Bidirectional modulation of hippocampal and amygdala synaptic plasticity by post‐weaning obesogenic diet intake in male rats: Influence of the duration of diet exposure

Hippocampus ◽  
2020 ◽  
Author(s):  
Rose‐Marie Vouimba ◽  
Ioannis Bakoyiannis ◽  
Eva‐Gunnel Ducourneau ◽  
Mouna Maroun ◽  
Guillaume Ferreira
2017 ◽  
Vol 330 ◽  
pp. 46-55 ◽  
Author(s):  
Alberto Camacho ◽  
Larisa Montalvo-Martinez ◽  
Robbi E. Cardenas-Perez ◽  
Lizeth Fuentes-Mera ◽  
Lourdes Garza-Ocañas

2007 ◽  
Vol 292 (5) ◽  
pp. R1810-R1818 ◽  
Author(s):  
Claire J. Stocker ◽  
Ed Wargent ◽  
Jacqueline O'Dowd ◽  
Claire Cornick ◽  
John R. Speakman ◽  
...  

Absence of leptin is known to disrupt the development of energy balance regulatory mechanisms. We investigated whether administration of leptin to normally nourished rats affects energy balance in their offspring. Leptin (2 mg·kg−1·day−1) was administered from day 14 of pregnancy and throughout lactation. Male and female offspring were fed either on chow or on high-fat diets that elicited similar levels of obesity in the sexes from 6 wk to 15 mo of age. Treatment of the dams with leptin prevented diet-induced increases in the rate of weight gain, retroperitoneal fat pad weight, area under the intraperitoneal glucose tolerance curve, and fasting plasma insulin concentration in female offspring. In the male offspring, the diet-induced increase in weight gain was prevented and increased fat pad weight was reduced. Energy intake per rat was higher in response to the obesogenic diet in male offspring of saline-treated but not leptin-treated dams. A similar trend was seen in 3-mo-old female offspring. Energy expenditure at 3 mo of age was higher for a given body weight in female offspring of leptin-treated compared with saline-treated dams when these animals were fed on the obesogenic diet. A similar trend was seen for male rats fed on the obesogenic diet. Thus leptin levels during pregnancy and lactation can affect the development of energy balance regulatory systems in their offspring.


Author(s):  
Sarieh Shahraki ◽  
Khadijeh Esmaeilpour ◽  
Mohammad Shabani ◽  
Gholamreza Sepehri ◽  
Mohammad Amin Rajizadeh ◽  
...  

1994 ◽  
Vol 267 (1) ◽  
pp. R44-R52
Author(s):  
L. L. Bellinger ◽  
G. Dula ◽  
F. E. Williams

The liver by way of afferent nerves is suggested to be a controller of food intake. In experiment 1, male rats were given a 15% fructose solution during the first 4 h of the dark phase, while chow was available the rest of the time, for 10 days, before total liver denervation (TLD) or sham operation. Postsurgery ingestion patterns (15-min measurements for 4 h) of fructose were similar in the two groups. However, chow intake in the TLD group was slightly attenuated the first 2 days after surgery. In experiment 2, rats were given chow in cups and vegetable oil in bottles for 8 days before TLD or sham operation. After surgery, hourly ingestion of chow and oil did not differ between the groups; however, there was a trend for the TLD group to take more oil in the dark phase on the first-day diet exposure. In experiment 3, rats were fed a high-protein diet for 21 days before TLD or sham operation. With the use of a computer-operated system, postsurgery meal size, meal duration, and frequency patterns were found to be comparable between the groups. In experiment 4, rats were given a diet of sweetened condensed milk mixed with water (3:1 vol/vol) and vitamins for 14 days before hepatic vagal branch transection (HVBX) or sham operation. After surgery the first-day milk intake of both groups was similar up to 3.5 h and then depressed at 4 and 24 h in the HVBX rats, but was again comparable over the next 13 days; body weights were similar throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)


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.


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