Effect of single or combined administration of resistant starch and chitosan oligosaccharides on insulin resistance in rats fed with a high‐fat diet. (16th December 2016)

• Record Type: Journal Article
• Authors: Wang, Junxuan; Si, Xu; Shang, Wenting; Zhou, Zhongkai; Strappe, Padraig; Blanchard, Chris
• Other Names: Bao Jinsong guestEditor.
• Is Part Of: Stärke. Volume 69:Number 7/8(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2016-12-16
• Subjects: Chitosan oligosaccharide -- Gene expression -- Gluconeogenesis -- Insulin resistance -- Resistant starch; Starch -- Periodicals; 572.566
• DOI: 10.1002/star.201600209
• Languages: English
• ISSNs: 0038-9056

Abstract

Abstract : In this study, rats fed with a high‐fat diet were treated with resistant starch (RS), chitosan oligosaccharide (COS), and a combination of these complexes with the aim of determining their effect on controlling blood glucose levels and improving insulin resistance (IR). Scanning electron microscopy (SEM) analysis demonstrated that an outer thin layer of film produced by COS covered the surface of RS granules and resulted in an increased particle size distribution. Cross‐linking between RS and COS was confirmed by Fourier transform infrared (FTIR) spectroscopy analysis. Treatment of rats revealed that blood glucose concentration was lowered to almost normal levels following the administration of either COS or COS–RS complexes. Furthermore, the homeostasis model of assessment for insulin resistance index (HOMA‐IR) was reduced and the quantitative insulin sensitivity check index (QUICKI) was increased with administration of COS–RS complexes. In summary, the consumption of COS‐RS complexes exerted a more efficient recovery of insulin sensitivity compared to individual treatments. Gene expression in liver tissue harvested from treated rats suggested that the improvement in insulin resistance was associated with enhanced hepatic glucose conversion through upregulation of GS2 and GYG1, reduction in gluconeogenesis was related to an upregulation in G6PC1 gene expression, and an alteration in glucolipid metabolism was associated with increased expression of Insig‐2 .