulin secretion.
  • Mechanistic studies revealed that SFGG attenuates beta cell senescence and enhances function through modulation of the PI3K/AKT/FoxO1 signaling pathway.
  • SFGG treatment reversed established senescence markers and restored normal beta cell function.

Conclusions:

  • SFGG is a potent agent for combating beta cell senescence and dysfunction.
  • SFGG holds significant therapeutic potential for the treatment of type 2 diabetes (T2D).
  • Targeting beta cell senescence with SFGG represents a promising strategy for alleviating T2D progression.
Keywords:
PI3K/AKT/FoxO1Pancreatic beta cell senescenceSulfated fuco-manno-glucuronogalactan

More Related Videos

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds12:32

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

Published on: January 23, 2018

12.1K
Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres09:31

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres

Published on: November 5, 2016

7.3K

Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
1.4K
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
5.1K
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
3.6K
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
224