Abstract
Dietary fats and sugars were identified as risk factors for overweight and neurodegeneration, especially in middle-age, an earlier stage of the aging process. Therefore, our aim was to study the metabolic response of both white adipose tissue and brain in middle aged rats fed a typical Western diet (high in saturated fats and fructose, HFF) and verify whether a similarity exists between the two tissues. Specific cyto/adipokines (tumor necrosis factor alpha (TNF-α), adiponectin), critical obesity-inflammatory markers (haptoglobin, lipocalin), and insulin signaling or survival protein network (insulin receptor substrate 1 (IRS), Akt, Erk) were quantified in epididymal white adipose tissue (e-WAT), hippocampus, and frontal cortex. We found a significant increase of TNF-α in both e-WAT and hippocampus of HFF rats, while the expression of haptoglobin and lipocalin was differently affected in the various tissues. Interestingly, adiponectin amount was found significantly reduced in e-WAT, hippocampus, and frontal cortex of HFF rats. Insulin signaling was impaired by HFF diet in e-WAT but not in brain. The above changes were associated with the decrease in brain derived neurotrophic factor (BDNF) and synaptotagmin I and the increase in post-synaptic protein PSD-95 in HFF rats. Overall, our investigation supports for the first time similarities in the response of adipose tissue and brain to Western diet.
Highlights
Lifestyle, nutrition and lack of physical exercise is increasing the number of overweight or obese people in the global population
We further investigated whether the dietary treatment could affect the amount of TrkB receptor, as brain derived neurotrophic factor (BDNF) activities, such as enhancement of synaptic plasticity, neuroprotection, and stimulation of neuronal fibers growth, are mediated by neurotrophin binding to this receptor [20]
It has been suggested that the molecules released or produced by the adipose tissue could be the molecular link between obesity and brain dysfunction [29]
Summary
Nutrition and lack of physical exercise is increasing the number of overweight or obese people in the global population. Dietary fats and sugars were identified as risk factors for cognitive decline and neurodegeneration, through altered brain metabolism, neuroinflammation and neuronal dysfunction [2,3,4,5,6]. Proinflammatory cytokines, namely tumor necrosis factor alpha (TNFα), are implicated in the development of neuronal insulin resistance [7,8]. Since both cytokines and insulin in the brain regulate synaptic plasticity, learning and memory, neuroinflammation and neuronal insulin resistance have been proposed to be involved in obesity-associated brain impairment [9]
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