Time-course study of high fat diet induced alterations in spatial memory, hippocampal JNK, P38, ERK and Akt activity

Abbasnejad, Zahra; Nasseri, Behzad; Zardooz, Homeira; Ghasemi, Rasoul

doi:10.1007/s11011-018-0369-1

Cited by 14 publications

(8 citation statements)

References 66 publications

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“…Currently, many reports have indicated that MAPK signaling are involved in response to metabolic stresses changes of extracellular or intracellular signals, such as glucose, circulating free fatty acids (FFAs) and intake HFD, which affect cell and organ metabolism [ 17 , 44 ]. In agreement with previous research reported that an increase in the activity of ERK1/2 after long-term HFD (20weeks) in hippocampus [ 19 ], our studies also revealed that 21 days HFD feeding increased the level of phospho-ERK1/2 significantly in cerebral cortex. However, other evidence have shown that after 16weeks of HFD feeding decrease ERK activity in the entire brain [ 20 ].…”

Section: Discussionsupporting

confidence: 93%

“…However, the limitations of current study should be stated. First, because similar results have been described in some literature [ 12 , 13 , 19 ], we did not explore the changes of metabolic parameters, such as glucose, cholesterol, insulin and triglyceride levels in blood, which may reflect changes of metabolic variables in short-term HFD-fed mice. Nevertheless, more recent studies suggest that cholesterol and triglyceride can induce neuroinflammation [ 40 , 50 ].…”

Section: Discussionmentioning

confidence: 98%

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Short-term high-fat diet favors the appearances of apoptosis and gliosis by activation of ERK1/2/p38MAPK pathways in brain

LiZhao

et al. 2021

Aging

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High-fat diet (HFD) has been associated with neuroinflammation and apoptosis in distinct brain regions. To explore the effect of short-term (7, 14 and 21 days) high-fat overfeeding on apoptosis, inflammatory signaling proteins, APP changes and glial cell activities in cerebral cortex and cerebellum. Mice were fed with HFD for different lengths (up to 21 days) and after each time body weights of mice was tested, then the apoptotic proteins, IL-1β, APP, BACE1and MAPKs, Akt and NF-κB signaling activity were evaluated by western blots. Results demonstrate that short period of high-fat overnutrition significantly promotes apoptosis, APP expression at day 21 of cerebral cortex and at day 7 of cerebellum compared to chow diet. In addition, increased GFAP + astrocytes, Iba-1 + microglia and IL-1β 30 were observed in cerebral cortex after 21 days HFD, but no changes for 7 days overfeeding of cerebellum. Serendipitously, ERK1/2 pathway was activated both in cerebral cortex and cerebellum for different time course of HFD. Furthermore, increased phospho-p38 MAPK level was observed in cerebellum only. In consistent with in vivo results, SH-SY5Y cells treatment with cholesterol (50 μM, 100 μM) for 48 h culture in vitro demonstrated that pro-apoptotic proteins were enhanced as well. In brief, short-term HFD consumption increases sensitivity to apoptosis, APP and IL-1β production as well as gliosis in cerebral cortex and cerebellum, which may be related to enhancement of ERK1/2 and p38 MAPK activation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Short-term high-fat diet favors the appearances of apoptosis and gliosis by activation of ERK1/2/p38MAPK pathways in brain

LiZhao

et al. 2021

Aging

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“…n = 5-7 per group did not alter pAkt Ser473 levels was in agreement with our results for the first two time points. Also, previous reports demonstrated that 16 and 20 weeks of a HFD or HFD/high fructose diet inhibited phosphorylation of Akt [26,27], whereas 26 weeks of a HFD increased pAkt Ser473 levels [25]. Although these studies differ from our study in terms of certain methodological factors such as species and dietary composition, the collected findings indicate that HFD-induced phosphorylation of Akt might be bimodal.…”

Section: Discussioncontrasting

confidence: 89%

“…Several recent studies reported similar kinetics in HFD-induced hippocampal pAkt Ser473 levels. Abbasnejad et al showed that a 2-week but not a 3-week HFD increased hippocampal pAkt Ser473 levels [25]. Their report that HFD-induced alterations can take place within 1 week might support our finding of substantial differences in hippocampal pAkt Ser473 and nNOS expression levels between 6 and 7 weeks of HFD treatment.…”

