Figure 25.

A) Schematic diagram of nanocarrier transport. Five potential pathways for the transepithelial transport of nanocarriers: a) transcellular pathway; b) paracellular pathway through TJs located between epithelial cells; c) receptor‐mediated endocytosis; d) adsorptive‐mediated endocytosis; and e) M cell‐associated pathway across the epithelium. B) Mechanisms of stimulus‐responsive drug release: pH, temperature, redox potential, enzyme, light, or ultrasound stimulation changes nanocarrier structure (swelling or degradation), which leads to drug release. C) The potential antidiabetic mechanisms of NPs containing elements with insulin‐like activities (selenium, zinc, chromium, vanadium, and so forth). (↑): activation or increase, (↓): inhibition or decrease, (┤): inhibition, (?): not clear, HbA_1c: Hemoglobin A_1c, IRS‐1: insulin receptor substrate‐1, NPs: nanoparticles, SeCys: selenocysteine, GPx: glutathione peroxidase, and NO: nitric oxide. D) Inhibition of diabetes and the complications through the antioxidant activity of NPs. (↑): activation or increase, (↓): inhibition or decrease, (┤): inhibition, P38 MAPK: P38‐mitogen‐activated protein kinase, JAK: Janus tyrosine kinase, JNK: Jun N‐terminal kinase, Nf‐ĸB: nuclear factor‐ĸB, NPs: nanoparticles, and TGF‐β: transforming growth factor beta. Signal transduction pathways mediated by P38 MAPK, JAK, JNK, JUN, Nf‐kB and TGF‐β promote the occurrence and/or development of diabetic complications.