4.8 Article

Biomimetic Glucose Trigger-Insulin Release System Based on Hydrogel Loading Bidentate β-Cyclodextrin

Journal

ADVANCED FUNCTIONAL MATERIALS
Volume 31, Issue 38, Pages -

Publisher

WILEY-V C H VERLAG GMBH
DOI: 10.1002/adfm.202104488

Keywords

diabetes; glucose receptors; hydrogels; insulin release; beta-cyclodextrin

Funding

  1. International Science AMP
  2. Technology Key Research and Development Program of Shaanxi [2020KWZ-006]
  3. Project of Foreign Experts [G20200241017]
  4. National Natural Science Foundation of China [11674263, 31700312, U1704192]
  5. Natural Science Foundation of Shaanxi Province [2021JM-385]
  6. Research Project Grant of the Joint Logistic Support [BLB18J014]
  7. Key Intergovernmental Special Projects of the National Key R AMP
  8. D Plan of the People's Republic of China [2018YFE0114200]
  9. Shaanxi University of Science and Technology
  10. Xi'an Weiyang District Science and Technology Fund [201927]

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Initiated by the specific binding between D-glucose and biological receptors, the delicate metabolic system in the human body regulates blood D-glucose levels, with insulin release playing a crucial role in preventing hyperglycemia and type I diabetes. A novel hydrogel system is presented, which responds specifically to D-glucose and releases insulin on demand, showing potential therapeutic efficacy in treating hyperglycemia.
Initiated by the specific binding between D-glucose and biological receptors, the human body has a delicate metabolic system to regulate blood D-glucose levels, but failing to release insulin would induce hyperglycemia or type I diabetes. While insulin delivery is an effective form of hyperglycemia therapy, the self-regulated triggering of insulin release for on-demand supplementation remains inadequate. Here, a biomimetic glucose trigger-insulin release system, that is, a bidentate beta-cyclodextrin-based hydrogel with preloaded insulin is presented; the dual self-regulated system shows a specific D-glucose response to realize accurate monitoring and simultaneous on-demand trigger insulin release. The specific binding between D-glucose and the bidentate beta-cyclodextrin induces the release of protons, causing macroscopic swelling of the hydrogel, subsequently triggering the on-demand and long-term supplementation of insulin. On the contrary, isomers of D-glucose, such as D-fructose and D-galactose, cause shrinking of the hydrogel, and retard insulin release. In-vivo studies in type I diabetic mice model ascertain that although the bidentate beta-CD hydrogel is preloaded with short-activity insulin, it exerts long-activity control of blood glucose level over 12 h.

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