Diet-induced obesity alters memory consolidation in female rats

Abstract

Obesity is a multifactorial disease characterized by the abnormal or excessive fat accumulation, which is caused by an energy imbalance between consumed and expended calories. Obesity leads to an inflammatory response that may result in peripheral and central metabolic changes, including insulin and leptin resistance. Insulin and leptin resistance have been associated with metabolic and cognitive dysfunctions. Obesity and some neurodegenerative diseases that lead to dementia affect mainly women. However, the effects of diet-induced obesity on memory consolidation in female rats are poorly understood. Therefore, the aim of this study was to evaluate the effect of a hypercaloric diet on the object recognition memory of female rats and on possible related metabolic changes. The animals submitted to the hypercaloric diet presented a higher food intake in grams and in calories, resulting in increased weight gain and liposomatic index in comparison with the animals exposed to the control diet. These animals presented a memory deficit in the object recognition test and increased serum levels of glucose and leptin. However, no significant differences were found in the serum levels of insulin, TNF-α and IL-1β, in the index of insulin resistance (HOMA), in the hippocampal levels of insulin, TNF-α and IL-1β, as well as on Akt expression or activation in the hippocampus. Our findings indicate that adult female rats submitted to a hypercaloric diet present memory consolidation impairment, which could be associated with diet-induced weight gain and leptin resistance, even without the development of insulin resistance.

Selegiline reduces adiposity induced by high‐fat, high‐sucrose diet in male rats

“…In our present study, neither selegiline treatment nor HFS diet‐induced moderate obesity had significant effects on motor activity or recognition memory. Although previous articles showed that extreme obesity induced cognitive dysfunction (Wang et al ., ; Zanini et al ., ), these changes could not be observed in our model of moderate obesity.…”

Neural Underpinnings of Obesity: The Role of Oxidative Stress and Inflammation in the Brain

“…Neuroimaging studies have shown that hippocampal volume is diminished with aberrant neural activity in obese individuals compared to lean healthy individuals [ 48 , 49 , 50 ], indicating a potential mechanistic link between hippocampal function and metabolic health. Consistent with these results, rodent studies indicate that diet-induced obesity (via HFD or high-sucrose diet) manifests impaired memory consolidation [ 51 , 52 , 53 ] that is associated with hippocampal BBB disruption [ 54 , 55 ], thereby potentially increasing the entry of systemic inflammatory mediators into the hippocampus. Indeed, diet-induced obese animals exhibit microglial activation, increased production of ROS, and pro-inflammatory cytokines including IL-1β and TNF-α in the hippocampus [ 54 , 55 ].…”

The Angiotensin Type 1 Receptor Antagonist Losartan Prevents Ovariectomy-Induced Cognitive Dysfunction and Anxiety-Like Behavior in Long Evans Rats

“…Accordingly, we found Ovx rats gained more than twice as much weight compared to Sham animals over the 10-week experiment. Excessive BW is a risk factor for mood disorders (Rocca et al 2009) and cognitive impairment (Zanini et al 2017) in humans and animals (Zanini et al 2017). However, it has been difficult to tease apart BW gain from ovarian hormone loss in the mechanisms contributing to Ovx-induced neurocognitive dysfunction.…”

“…The NOR test was adapted from Drumond et al and Zanini et al (Drumond et al 2012;Zanini et al 2017). This test uses the same apparatus and software (EthoVision XT; Noldus Information Technology) as for the OF test.…”