ABSTRACT
Silkworm silk protein fibroin is widely exploited to develop novel silk-based biomaterials due to its stable b-sheetstructure, providing high crystallinity and tensile strength. The polymorphic behaviour of silk fibroin provides awindow to modulate its structural transitions during self-assembly for different functional outcomes. Most studiesare therefore mainly focused on formation of well-developed b-sheet structure and self-assembly of silk fibroinwhich are regulated by many parameters. Glyoxal, a highly reactive a-oxoaldehyde, reacts with different proteinsto form advanced glycation end products (AGEs) following Maillard-like reaction. Considering the significanceof protein modification by glyoxal-derived AGEs, in the present study the effect of glyoxal (250, 500 and1000 lM) on the structure of silk fibroin has been investigated. CD and fluorescence studies reveal that higherconcentrations of the a-oxoaldehyde induce considerable alterations of secondary and tertiary structure of theprotein leading to aggregation following incubation with for 3 weeks. The aggregates exhibit fibrillar morphologywith amyloidal nature as evident from SEM, FTIR and XRD experiments. The findings highlight that glycationinduced modification can be a possible approach for modulating the conformation of the silk protein which may berelevant in connection to clinical, biomedical or synthetic biology based applications.
ABSTRACT
Acceleration of natural ageing occurs due to multiple reasons such as stress, obesity and Type 2 diabetes working in a vicious cycle. In the present study, we tested if superimposing type 2 diabetes in a rat model of obesity accelerates ageing or not. We aggravated insulin resistance/ induced type 2 diabetes by feeding high sucrose diet (HSD) to 9-10 wk old, male, WNIN/Gr-Ob obese rats. We report here the changes in physiological, biochemical and histological parameters after 3 and 6 months of feeding. Rats fed HSD had the highest insulin resistance as evident from increased HOMA IR and AUC insulin during OGTT. Body weight gain and Food efficiency ratio (FER) were also significantly higher in HSD fed than the control rats after 6 months of feeding. Further, liver steatosis and kidney damage were the highest in the HSD fed rats as evident from ORO staining. Interestingly, HSD fed rats also had the highest intensity of ß-cell staining and functioning (as indicated by higher HOMA-ß). The findings indicate that parameters associated with ageing were accelerated in WNIN/Gr-Ob rats fed HSD, implying that aggravating insulin resistance in obese rats may be associated with accelerated ageing.