scholarly journals La capacidad de inhibición de respuesta y la memoria a corto plazo son robustos a los efectos de la dieta alta en grasa (HFD) durante la pre y periadolescencia

2014 ◽  
Vol 13 (3) ◽  
Author(s):  
Elizabeth Watterson ◽  
Arturo R Zavala ◽  
Gregory J Privitera ◽  
Federico Sanabria

Several lines of evidence demonstrate that high fat diet exposure can be detrimental to cognition across the lifespan. We have previously shown that context-stimulus learning is sensitive to high fat diet effects during adolescence but not adulthood. In the present study we determined if pre and periadolescent high fat diet exposure interferes with response-inhibition capacity, rule- learning, and memory during adulthood. Rats were fed a high fat or low fat diet during pre and periadolescence and completed behavioral testing as adults to assess response-inhibition capacity and reinforcer efficacy rule-learning and short-term memory. Results indicate pre and periadolescent high fat diet may have long-term effects on reinforcer efficacy and sustained attention. However, results indicate that either the pre and periadolescence period is too short for a high fat diet to induce long-term deficits in response-inhibition, rule-learning, or memory, or that maturation in the absence of a high fat diet rescued these deficits.

2019 ◽  
Vol 29 ◽  
pp. S225-S226
Author(s):  
M. Mazzelli ◽  
N. Cattane ◽  
C. Mora ◽  
V. Begni ◽  
A. Berry ◽  
...  

2007 ◽  
Vol 293 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
Michelle Lee ◽  
Andrea Kim ◽  
Streamson C. Chua ◽  
Silvana Obici ◽  
Sharon L. Wardlaw

To determine whether long-term melanocortinergic activation can attenuate the metabolic effects of a high fat diet, mice overexpressing an NH2-terminal POMC transgene that includes α- and γ3-MSH were studied on either a 10% low-fat diet (LFD) or 45% high-fat diet (HFD). Weight gain was modestly reduced in transgenic (Tg-MSH) male and female mice vs. wild type (WT) on HFD ( P < 0.05) but not LFD. Substantial reductions in body fat percentage were found in both male and female Tg-MSH mice on LFD ( P < 0.05) and were more pronounced on HFD ( P < 0.001). These changes occurred in the absence of significant feeding differences in most groups, consistent with effects of Tg-MSH on energy expenditure and partitioning. This is supported by indirect calorimetry studies demonstrating higher resting oxygen consumption and lower RQ in Tg-MSH mice on the HFD. Tg-MSH mice had lower fasting insulin levels and improved glucose tolerance on both diets. Histological and biochemical analyses revealed that hepatic fat accumulation was markedly reduced in Tg-MSH mice on the HFD. Tg-MSH also attenuated the increase in corticosterone induced by the HFD. Higher levels of Agrp mRNA, which might counteract effects of the transgene, were measured in Tg-MSH mice on LFD ( P = 0.02) but not HFD. These data show that long-term melanocortin activation reduces body weight, adiposity, and hepatic fat accumulation and improves glucose metabolism, particularly in the setting of diet-induced obesity. Our results suggest that long-term melanocortinergic activation could serve as a potential strategy for the treatment of obesity and its deleterious metabolic consequences.


2016 ◽  
Vol 310 (11) ◽  
pp. E886-E899 ◽  
Author(s):  
Pia Kiilerich ◽  
Lene Secher Myrmel ◽  
Even Fjære ◽  
Qin Hao ◽  
Floor Hugenholtz ◽  
...  

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.


Neurology ◽  
2019 ◽  
Vol 93 (14 Supplement 1) ◽  
pp. S2.3-S3
Author(s):  
Clara Alexandra Stafford ◽  
Bobby Stojanoski ◽  
Conor Wild ◽  
Adrian Owen

