The metabolic and neuroinflammatory changes induced by consuming a cafeteria diet are age-dependent

Teixeira, D; Cecconello, Ana Lúcia; Partata, Wania Aparecida; Fraga, Luciano Stürmer de; Ribeiro, Maria Flávia Marques; Guedes, Renata Padilha

doi:10.1080/1028415x.2017.1380892

Cited by 21 publications

(17 citation statements)

References 68 publications

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“…www.nature.com/scientificreports/ Mice that consumed HFHS as adults showed increased microgliosis in the PrL PFC and all hippocampal subregions measured by IBA-1 fluorescence compared to the adolescent cohort, which was also associated with increased adiposity. Given that microglia respond to cytokines, this observation suggests that there may be some resistance to HFHS-induced neuroinflammation in younger animals, which has been previously observed in rats 44 . However, when we examined morphological changes in microglia-from resting (ramified) to active (hypertrophied) states-we found a significant reduction in ramified microglia and related increases in hypertrophied microglia within the PFC of mice exposed to the HFHS-diet during adolescence, but not as adults, which was positively correlated with adiposity.…”

Section: Discussionsupporting

confidence: 73%

“…Obesity is also associated with chronic inflammation due to the systemic release of inflammatory cytokines by adipocytes 42 , which then enter the brain via the blood brain barrier causing neuroinflammation 43 . The effects of obesogenic diets on neuroinflammation might occur in an age-dependent manner, with younger rats being more resistant to obesity-induced neuroinflammation, indicated by an increase in cortical interleukin-1β levels in 18-month-old, but not 3-month-old rats 44 . What has not yet been examined, however, is the role of microglia in HFHS-induced pathology across age groups.…”

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confidence: 99%

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Age-dependent and region-specific alteration of parvalbumin neurons, perineuronal nets and microglia in the mouse prefrontal cortex and hippocampus following obesogenic diet consumption

Reichelt

Lemieux

Princz-Lebel

et al. 2021

Sci Rep

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Emergent evidence demonstrates that excessive consumption of high fat and high sugar (HFHS) diets has negative consequences on hippocampal and prefrontal cortex (PFC) function. Moreover, the delayed maturation of the PFC including the late development of parvalbumin-expressing (PV) interneurons and perineuronal nets (PNNs) may promote vulnerability to HFHS diet-induced nutritional stress. However, the young brain may have some resistance to diet-induced neuroinflammation. Thus, we examined the impact of a HFHS diet commencing either in adolescence or adulthood in male mice. PV interneurons, PNNs and microglia were assessed using immunohistochemistry. We observed greater numbers of PV neurons and PNNs in the hippocampus and the prelimbic and infralimbic PFC in adult mice in comparison to our younger cohort. Mice that consumed HFHS diet as adults had reduced numbers of hippocampal PV neurons and PNNs, which correlated with adiposity. However, we saw no effects of diet on PV and PNNs in the PFC. HFHS diet increased microgliosis in the adult cohort, and morphological changes to microglia were observed in the PFC and hippocampus of the adolescent cohort, with a shift to activated microglia phenotypes. Taken together, these findings demonstrate different regional and age-specific effects of obesogenic diets on PV neurons, PNNs and microglia.

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Section: Discussionsupporting

confidence: 73%

mentioning

confidence: 99%

Age-dependent and region-specific alteration of parvalbumin neurons, perineuronal nets and microglia in the mouse prefrontal cortex and hippocampus following obesogenic diet consumption

Reichelt

Lemieux

Princz-Lebel

et al. 2021

Sci Rep

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“…It has also been shown that this response is age-dependent. Though, normally aged individuals are more prone to diet-induced neuroinflammation than young individuals 71 . Here, younger mice show a more pronounced inflammatory response to SRD.…”

Section: Discussionmentioning

confidence: 97%

Chia seeds as a potential cognitive booster in the APP23 Alzheimer’s disease model

Schreyer

Klein

Pfeffer

et al. 2020

Sci Rep

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Glucose hypometabolism potentially contributes to Alzheimer’s disease (AD) and might even represent an underlying mechanism. Here, we investigate the relationship of diet-induced metabolic stress and AD as well as the therapeutic potential of chia seeds as a modulator of glucose metabolism in the APP23 mouse model. 4–6 (pre-plaque stage, PRE) and 28–32 (advanced-plaque stage, ADV) weeks old APP23 and wild type mice received pretreatment for 12 weeks with either sucrose-rich (SRD) or control diet, followed by 8 weeks of chia seed supplementation. Although ADV APP23 mice generally showed functioning glucose homeostasis, they were more prone to SRD-induced glucose intolerance. This was accompanied by elevated corticosterone levels and mild insulin insensitivity. Chia seeds improved spatial learning deficits but not impaired cognitive flexibility, potentially mediated by amelioration of glucose tolerance, attenuation of corticosterone levels and reversal of SRD-induced elevation of pro-inflammatory cytokine levels. Since cognitive symptoms and plaque load were not aggravated by SRD-induced metabolic stress, despite enhanced neuroinflammation in the PRE group, we conclude that impairments of glucose metabolism do not represent an underlying mechanism of AD in this mouse model. Nevertheless, chia seeds might provide therapeutic potential in AD as shown by the amelioration of cognitive symptoms.

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“…In contrast, some studies have not observed significant differences in inflammatory biomarkers following adolescent HFD access (Kaczmarczyk et al, 2013; Wang et al, 2015). Recent evidence suggests that aged animals may be more susceptible to neuroinflammation following access to a cafeteria diet (Teixeira et al, 2019), suggesting an additional developmental period of vulnerability to high fat, high sugar diets.…”

Section: Discussionmentioning

confidence: 99%

Examining Adolescence as a Sensitive Period for High-Fat, High-Sugar Diet Exposure: A Systematic Review of the Animal Literature

Murray

Chen

2019

Front. Neurosci.

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Animal studies suggest that poor nutrition (e.g., high-fat, high-sugar diets) may lead to impairments in cognitive functioning. Accumulating evidence suggests that the deleterious effects of these diets appear more pronounced in animals maintained on this diet early in life, consistent with the notion that the developing brain may be especially vulnerable to environmental insults. The current paper provides the first systematic review of studies comparing the effects of high-fat, high-sugar diet exposure during adolescence and adulthood on memory performance. The majority of studies (7/8) identified here report diet-induced memory problems when diet exposure began in adolescence but not adulthood. These findings lend support to the hypothesis that adolescence is a sensitive period during which palatable diets may contribute to negative neurocognitive effects. The current review explores putative mechanisms involved in diet-induced cognitive dysfunction and highlights promising areas for further research.

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The metabolic and neuroinflammatory changes induced by consuming a cafeteria diet are age-dependent

Cited by 21 publications

References 68 publications

Age-dependent and region-specific alteration of parvalbumin neurons, perineuronal nets and microglia in the mouse prefrontal cortex and hippocampus following obesogenic diet consumption

Age-dependent and region-specific alteration of parvalbumin neurons, perineuronal nets and microglia in the mouse prefrontal cortex and hippocampus following obesogenic diet consumption

Chia seeds as a potential cognitive booster in the APP23 Alzheimer’s disease model

Examining Adolescence as a Sensitive Period for High-Fat, High-Sugar Diet Exposure: A Systematic Review of the Animal Literature

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