Uskoković Vuk
TardigradeNano LLC, 7 Park Vista, Irvine, CA 92604, USA.
Department of Mechanical Engineering, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182, USA.
Materials (Basel). 2023 Jan 13;16(2):786. doi: 10.3390/ma16020786.
Type 1 diabetes is caused by the inability of the pancreatic beta cells to produce sufficient amounts of insulin, an anabolic hormone promoting the absorption of the blood glucose by various cells in the body, primarily hepatocytes and skeletal muscle cells. This form of impaired metabolism has been traditionally treated with subcutaneous insulin injections. However, because one such method of administration does not directly correspond to the glucose concentrations in the blood and may fail to reduce hyperglycemia or cause hypoglycemia, the delivery of insulin in a glucose-dependent manner has been researched intensely in the present and past. This study tested the novel idea that the supplementation of polymeric reservoirs containing insulin with metallic nanoparticle precursors responsive to the redox effect of glucose could be used to create triggers for the release of insulin in direct response to the concentration of glucose in the tissue. For that purpose, manganese oxide nanoparticles were dispersed inside a poly(ε-caprolactone) matrix loaded with an insulin proxy and the resulting composite was exposed to different concentrations of glucose. The release of the insulin proxy occurred in direct proportion to the concentration of glucose in the medium. Mechanistically, as per the central hypothesis of the study, glucose reduced the manganese cations contained within the metal oxide phase, forming finer and more dissipative zero-valent metallic nanoparticles, thus disrupting the polymeric network, opening up pores in the matrix and facilitating the release of the captured drug. The choice of manganese for this study over other metals was justified by its use as a supplement for protection against diabetes. Numerical analysis of the release mechanism revealed an increasingly nonlinear and anomalous release accompanied by a higher diffusion rate at the expense of chain rigidity as the glucose concentration increased. Future studies should focus on rendering the glucose-controlled release (i) feasible within the physiological pH range and (ii) sensitive to physiologically relevant glucose concentrations. These technical improvements of the fundamental new concept proven here may bring it closer to a real-life application for the mitigation of symptoms of hyperglycemia in patients with diabetes.
1型糖尿病是由胰腺β细胞无法产生足够量的胰岛素引起的。胰岛素是一种合成代谢激素,可促进身体各细胞(主要是肝细胞和骨骼肌细胞)对血糖的吸收。这种代谢受损形式传统上通过皮下注射胰岛素进行治疗。然而,由于这种给药方法之一与血液中的葡萄糖浓度没有直接对应关系,可能无法降低高血糖或导致低血糖,因此目前和过去都在深入研究以葡萄糖依赖方式递送胰岛素。本研究测试了一个新想法,即向含有胰岛素的聚合物储库中添加对葡萄糖氧化还原作用有响应的金属纳米颗粒前体,可用于创建直接响应组织中葡萄糖浓度释放胰岛素的触发机制。为此,将氧化锰纳米颗粒分散在负载有胰岛素替代物的聚(ε-己内酯)基质中,并将所得复合材料暴露于不同浓度的葡萄糖中。胰岛素替代物的释放与培养基中葡萄糖的浓度成正比。从机制上讲,根据该研究的核心假设,葡萄糖还原了金属氧化物相中所含的锰阳离子,形成更细小且更易分散的零价金属纳米颗粒,从而破坏了聚合物网络,在基质中打开孔隙并促进捕获药物的释放。本研究选择锰而不是其他金属的理由是其可作为预防糖尿病的补充剂。对释放机制的数值分析表明,随着葡萄糖浓度的增加,释放呈现出越来越非线性和异常的特征,同时伴随着更高的扩散速率,但以链刚性为代价。未来的研究应专注于使葡萄糖控释(i)在生理pH范围内可行,以及(ii)对生理相关的葡萄糖浓度敏感。此处证明的这一基本新概念的这些技术改进可能使其更接近用于减轻糖尿病患者高血糖症状的实际应用。