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World J Diabetes. Oct 15, 2025; 16(10): 110041
Published online Oct 15, 2025. doi: 10.4239/wjd.v16.i10.110041
Figure 5
Figure 5 Insulin signaling cascade and glucose transporter type 4 translocation in type 1 diabetes. This figure illustrates the effects of healthy vs impaired pancreatic function on glucose metabolism in type 1 diabetes. In the healthy pancreas (panel A, left), functional β cells secrete insulin, which binds to its receptor on the cell membrane and activates a signaling cascade via insulin receptor substrate 1 (IRS-1) and IRS-2. This triggers the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB) pathway, promoting the translocation of glucose transporter type 4 (GLUT4) to the membrane and facilitating glucose entry into muscle cells. By contrast, panel B (right) depicts the absence of insulin secretion due to β-cell destruction, which disrupts activation of the IRS-1/IRS-2 and PI3K/PKB pathways. As a result, GLUT4 translocation is impaired, preventing glucose uptake and leading to hyperglycemia. This dysfunction is closely associated with inflammatory and oxidative stress in type 1 diabetes, reinforcing the importance of therapeutic strategies that preserve β-cell function or modulate inflammation.


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