Actions of exendin-4 therapy on cognitive function and hippocampal synaptic plasticity in mice fed a high-fat diet

2010 ◽  
Vol 34 (8) ◽  
pp. 1341-1344 ◽  
Author(s):  
V A Gault ◽  
W D Porter ◽  
P R Flatt ◽  
C Hölscher
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
High Fat Diet ◽  
High Fat ◽  
Hippocampal Synaptic Plasticity

Maternal High-Fat Diet Multigenerationally Impairs Hippocampal Synaptic Plasticity and Memory in Male Rat Offspring

Endocrinology ◽  
2020 ◽  
Vol 162 (1) ◽  
Author(s):  
Cheng Lin ◽  
YanYan Lin ◽  
Ji Luo ◽  
JunRu Yu ◽  
YaNi Cheng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Learning And Memory ◽  
High Fat Diet ◽  
Maternal Diet ◽  
High Fat ◽  
Hippocampal Synaptic Plasticity ◽  
Insulin Replacement

Abstract As advances are made in the field of developmental origins of health and disease, there is an emphasis on long-term influence of maternal environmental factors on offspring health. Maternal high-fat diet (HFD) consumption has been suggested to exert detrimental effects on cognitive function in offspring, but whether HFD-dependent brain remodeling can be transmitted to the next generations is still unclear. This study tested the hypothesis that HFD consumption during rat pregnancy and lactation multigenerationally influences male offspring hippocampal synaptic plasticity and cognitive function. We observed that hippocampus-dependent learning and memory was impaired in 3 generations from HFD-fed maternal ancestors (referred as F1-F3), as assessed by novel object recognition and Morris water maze tests. Moreover, maternal HFD exposure also affected electrophysiological and ultrastructure measures of hippocampal synaptic plasticity across generations. We observed that intranasal insulin replacement partially rescued hippocampal synaptic plasticity and cognitive deficits in F3 rats, suggesting central insulin resistance may play an important role in maternal diet-induced neuroplasticity impairment. Furthermore, maternal HFD exposure enhanced the palmitoylation of GluA1 critically involved in long-term potentiation induction, while palmitoylation inhibitor 2-bromopalmitate counteracts GluA1 hyperpalmitoylation and partially abolishes the detrimental effects of maternal diet on learning and memory in F3 offspring. Importantly, maternal HFD-dependent GluA1 hyperpalmitoylation was reversed by insulin replacement. Taken together, our data suggest that maternal HFD exposure multigenerationally influences adult male offspring hippocampal synaptic plasticity and cognitive performance, and central insulin resistance may serve as the cross-talk between maternal diet and cognitive impairment across generations.

scholarly journals Necrostatin-1 Mitigates Cognitive Dysfunction in Prediabetic Rats With no Alteration in Insulin Sensitivity

2020 ◽  
Author(s):  
Ada Admin ◽  
Kewarin Jinawong ◽  
Nattayaporn Apaijai ◽  
Supawit Wongsuchai ◽  
Wasana Pratchayasakul ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Insulin Sensitivity ◽  
Cognitive Decline ◽  
High Fat Diet ◽  
Spine Density ◽  
High Fat ◽  
Dendritic Spine Density ◽  
Microglial Morphology ◽  
Brain Mitochondrial Function

Previous studies show that 12-week of high-fat diet (HFD) consumption caused not only prediabetes, but also cognitive decline and brain pathologies. Recently, necrostatin-1 (nec-1), a necroptosis inhibitor, showed beneficial effects in brain against stroke. However, the comparative effects of nec-1 and metformin on cognition and brain pathologies in prediabetes have not been investigated. We hypothesized that nec-1 and metformin equally attenuated cognitive decline and brain pathologies in prediabetic rats. Rats (n=32) were fed with either normal diet (ND) or high-fat diet (HFD) for 20 weeks. At week 13, ND-fed rats were given a vehicle (n=8) and HFD-fed rats were randomly assigned into 3 subgroups (n=8/subgroup) with vehicle, nec-1 or metformin for 8 weeks. Metabolic parameters, cognitive function, brain insulin receptor function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, Alzheimer’s protein, and cell death were determined.<b> </b>HFD-fed rats exhibited prediabetes, cognitive decline, and brain pathologies. Nec-1 and metformin equally improved cognitive function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, reduced hyperphosphorylated-tau and necroptosis in HFD-fed rats. Interestingly metformin, but not nec-1, improved brain insulin sensitivity in those rats.<b> </b><b> </b>In conclusion, necroptosis inhibition directly improved cognition in prediabetic rats without alteration in insulin sensitivity.

