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Ocular manifestations of central insulin resistance

Neural Regeneration Research 2023年第5期18卷 1139-1146页

作者： Muneeb A.Faiq trina sengupta Madhu Nath Thirumurthy Velpandian Daman Saluja Rima Dada Tanuj Dada Kevin C.Chan Dr.Rajendra Prasad Centre for Ophthalmic Sciences All India Institute of Medical SciencesNew DelhiIndia Neuroimaging and Visual Science Laboratory Department of OphthalmologyNYU Grossman School of MedicineNYU Langone HealthNew York UniversityNew YorkNYUSA Medical Biotechnology Laboratory Dr.B.R.Ambedkar Center for Biomedical ResearchUniversity of DelhiDelhiIndia Dr.Baldev Singh Sleep Laboratory Department of PhysiologyAll India Institute of Medical SciencesNew DelhiIndia Department of Ocular Pharmacology Dr.Rajendra Prasad Center for Ophthalmic SciencesAll India Institute of Medical SciencesNew DelhiIndia Laboratory for Molecular Reproduction and Genetics Department of AnatomyAll India Institute of Medical SciencesNew DelhiIndia

Central insulin resistance, the diminished cellular sensitivity to insulin in the brain, has been implicated in diabetes mellitus, Alzheimer’s disease and other neurological disorders. However, whether and how central insulin resistance plays a role in the eye remains unclear. Here, we performed intracerebroventricular injection of S961, a potent and specific blocker of insulin receptor in adult Wistar rats to test if central insulin resistance leads to pathological changes in ocular structures. 80 mg of S961 was stereotaxically injected into the lateral ventricle of the experimental group twice at 7 days apart, whereas buffer solution was injected to the sham control group. Blood samples, intraocular pressure, trabecular meshwork morphology, ciliary body markers, retinal and optic nerve integrity, and whole genome expression patterns were then evaluated. While neither blood glucose nor serum insulin level was significantly altered in the experimental or control group, we found that injection of S961 but not buffer solution significantly increased intraocular pressure at 14 and 24 days after first injection, along with reduced porosity and aquaporin 4 expression in the trabecular meshwork, and increased tumor necrosis factor α and aquaporin 4 expression in the ciliary body. In the retina, cell density and insulin receptor expression decreased in the retinal ganglion cell layer upon S961 injection. Fundus photography revealed peripapillary atrophy with vascular dysregulation in the experimental group. These retinal changes were accompanied by upregulation of pro-inflammatory and pro-apoptotic genes, downregulation of anti-inflammatory, anti-apoptotic, and neurotrophic genes, as well as dysregulation of genes involved in insulin signaling. Optic nerve histology indicated microglial activation and changes in the expression of glial fibrillary acidic protein, tumor necrosis factor α, and aquaporin 4. Molecular pathway architecture of the retina revealed the three most s

关键词： brain ciliary bodies gene expression inflammation insulin receptor insulin resistance intraocular pressure neurodegeneration optic nerve retina retinal ganglion cells trabecular meshwork

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