Improving glycemic control in model mice with type 2 diabetes by increasing superoxide dismutase (SOD) activity using silk fibroin hydrolysate (SFH).

Biochem Biophys Res Commun

Department of Medical Genetics, College of Medicine, Hallym University, Chuncheon, Gangwon-do, 24252, Republic of Korea. Electronic address:

Published: November 2017

AI Article Synopsis

  • * Mice treated with SFH had significantly lower fasting blood glucose and HbA1c levels, improved glucose and insulin tolerance, and a decrease in pancreatic islet cell death compared to untreated diabetic mice.
  • * The treatment also increased antioxidant enzyme activities and important proteins related to beta cell health, suggesting SFH helps protect pancreatic islets and manage blood sugar levels in type 2 diabetes.

Article Abstract

Islet cell dysfunction in type 2 diabetes is primarily attributed to the increased apoptosis of pancreatic beta cells. Silk fibroin hydrolysate (SFH) has an effect on blood in type 2 diabetes model mice (C57BL/KsJ-db/db). However, its exact mechanism is unknown. The type 2 diabetes model mice were randomly divided into non-diabetic mice (ND), diabetic mice (DB), and diabetic mice treated with silk fibroin hydrolysate (DB-SFH). The results showed that SFH significantly decreased fasting blood glucose and hemoglobin A1c (HbA1c). The oral glucose tolerance and insulin tolerance were significantly improved in the DB-SFH group. The DB-SFH group exhibited increased superoxide dismutase (SOD) activity in the plasma, as well as increased Mn-SOD and CuZn-SOD activities in the pancreatic islets. Furthermore, the pancreatic islet cells' death was decreased in the DB-SFH group. In the DB-SFH group, the protein expression of caspase-3 was significantly decreased compared with the DB group. The expression of the Nkx6.1 and Pdx1 proteins were increased in the DB-SFH group. The results suggest that SFH prevents the degeneration of pancreatic islets via increasing SOD while hyperglycemia is alleviated by maintaining beta cell mass in type 2 diabetes model mice.

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Source
http://dx.doi.org/10.1016/j.bbrc.2017.09.066DOI Listing

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