INTRODUCTION. Obesity, is considered a medical challenge for its increase worldwide. It represents also an independent risk factor for the development of cerebrovascular disease and of cognitive im-pairment. This work has assessed the relationships between obesity and brain injury by investigating brain morphology in rats developing obesity (diet-induced obesity, DIO) or resistant (DR), when they were fed with a high fat diet for 17 weeks. DIO rats were compared to control rats not receiving fat-diet (CHOW). METHODS. Ultrasonographic and computed tomography techniques were used to detect deposition of adipose tissue. Magnetic resonance imaging (MRI) has investigated possible changes in brain gross anatomy, whereas morphological changes of selected cerebral areas were evaluated by immu-nohistochemistry. Different behavioural tests were used to estimate cognitive performance. RESULTS. After long-term high fat diet exposure, body weight was remarkably increased in DIO rats compared to the control group and DR rats. MRI did not show significant morphological and vascular brain changes. In contrast, immunohistochemical and immunochemical analysis showed an increased expression of glial-fibrillary acid protein in the frontal cortex and hippocampus of older DIO rats compared to age-matched CHOW and DR rats. A decrease of neurofilament expression was found in the hippocampus of 17-week-old DIO rats. In DIO rats emotional learning and cognitive task impairment was also noticeable. CONCLUSION. These results indicate that overweight in rats, causes brain injury characterized by astrogliosis and neurodegeneration and is accompanied by impaired learning and memory tasks. A better knowledge of the mechanisms of brain injury in obesity may contribute to identify possible strategies to prevent target organ damage in overweight subject.

OVERWEIGHT LEADS TO BRAIN INJURY IN HIGH FAT DIET-INDUCED OBESITY (DIO) RATS

Daniele Tomassoni;Maria Vittoria Micioni di Bonaventura;Michele Moruzzi;Ilenia Martinelli;Fabrizio Dini;Alessandro Fruganti;Andrea Marchegiani;Maria Elena Giusepponi;Carlotta Marini;Carlo Polidori;Giulio Lupidi;Seyed Khosrow Tayebati;Francesco Amenta;Carlo Cifani.
2017-01-01

Abstract

INTRODUCTION. Obesity, is considered a medical challenge for its increase worldwide. It represents also an independent risk factor for the development of cerebrovascular disease and of cognitive im-pairment. This work has assessed the relationships between obesity and brain injury by investigating brain morphology in rats developing obesity (diet-induced obesity, DIO) or resistant (DR), when they were fed with a high fat diet for 17 weeks. DIO rats were compared to control rats not receiving fat-diet (CHOW). METHODS. Ultrasonographic and computed tomography techniques were used to detect deposition of adipose tissue. Magnetic resonance imaging (MRI) has investigated possible changes in brain gross anatomy, whereas morphological changes of selected cerebral areas were evaluated by immu-nohistochemistry. Different behavioural tests were used to estimate cognitive performance. RESULTS. After long-term high fat diet exposure, body weight was remarkably increased in DIO rats compared to the control group and DR rats. MRI did not show significant morphological and vascular brain changes. In contrast, immunohistochemical and immunochemical analysis showed an increased expression of glial-fibrillary acid protein in the frontal cortex and hippocampus of older DIO rats compared to age-matched CHOW and DR rats. A decrease of neurofilament expression was found in the hippocampus of 17-week-old DIO rats. In DIO rats emotional learning and cognitive task impairment was also noticeable. CONCLUSION. These results indicate that overweight in rats, causes brain injury characterized by astrogliosis and neurodegeneration and is accompanied by impaired learning and memory tasks. A better knowledge of the mechanisms of brain injury in obesity may contribute to identify possible strategies to prevent target organ damage in overweight subject.
2017
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11581/424371
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