Effects of thymol on amyloid-β-induced impairments in hippocampal synaptic plasticity in rats fed a high-fat diet

2018 ◽  
Vol 137 ◽  
pp. 338-350 ◽  
Author(s):  
Masoumeh Asadbegi ◽  
Alireza Komaki ◽  
Iraj Salehi ◽  
Parichehreh Yaghmaei ◽  
Azadeh Ebrahim-Habibi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
High Fat Diet ◽  
Amyloid Β ◽  
High Fat ◽  
Hippocampal Synaptic Plasticity

scholarly journals Necrostatin-1 Mitigates Cognitive Dysfunction in Prediabetic Rats With no Alteration in Insulin Sensitivity

2020 ◽  
Author(s):  
Ada Admin ◽  
Kewarin Jinawong ◽  
Nattayaporn Apaijai ◽  
Supawit Wongsuchai ◽  
Wasana Pratchayasakul ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Insulin Sensitivity ◽  
Cognitive Decline ◽  
High Fat Diet ◽  
Spine Density ◽  
High Fat ◽  
Dendritic Spine Density ◽  
Microglial Morphology ◽  
Brain Mitochondrial Function

Previous studies show that 12-week of high-fat diet (HFD) consumption caused not only prediabetes, but also cognitive decline and brain pathologies. Recently, necrostatin-1 (nec-1), a necroptosis inhibitor, showed beneficial effects in brain against stroke. However, the comparative effects of nec-1 and metformin on cognition and brain pathologies in prediabetes have not been investigated. We hypothesized that nec-1 and metformin equally attenuated cognitive decline and brain pathologies in prediabetic rats. Rats (n=32) were fed with either normal diet (ND) or high-fat diet (HFD) for 20 weeks. At week 13, ND-fed rats were given a vehicle (n=8) and HFD-fed rats were randomly assigned into 3 subgroups (n=8/subgroup) with vehicle, nec-1 or metformin for 8 weeks. Metabolic parameters, cognitive function, brain insulin receptor function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, Alzheimer’s protein, and cell death were determined.<b> </b>HFD-fed rats exhibited prediabetes, cognitive decline, and brain pathologies. Nec-1 and metformin equally improved cognitive function, synaptic plasticity, dendritic spine density, microglial morphology, brain mitochondrial function, reduced hyperphosphorylated-tau and necroptosis in HFD-fed rats. Interestingly metformin, but not nec-1, improved brain insulin sensitivity in those rats.<b> </b><b> </b>In conclusion, necroptosis inhibition directly improved cognition in prediabetic rats without alteration in insulin sensitivity.

Actions of incretin metabolites on locomotor activity, cognitive function and in vivo hippocampal synaptic plasticity in high fat fed mice

Peptides ◽  
2012 ◽  
Vol 35 (1) ◽  
pp. 1-8 ◽  
Author(s):  
David Porter ◽  
Emilie Faivre ◽  
Peter R. Flatt ◽  
Christian Hölscher ◽  
Victor A. Gault
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Locomotor Activity ◽  
High Fat ◽  
Hippocampal Synaptic Plasticity

scholarly journals Effects of glucose-dependent insulinotropic polypeptide receptor knockout and a high-fat diet on cognitive function and hippocampal gene expression in mice

2012 ◽  
Vol 12 (1) ◽  
pp. 1544-1548 ◽  
Author(s):  
RACHAEL R. LENNOX ◽  
CHARLOTTE MOFFETT ◽  
DAVID W. PORTER ◽  
NIGEL IRWIN ◽  
VICTOR A. GAULT ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cognitive Function ◽  
High Fat Diet ◽  
High Fat

scholarly journals Neurodevelopmental Disorders: Effect of High-Fat Diet on Synaptic Plasticity and Mitochondrial Functions

2020 ◽  
Vol 10 (11) ◽  
pp. 805 ◽  
Author(s):  
Eduardo Penna ◽  
Amelia Pizzella ◽  
Fabiano Cimmino ◽  
Giovanna Trinchese ◽  
Gina Cavaliere ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neurodevelopmental Disorders ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Low Grade ◽  
High Fat ◽  
Mitochondrial Functions ◽  
Diet Pattern ◽  
Metabolic Dysfunctions ◽  
And Mitochondrial Functions

Neurodevelopmental disorders (NDDs) include diverse neuropathologies characterized by abnormal brain development leading to impaired cognition, communication and social skills. A common feature of NDDs is defective synaptic plasticity, but the underlying molecular mechanisms are only partially known. Several studies have indicated that people’s lifestyles such as diet pattern and physical exercise have significant influence on synaptic plasticity of the brain. Indeed, it has been reported that a high-fat diet (HFD, with 30–50% fat content), which leads to systemic low-grade inflammation, has also a detrimental effect on synaptic efficiency. Interestingly, metabolic alterations associated with obesity in pregnant woman may represent a risk factor for NDDs in the offspring. In this review, we have discussed the potential molecular mechanisms linking the HFD-induced metabolic dysfunctions to altered synaptic plasticity underlying NDDs, with a special emphasis on the roles played by synaptic protein synthesis and mitochondrial functions.

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