Section: Discussionsupporting

confidence: 87%

Anxiety-like behaviors and hippocampal nNOS in response to diet-induced obesity combined with exercise

Tobisawa

Yoshimura

et al. 2019

J Physiol Sci

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A high-fat diet (HFD) and overweight status can induce hippocampal dysfunction, leading to depression and anxiety. Exercise has beneficial effects on emotional behaviors. We previously reported that exercise training rescues HFD-induced excess hippocampal neuronal nitric oxide synthase (nNOS) expression, which is a key regulator of anxiety. Here, we investigated anxiety-like behaviors and hippocampal nNOS expression in response to HFD combined with exercise. Mice were assigned to standard diet, HFD, or HFD with exercise groups for 12 weeks. We found that exercise during the final 6 weeks of the HFD regime improved 12 weeks of HFD-induced defecation, accompanied by rescue of excess nNOS expression. However, anxiety indicators in the elevated plus maze were unchanged. These effects were not apparent after only 1 week of exercise. In conclusion, 6 weeks of exercise training reduced HFD-related anxiety according to one of our measures (defecation), and reversed changes in the hippocampal nNOS/NO pathway.

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“…The 7-9-year-old adolescents with the long-term intake of saturated fatty acids present a negative correlation with learning and memory function [25], as confirmed by the same performance in Zebrafish [26], which stimulates the interest in exploring the beneficial effect of regular exercise intervention on the mitigation of the HFD-induced impairment of learning and memory function and precision mechanisms through the mouse model, thereby providing a reference or guidance for health promotion. However, in 12-month-term HFD feeding, rats showed better learning and memory capacity and larger hippocampal volume [27], and the consumption of HFD for 6 months showed no spatial memory impairment [28]. This phenomenon, that a long-term high-fat diet does not trigger the changes in learning and memory capacity, may be related to stress, self-resistance, and the adaptation of neurons to high-fat diets, but the specific mechanisms need to be further explored.…”

Section: Discussionmentioning

confidence: 94%

Swimming Suppresses Cognitive Decline of HFD-Induced Obese Mice through Reversing Hippocampal Inflammation, Insulin Resistance, and BDNF Level

Zhang

Liang

et al. 2022

Nutrients

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Obesity is an important public health problem nowadays. Long-term obesity can trigger a series of chronic diseases and impair the learning and memory function of the brain. Current studies show that scientific exercise can effectively improve learning and memory capacity, which also can provide benefits for obese people. However, the underlying mechanisms for the improvement of cognitive capacity under the status of obesity still need to be further explored. In the present study, the obesity-induced cognition-declined model was established using 4-week-old mice continuously fed with a high-fat diet (HFD) for 12 weeks, and then the model mice were subjected to an 8-week swimming intervention and corresponding evaluation of relevant indicators, including cognitive capacity, inflammation, insulin signal pathway, brain-derived neurotrophic factor (BNDF), and apoptosis, for exploring potential regulatory mechanisms. Compared with the mice fed with regular diets, the obese mice revealed the impairment of cognitive capacity; in contrast, swimming intervention ameliorated the decline in cognitive capacity of obese mice by reducing inflammatory factors, inhibiting the JNK/IRS-1/PI3K/Akt signal pathway, and activating the PGC-1α/BDNF signal pathway, thereby suppressing the apoptosis of neurons. Therefore, swimming may be an important interventional strategy to compensate for obesity-induced cognitive impairment.

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Time-course study of high fat diet induced alterations in spatial memory, hippocampal JNK, P38, ERK and Akt activity

Cited by 14 publications

References 66 publications

Short-term high-fat diet favors the appearances of apoptosis and gliosis by activation of ERK1/2/p38MAPK pathways in brain

Short-term high-fat diet favors the appearances of apoptosis and gliosis by activation of ERK1/2/p38MAPK pathways in brain

Anxiety-like behaviors and hippocampal nNOS in response to diet-induced obesity combined with exercise

Swimming Suppresses Cognitive Decline of HFD-Induced Obese Mice through Reversing Hippocampal Inflammation, Insulin Resistance, and BDNF Level

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