Obesogenic diet intake during pregnancy programs aberrant synaptic plasticity and addiction-like behavior to a palatable food in offspring

2017 ◽  
Vol 330 ◽  
pp. 46-55 ◽  
Author(s):  
Alberto Camacho ◽  
Larisa Montalvo-Martinez ◽  
Robbi E. Cardenas-Perez ◽  
Lizeth Fuentes-Mera ◽  
Lourdes Garza-Ocañas
2018 ◽  
Vol 119 (4) ◽  
pp. 368-380 ◽  
Author(s):  
Gilles Fouret ◽  
Sylvie Gaillet ◽  
Jerome Lecomte ◽  
Beatrice Bonafos ◽  
Ferdinand Djohan ◽  
...  

AbstractThe incidence of obesity and its metabolic complications are rapidly increasing and become a major public health issue. This trend is associated with an increase in the prevalence of non-alcoholic fatty liver disease (NAFLD), insulin resistance and diabetes. The sequence of events leading to NAFLD progression and mitochondrial dysfunction and their interrelation remains to be elucidated. This study aimed to explore the installation and progression of NAFLD and its association with the liver mitochondrial structure and activity changes in rats fed an obesogenic diet up to 20 weeks. Male Wistar rats were fed either a standard or high-fat–high-fructose (HFHFR) diet and killed on 4, 8, 12, 16 and 20 weeks of diet intake. Rats fed the HFHFR diet developed mildly overweight, associated with increased adipose tissue weight, hepatic steatosis, hyperglycaemia and hyperinsulinaemia after 8 weeks of HFHFR diet. Hepatic steatosis and many biochemical modifications plateaued at 8–12 weeks of HFHFR diet with slight amelioration afterwards. Interestingly, several biochemical and physiological parameters of mitochondrial function, as well as its phospholipid composition, in particular cardiolipin content, were tightly related to hepatic steatosis installation. These results showed once again the interrelation between hepatic steatosis development and mitochondrial activity alterations without being able to say whether the mitochondrial alterations preceded or followed the installation/progression of hepatic steatosis. Because both hepatic steatosis and mitochondrial alterations occurred as early as 4 weeks of diet, future studies should consider these four 1st weeks to reveal the exact interconnection between these major consequences of obesogenic diet intake.


2020 ◽  
Vol 319 (3) ◽  
pp. E485-E493
Author(s):  
Breno P. Casagrande ◽  
Debora Estadella

There is accumulating evidence of dietary impact on several metabolic parameters. Unhealthy diets are estimated to be responsible for about 20% of the deaths worldwide. The recommendation is to improve the dietary pattern, aiming to prevent further harm. In this context, we reviewed the benefits and barriers of withdrawing from continuous obesogenic diet intake in the short- and long-term, which were found in rodent models. Although dietary modifications demand a re-establishment of the equilibrium, withdrawing was seen as a homeostatic insult and thus elicited several responses to protect the organism. In the short-term, withdrawal presented stressful and reward destimulating responses. The intake of obesogenic diets presented rewarding and stress destimulating responses. Whereas withdrawing in the long term ameliorated several biological functions and histopathologic features, it was not effective at reestablishing food intake and normalizing feeding behaviors or reward pathways. Altogether, terminating obesogenic diet intake does not immediately extinguish all negative consequences, and it even elicits brain behavioral and metabolic modifications. These modifications can hinder the maintenance of habits’ change and prevent reaching the long-term benefits of diet improvement.


2011 ◽  
Vol 42 (S 01) ◽  
Author(s):  
F Mainberger ◽  
N Jung ◽  
M Zenker ◽  
I Delvendahl ◽  
U Wahlländer-Danek ◽  
...  
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