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Aim:The study hypothesized that testosterone deprivation aggravates cognitive decline in obesity through increasing oxidative stress, glial activation, and apoptosis. Methods: Male Wistar rats (n = 24) were fed with either normal-diet (ND) or high-fat diet (HFD) for 24 weeks. At week 13, ND-fed rats and HFD-fed rats were randomly assigned to two subgroups to receive either a sham-operation or bilateral-orchiectomy (ORX). Rats were evaluated for metabolic parameters and cognition at 4, 8, and 12 weeks after the operation. At the end of protocol, the reactive oxygen species (ROS), glial morphology, and cell apoptosis were determined in hippocampus and cortex. Results: Both HFD-fed groups developed obese-insulin resistance, but ND-fed rats did not. HFD-fed rats with sham-operation showed cognitive decline, when compared to ND-fed rats with sham-operation at all time points. At 4-and 8-week after ORX, the cognitive impairment of ND-fed rats and both HFD-fed groups was not different. However, 12-week after ORX, cognitive decline and of glial hyperactivity of HFD-fed rats had the greatest increase among all groups. Hippocampal ROS levels and apoptotic cells in both HFD-fed groups were equally increased, but the cortical ROS levels and apoptotic cells of HFD-fed rats with ORX were the highest ones. Conclusions: These findings suggest that testosterone deprivation aggravates cognitive decline in obesity via increasing oxidative stress, glial activity and apoptosis. K E Y W O R D Sapoptosis, cognitive function, glia function, obesity, reactive oxygen species, testosterone deprivation

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Scope It has been hypothesized that a high‐saturated‐fat, high‐sugar diet (HFHS) causes worse cardiometabolic dysfunction than a high‐saturated‐fat diet (HFD) due to severe mitochondrial dysfunction, oxidative stress, and apoptosis in obese insulin‐resistant rats. Methods and Results Rats are divided into three groups to receive normal diet (ND), HFD, or HFHS for 24 weeks. Cardiometabolic parameters are determined at baseline and every 4 weeks until the end of the feeding protocol. At week 24, hearts are removed to determine mitochondrial function and dynamics, apoptosis, and insulin signaling. HFD and HFHS rats develop obese insulin‐resistance at week 8. However, fasting plasma glucose level is increased only in HFHS rats. Myocardial insulin signaling is markedly impaired in HFHS rats compared to other groups. Cardiac autonomic imbalance is observed in both HFD and HFHS rats beginning at week 8. However, cardiac dysfunction is observed earlier (week 8) in HFHS rats, and later at week 12 in HFD rats. Moreover, cardiac and mitochondrial oxidative stress levels, and apoptosis are greater in HFHS rats than HFD rats. Conclusion Both HFD and HFHS cause cardiometabolic dysfunction. HFHS causes more severe metabolic disturbance, oxidative stress, and apoptosis than HFD, which leads to an accelerated LV dysfunction in HFHS rats.

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