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. 2023 May 23;19(1):16–24. doi: 10.17925/EE.2023.19.1.16

Figure 2: Mechanisms of insulin-i nduced neuroprotective actions.

Figure 2:

Insulin-induced phosphorylation of insulin receptor substrate activates phosphoinositide-3 kinase (PI3K)/protein kinase B (Akt) and mitogen-activated kinase (MAPK) pathways. PI3K/ Akt pathway then inactivates glycogen synthase kinase 3β and forkhead box O and activates mammalian target of rapamycin. Altogether, insulin sensitive-dependent intracellular pathways regulate many mechanisms involved in cell survival, proliferation, apoptosis, protein synthesis, inflammation, endoplasmic reticulum stress, autophagy and mitochondrial function. Through cyclic adenosine monophosphate response element-binding protein, Akt also stimulates B cell lymphoma 2, B cell lymphoma extra-large and B cell lymphoma 2 antagonist of death, which regulates learning, memory and neuron survival. MAPK influences mechanisms involved in cell proliferation, differentiation, apoptosis or survival, and neuroinflammation.

Akt = protein kinase B; BAD = Bcl-2 antagonist of death; Bcl-2 = B cell lymphoma 2; Bcl-XL = B cell lymphoma extra-large; CREB = cyclic adenosine monophosphate response element-binding protein; ER = endoplasmic reticulum; FoxO = forkhead box O; GSK-3β = glycogen synthase kinase 3β; IRS = insulin receptor substrate; MAPK = mitogen-activated kinase; mTOR = mammalian target of rapamycin; PI3K = phosphoinositide-3 kinase.