Abstract
The pathology and neurodegeneration in type 2 diabetes- (T2D-) mediated Alzheimer's disease (AD) have been reported in several studies. Despite the lack of information regarding the basic underlying mechanisms involved in the development of T2D-mediated AD, some common features of the two conditions have been reported, such as brain atrophy, reduced cerebral glucose metabolism, and insulin resistance. T2D phenotypes such as glucose dyshomeostasis, insulin resistance, impaired insulin signaling, and systemic inflammatory cytokines have been shown to be involved in the progression of AD pathology by increasing amyloid-beta accumulation, tau hyperphosphorylation, and overall neuroinflammation. Similarly, oxidative stress, mitochondrial dysfunction, and the generation of advanced glycation end products (AGEs) and their receptor (RAGE) as a result of chronic hyperglycemia may serve as critical links between diabetes and AD. The natural dietary polyflavonoid anthocyanin enhances insulin sensitivity, attenuates insulin resistance at the level of the target tissues, inhibits free fatty acid oxidation, and abrogates the release of peripheral inflammatory cytokines in obese (prediabetic) individuals, which are responsible for insulin resistance, systemic hyperglycemia, systemic inflammation, brain metabolism dyshomeostasis, amyloid-beta accumulation, and neuroinflammatory responses. In this review, we have shown that obesity may induce T2D-mediated AD and assessed the recent therapeutic advances, especially the use of anthocyanin, against T2D-mediated AD pathology. Taken together, the findings of current studies may help elucidate a new approach for the prevention and treatment of T2D-mediated AD by using the polyflavonoid anthocyanin.
Highlights
Obesity and diabetes share the same pathways of activation of inflammatory mediators, which play a role in insulin resistance and the pathogenesis of type 2 diabetes (T2D)
A previous line of evidence suggested that adipose tissue macrophages release proinflammatory mediators to classically activate the M1 macrophages, which may contribute to insulin resistance and diabetes mellitus
Contagious diseases and contaminated foods increase the usage of broad-spectrum antibiotics, and prolonged usage of these drugs induces gut dysbiosis and reduces the abundance of beneficial bacteria, which are largely involved in the synthesis of multivitamins in the body
Summary
Obesity and diabetes share the same pathways of activation of inflammatory mediators, which play a role in insulin resistance and the pathogenesis of T2D. The pathogenesis of these disorders is associated with the number and phenotype of adipose tissue. A previous line of evidence suggested that adipose tissue macrophages release proinflammatory mediators to classically activate the M1 macrophages, which may contribute to insulin resistance and diabetes mellitus. Several basic mechanisms are involved in the development of T2D In one such mechanism, increased secretion of FFAs by adipose tissue in obese individuals induces the production of plasma malondialdehyde (MDA), which is a reactive product of lipid peroxidation. The daily consumption of natural dietary anthocyanin has been recently suggested to prevent various diseases and improve immune function [34,35,36,37]
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