Abstract

AbstractBackgroundHigh cardiorespiratory fitness (CRF) and behavioral modification exert a neuroprotective effect in obese condition. However, the interplay between CRF, obesity, and behavioral modification has never been identified. Therefore, this study investigated whether high CRF level provides the neuroprotective effect in obese rats receiving either caloric restriction or exercise.MethodSeven‐week‐old male Wistar rats were fed with either a normal diet (ND; n = 5) or a high‐fat diet (HFD; n = 25) to induce obesity for 12 weeks. At the end of week 12, baseline CRF was measured. The ND‐fed rats were continuously fed with a ND for an additional 16 weeks. The HFD‐fed rats were randomly assigned into 5 groups (n = 5/group) to receive either 1) a HFD without intervention for 16 weeks, 2) 40% caloric restriction for 6 weeks followed by an ad libitum ND for 10 weeks (short‐term caloric restriction followed by weight maintenance), 3) 40% caloric restriction for 16 weeks (long‐term caloric restriction), 4) a HFD plus an exercise for 6 weeks followed by a ND without exercise for 10 weeks (short‐term exercise followed by weight maintenance), or 5) a HFD plus an exercise for 16 weeks (long‐term exercise). At the end of interventions (week 28), CRF and cognitive function were determined. After that, the rats were euthanized for molecular studies in the brain.ResultThere was a significantly positive correlation between running distance at week 12 and week 28 (Figure A), indicating that CRF is highly intrinsic factor. When compared to the ND‐fed rats, CRF level was lower in the obese rats at week 12 (Figure B). At week 28, all types of behavioral modification significantly increased the CRF level in obese rats (Figure C). Interestingly, high baseline CRF level demonstrated a significant correlation with favorable brain profiles at follow‐up in obese rats, both with and without behavioral modification (Figure D).ConclusionRegardless of behavioral modification, high CRF exerts a neuroprotective effect against obesity. Hence, targeting on an enhancement of CRF may provide the better effective therapy for obesity‐induced neuronal impairment.

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