Different Effect of High Fat Diet and Physical Exercise in the Hippocampal Signaling

2007 ◽  
Vol 33 (5) ◽  
pp. 880-885 ◽  
Author(s):  
Alexandre Pastoris Muller ◽  
Martín Cammarota ◽  
Marcelo de Oliveira Dietrich ◽  
Liane N. Rotta ◽  
Luis Valmor Portela ◽  
...  
2018 ◽  
Vol 74 (2) ◽  
pp. 235-246 ◽  
Author(s):  
Sílvia Rocha-Rodrigues ◽  
Inês O. Gonçalves ◽  
Jorge Beleza ◽  
António Ascensão ◽  
José Magalhães

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1603 ◽  
Author(s):  
Hye-Sang Park ◽  
Sang-Seo Park ◽  
Chang-Ju Kim ◽  
Mal-Soon Shin ◽  
Tae-Woon Kim

Obesity, caused by a high-fat diet (HFD), leads to insulin resistance, which is a precursor of diabetes and a risk factor for impaired cognitive function, dementia, and brain diseases, such as Alzheimer’s disease. Physical exercise has positive effects on obesity and brain functions. We investigated whether the decline in cognitive function caused by a HFD could be improved through exercise by examining insulin signaling pathways and neuroplasticity in the hippocampus. Four-week-old C57BL/6 male mice were fed a HFD or a regular diet for 20 weeks, followed by 12 weeks of treadmill exercise. To ascertain the effects of treadmill exercise on impaired cognitive function caused by obesity, the present study implemented behavioral testing (Morris water maze, step-down). Moreover, insulin-signaling and neuroplasticity were measured in the hippocampus and dentate gyrus. Our results demonstrated that HFD-fed obesity-induced insulin resistance was improved by exercise. In addition, the HFD group showed a decrease in insulin signaling and neuroplasticity in the hippocampus and the dentate gyrus and increased cognitive function impairment, which were reversed by physical exercise. Overall, our findings indicate that physical exercise may act as a non-pharmacologic method that protects against cognitive dysfunction caused by obesity by improving hippocampal insulin signaling and neuroplasticity.


1996 ◽  
Vol 26 (3) ◽  
pp. 265-279 ◽  
Author(s):  
K. Kazakoff ◽  
T. Cardesa ◽  
J. Liu ◽  
T. E. Adrian ◽  
D. Bagchi ◽  
...  

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii164-iii164
Author(s):  
Rosemara S Ribeiro ◽  
Clevia S Passos ◽  
Maria Aparecida Gloria ◽  
Lila M Oyama ◽  
Mirian A Boim

Life Sciences ◽  
2016 ◽  
Vol 165 ◽  
pp. 100-108 ◽  
Author(s):  
Sílvia Rocha-Rodrigues ◽  
Amaia Rodríguez ◽  
Alexandra M. Gouveia ◽  
Inês O. Gonçalves ◽  
Sara Becerril ◽  
...  

2017 ◽  
Vol 250 ◽  
pp. 71-77 ◽  
Author(s):  
Hye-Sang Park ◽  
Jae-Min Lee ◽  
Han-Sam Cho ◽  
Sang-Seo Park ◽  
Tae-Woon Kim

2021 ◽  
Author(s):  
Maria Eduarda Almeida Tavares ◽  
Allice Santos Cruz Veras ◽  
Danilo Bianchini Baptista ◽  
Giovana Rampazzo Teixeira

Abstract Body fat resulting from the consumption of fatty foods develops inflammation, a precursor to obesity, diabetes mellitus and prostatic diseases, causing tissue changes. On the other hand, aerobic physical exercise in conjunction with PPARα promotes an increase in energy expenditure, modulating cellular metabolism by altering prostate cell metabolism. This study aimed to elucidate the effect of the gene transcription factor PPARα as a prostatic regulator associated with the effects of aerobic physical exercise in mice fed to a high-fat diet. Wild Type and PPARα -/- mice (C57BL/6J) were fed a high-fat diet and submitted to aerobic physical training for 8 weeks. Prostates of male mice were analyzed histologically and metabolically for PIN progression. These findings suggest that the absence of PPARα reduces adiposity and but does not modify the expression AR and GR, up-regulate prostate inflammation, and suppresses Fas (CD95/Apo-1) increase in TNF-α, induced by prostatic lesions. On the other hand, aerobic physical exercise was effective in protecting prostatic damage induced by a high-fat diet, both in wild type and in PPARα-/- animals. The absence PPARα induces an inflammatory process and prostatic changes and associated with a high-fat diet, however, these inflammatory processes induce increased apoptosis and may further inhibit cell growth associated with physical exercise.


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