Resistin Inhibits Insulin Secretion Through Inhibition of Insulin Granule Docking Via Downregulation of Rab3A in Pancreatic Beta-cells.
- Author:
Jae Hyung PARK
1
Author Information
1. Department of Physiology, Keimyung University School of Medicine, Daegu, Korea. physiopark@kmu.ac.kr
- Publication Type:Original Article
- Keywords:
Insulin secretion;
Obesity;
Rab3A;
Resistin;
Type 2 diabetes
- MeSH:
Adenosine Triphosphate;
Adipocytes;
Adipokines;
Calcium;
Cell Membrane;
Down-Regulation*;
Fluorescence;
Glucose;
Insulin Resistance;
Insulin*;
Muscle Cells;
Obesity;
Receptor, Insulin;
Resistin*
- From:Keimyung Medical Journal
2015;34(2):98-107
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Resistin is a recently described novel adipokine that has been suggested to play an important role in the development of insulin resistance and type 2 diabetes by inhibiting insulin receptor signaling in myocytes and adipocytes. In the present study, we evaluated the direct effect of resistin on insulin secretion in pancreatic beta-cells. After treatment with recombinant resistin for 30 min, changes in glucose uptake, intracellular ATP and calcium levels, and insulin secretion were measured in glucose-stimulated INS-1 cells. The number of insulin granules morphologically docked to the plasma membrane was measured using a total internal reflection fluorescence microscope. Resistin significantly inhibited glucose-stimulated insulin secretion in INS-1 cells. Although resistin had no effects on intracellular glucose uptake, ATP and calcium levels, it caused a significant decrease in the number of docked insulin granules. In addition, the expression of rab3A was decreased after treatment with resistin. These results suggest that resistin can inhibit insulin secretion through inhibition of insulin granule docking via downregulation of rab3A in pancreatic beta-cells. The present finding may also be an important mechanism of resistin for the development of type 2 diabetes.
