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These outcomes are in agreement with previous experiments, suggesting that diabetes-aggravated ischemic damage was resulting from multifactorial interactions and normalization of hyperglycemia alone is not the major mechanism of neuroprotective effects
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It is understood to be caused by dysregulation of the complement system, leading to abnormal deposition of complement protein C3 in the kidneys glomeruli
16,51 The anxiolytic effect of GLP-1 agonists has been hypothesized due to the preservation of brain-derived neurotrophic factor/nuclear factor erythroid 2related factor 2 levels, decreased oxidative stress, and lipocalin 2 levels in the hippocampus
