High-fat diet worsens the impact of aging on microglial function and morphology in a region-specific manner

Abstract

Hippocampal microglia are vulnerable to the effects of ageing, displaying a primed phenotype and hyper-responsiveness to various stimuli. We have previously shown that short-term high fat diet (HFD) significantly impairs hippocampal-and amygdala-based cognitive function in the aged without affecting it in the young. Here we assessed if morphological and functional changes in microglia might be responsible for this. We analysed hippocampus and amygdala from young and ageing rats that had been given three days HFD; a treatment sufficient to cause both hippocampaland amygdala-dependent cognitive and neuroinflammatory differences in the aged. Ageing led to the expected priming of hippocampal microglia in that it increased microglial numbers and reduced branching in this region. Ageing also increased microglial phagocytosis of microbeads in the hippocampus, but the only effect of HFD in this region was to increase the presence of enlarged synaptophysin boutons in the aged, indicative of neurodegeneration. In the amygdala, HFD exacerbated the effects of ageing on microglial priming (morphology) and markedly suppressed phagocytosis without notably affecting synaptophysin. These data reveal that, like the

Brain Metabolism Alterations in Type 2 Diabetes: What Did We Learn From Diet-Induced Diabetes Models?

“…Proliferation of microglia might also depend on the age of HFD exposure. Aged animals appear to be more susceptible to develop HFD-induced neuroinflammation (Spencer et al, 2019). Hsu et al (2015) also observed age-dependent inflammation effects of exposure to sugar-rich diets.…”

Glial remodeling enhances short-term memory performance in Wistar rats

“…For morphology in the 7and 14-day groups, all cells were categorized as ameboid (0-1 primary process), intermediate (2-4 primary processes), or ramified (five or more primary processes). We also assessed microglial complexity with a Sholl analysis on three cells per section from the same images as described in detail in [28]. Data were grouped into bins of 1-10 or 1-20 μm for analysis with repeated measures analyses of variance (ANOVA) followed, where significant, by Student's unpaired t tests.…”

Dietary fat exacerbates postprandial hypothalamic inflammation involving glial fibrillary acidic protein‐positive cells and microglia in male mice

“…While we focused on the HT because it is a well-known area involved in energy balance regulation (Gao & Horvath, 2008), we do not exclude the possibility that other brain areas may also display postprandial inflammation associated with neuropeptide modulation. Indeed, several studies have shown that chronic HFD consumption leads to hippocampal inflammatory responses and affects behavioral disorders associated with obesity (Abbink, van Deijk, Heine, Verheijen, & Korosi, 2019;Guillemot-Legris et al, 2016;Gzielo, Kielbinski et al 2017;Spencer, Basri et al 2019;Tsai, Wu et al 2018;Waise et al, 2015). Moreover, astrocytes in the brainstem dorsal vagal complex responds to acute nutritional excess (MacDonald et al, 2020).…”