PCR data.zip

Obesity's global rise brings attention to related health issues, including brain functionality deterioration due to hippocampal neurogenesis and neuroplasticity alterations, leading to cognitive decline. This study aims to counteract the negative effects of obesity <i>via</i> treadmill endurance training (ET) in the hippocampus of a rat genetic model of obesity. The findings after ET based on analyses of expression profiles of individual genes demonstrate differences in neurotrophin-associated signaling, significantly affecting PI3K/Akt expression within the trained lean group. In contrast, we noticed activity-dependent changes regarding PLCγ/PKC/CAMKII signaling. While sedentary obese animals utilized neurotrophin signaling towards the PLCγ/PKC pathway, ET of both lean and obese rats shifted PLCγ activation to the alternative branch, with CAMKII emerging as a preferred downstream target crucial for synaptic plasticity and memory formation. A concomitant mRNA increase in the presynaptic marker synaptophysin suggests the beneficial role of ET in synaptogenesis and plasticity. The microglial pro-inflammatory marker Iba1 was suppressed in obese trained rats, accompanied by the upregulation of regenerative markers for immature/mature oligodendrocytes, and neurofilaments. Furthermore, the passive avoidance test revealed improved learning and memory among trained obese animals. These findings suggest that ET can moderate obesity-induced hippocampal damage, exert neuroprotective effects, and support hippocampal functions.