ObjectiveWe investigated the long-term cognitive effects of concussion in almost 20,000 members of the general population, using tests that are known to be sensitive to small changes in performance.BackgroundConcussions are the most common type of mild traumatic brain injury, with clinical symptoms such as headaches, dizziness, and nausea, persisting for months post-injury. Despite a growing understanding of the severity and duration of these symptoms, very little is known about the long-term effects of concussion on higher level cognitive functioning and emotional lability.Design/MethodsWe asked 19,261 participants to complete a demographic questionnaire as well as the Cambridge Brain Sciences (CBS) cognitive battery. We divided our sample into two groups: those reporting at least one concussion in their lifetime (post-concussion) and those reporting no concussions in their lifetime (non-concussed). We compared the performance of the two groups on the 12 CBS tasks, as well as on four non-cognitive variables measuring levels of social contact, anxiety, depression, and concentration difficulties.ResultsWe found that post-concussion individuals performed significantly worse on a modified Stroop task that measures aspects of response inhibition, but were no worse on any other cognitive measure, including short-term memory, reasoning, and verbal abilities. Crucially, performance profiles of the post-concussion individuals indicated that they made more errors on trials that involved an incongruent colour/word pair. Beyond measures of cognition, we found that post-concussion participants also reported higher levels of anxiety, depression, and trouble concentrating when compared to the non-concussed group. The number of reported concussions also predicted task scores on this task only.ConclusionsOur results suggest that sustaining a concussion is not associated with long-term global effects on cognition. Those who report at least one concussion appear to have a modest, but statistically significant deficit of response inhibition. This impairment seems to be related to the number of concussions reported.


2009 ◽  
Vol 296 (4) ◽  
pp. E898-E903 ◽  
Author(s):  
Gabriel Paulino ◽  
Claire Barbier de la Serre ◽  
Trina A. Knotts ◽  
Pieter J. Oort ◽  
John W. Newman ◽  
...  

The vagal afferent pathway is important in short-term regulation of food intake, and decreased activation of this neural pathway with long-term ingestion of a high-fat diet may contribute to hyperphagic weight gain. We tested the hypothesis that expression of genes encoding receptors for orexigenic factors in vagal afferent neurons are increased by long-term ingestion of a high-fat diet, thus supporting orexigenic signals from the gut. Obesity-prone (DIO-P) rats fed a high-fat diet showed increased body weight and hyperleptinemia compared with low-fat diet-fed controls and high-fat diet-induced obesity-resistant (DIO-R) rats. Expression of the type I cannabinoid receptor and growth hormone secretagogue receptor 1a in the nodose ganglia was increased in DIO-P compared with low-fat diet-fed controls or DIO-R rats. Shifts in the balance between orexigenic and anorexigenic signals within the vagal afferent pathway may influence food intake and body weight gain induced by high fat diets.


2018 ◽  
Vol 507 (1-4) ◽  
pp. 291-296 ◽  
Author(s):  
Saki Yoshimura ◽  
Shihoko Nakashima ◽  
Yuki Tomiga ◽  
Shotaro Kawakami ◽  
Yoshinari Uehara ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Darren J. Fernandes ◽  
Shoshana Spring ◽  
Anna R. Roy ◽  
Lily R. Qiu ◽  
Yohan Yee ◽  
...  

AbstractMaternal environmental exposures, such as high-fat diets, diabetes and obesity, can induce long-term effects in offspring. These effects include increased risk of neurodevelopmental disorders (NDDs) including autism spectrum disorder (ASD), depression and anxiety. The mechanisms underlying these late-life neurologic effects are unknown. In this article, we measured changes in the offspring brain and determined which brain regions are sensitive to maternal metabolic milieu and therefore may mediate NDD risk. We showed that mice exposed to a maternal high-fat diet display extensive brain changes in adulthood despite being switched to a low-fat diet at weaning. Brain regions impacted by early-life diet include the extended amygdalar system, which plays an important role in reward-seeking behaviour. Genes preferentially expressed in these regions have functions related to feeding behaviour, while also being implicated in human NDDs, such as autism. Our data demonstrated that exposure to maternal high-fat diet in early-life leads to brain alterations that persist into adulthood, even after dietary modifications.


2020 ◽  
Author(s):  
Darren J. Fernandes ◽  
Shoshana Spring ◽  
Anna R. Roy ◽  
Lily R. Qiu ◽  
Yohan Yee ◽  
...  

AbstractMaternal environmental exposures, such as high-fat diets, diabetes and obesity, can induce long term effects in offspring. These effects include increased risk of neurodevelopmental disorders (NDDs) including autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), depression and anxiety. The mechanisms underlying these late-life neurologic effects are unknown. In this article, we measured changes in the offspring brain and determined which brain regions are sensitive to maternal metabolic milieu and therefore may mediate NDD risk. We showed that mice exposed to maternal high-fat diet display extensive brain changes in adulthood despite being switched to low-fat diet at weaning. Brain regions impacted by early-life diet include the extended amygdalar system, which plays an important role in reward-seeking behaviour. Genes preferentially expressed in these regions have functions related to feeding behavior, while also being implicated in human NDDs, such as autism. Our data demonstrated that exposure to maternal high-fat diet in early-life leads to brain alterations that persist into adulthood, even after dietary modifications.


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