Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity
The incidence of metabolic disorders including obesity, type 2 diabetes and metabolic syndrome have seriously increased in the last decades. These diseases – with growing impact in modern societies – constitute major risk factors for neurodegenerative disorders such as Alzheimer's disease (AD),...
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2016
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064530_v72_n_p22_Vinuesa http://hdl.handle.net/20.500.12110/paper_03064530_v72_n_p22_Vinuesa |
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paper:paper_03064530_v72_n_p22_Vinuesa |
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dspace |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Cognitive performance Emotionality High fat diet Hippocampal neuroinflammation Neurogenesis Periadolescence insulin receptor substrate 1 insulin receptor substrate 2 interleukin 1beta Ki 67 antigen phospholipase A2 protein c fos protein kinase B tumor necrosis factor alpha adult amygdala animal experiment animal model animal tissue anxiety Article behavior change cell proliferation controlled study dentate gyrus depression disease association dyslipidemia enzyme activity enzyme phosphorylation gene expression insulin resistance lipid composition lipid diet male memory disorder motivation mouse nervous system inflammation nonhuman obesity population exposure priority journal protein blood level protein expression protein phosphorylation short term memory spatial memory amygdala animal animal behavior C57BL mouse cognitive defect dyslipidemia hippocampus hyperinsulinism inflammation lipid diet metabolism nervous system development pathology pathophysiology physiology Amygdala Animals Behavior, Animal Cognitive Dysfunction Diet, High-Fat Dyslipidemias Hippocampus Hyperinsulinism Inflammation Male Mice Mice, Inbred C57BL Neurogenesis |
| spellingShingle |
Cognitive performance Emotionality High fat diet Hippocampal neuroinflammation Neurogenesis Periadolescence insulin receptor substrate 1 insulin receptor substrate 2 interleukin 1beta Ki 67 antigen phospholipase A2 protein c fos protein kinase B tumor necrosis factor alpha adult amygdala animal experiment animal model animal tissue anxiety Article behavior change cell proliferation controlled study dentate gyrus depression disease association dyslipidemia enzyme activity enzyme phosphorylation gene expression insulin resistance lipid composition lipid diet male memory disorder motivation mouse nervous system inflammation nonhuman obesity population exposure priority journal protein blood level protein expression protein phosphorylation short term memory spatial memory amygdala animal animal behavior C57BL mouse cognitive defect dyslipidemia hippocampus hyperinsulinism inflammation lipid diet metabolism nervous system development pathology pathophysiology physiology Amygdala Animals Behavior, Animal Cognitive Dysfunction Diet, High-Fat Dyslipidemias Hippocampus Hyperinsulinism Inflammation Male Mice Mice, Inbred C57BL Neurogenesis Bonaventura, María Marta Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| topic_facet |
Cognitive performance Emotionality High fat diet Hippocampal neuroinflammation Neurogenesis Periadolescence insulin receptor substrate 1 insulin receptor substrate 2 interleukin 1beta Ki 67 antigen phospholipase A2 protein c fos protein kinase B tumor necrosis factor alpha adult amygdala animal experiment animal model animal tissue anxiety Article behavior change cell proliferation controlled study dentate gyrus depression disease association dyslipidemia enzyme activity enzyme phosphorylation gene expression insulin resistance lipid composition lipid diet male memory disorder motivation mouse nervous system inflammation nonhuman obesity population exposure priority journal protein blood level protein expression protein phosphorylation short term memory spatial memory amygdala animal animal behavior C57BL mouse cognitive defect dyslipidemia hippocampus hyperinsulinism inflammation lipid diet metabolism nervous system development pathology pathophysiology physiology Amygdala Animals Behavior, Animal Cognitive Dysfunction Diet, High-Fat Dyslipidemias Hippocampus Hyperinsulinism Inflammation Male Mice Mice, Inbred C57BL Neurogenesis |
| description |
The incidence of metabolic disorders including obesity, type 2 diabetes and metabolic syndrome have seriously increased in the last decades. These diseases – with growing impact in modern societies – constitute major risk factors for neurodegenerative disorders such as Alzheimer's disease (AD), sharing insulin resistance, inflammation and associated cognitive impairment. However, cerebral cellular and molecular pathways involved are not yet clearly understood. Thus, our aim was to study the impact of a non-severe high fat diet (HFD) that resembles western-like alimentary habits, particularly involving juvenile stages where the brain physiology and connectivity are in plain maturation. To this end, one-month-old C57BL/6J male mice were given either a control diet or HFD during 4 months. Exposure to HFD produced metabolic alterations along with changes in behavioral and central parameters, in the absence of obesity. Two-month-old HFD mice showed increased glycemia and plasmatic IL1β but these values normalized at the end of the HFD protocol at 5 months of age, probably representing an acute response that is compensated at later stages. After four months of HFD exposure, mice presented dyslipidemia, increased Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity, hepatic insulin resistance and inflammation. Alterations in the behavioral profile of the HFD group were shown by the impediment in nest building behavior, deficiencies in short and mid-term spatial memories, anxious and depressive- like behavior. Regarding the latter disruptions in emotional processing, we found an increased neural activity in the amygdala, shown by a greater number of c-Fos+ nuclei. We found that hippocampal adult neurogenesis was decreased in HFD mice, showing diminished cell proliferation measured as Ki67+ cells and neuronal differentiation in SGZ by doublecortin labeling. These phenomena were accompanied by a neuroinflammatory and insulin-resistant state in the hippocampus, depicted by a reactive phenotype in Iba1+ microglia cells (increased in number and soma size) and an impaired response to insulin given by decreased phosphorylated Akt levels and increased levels of inhibitory phosphorylation of IRS1. Our data portray a set of alterations in behavioral and neural parameters as a consequence of an early-life exposure to a quite moderate high fat diet, many of which can resemble AD-related features. These results highly emphasize the need to study how metabolic and neurodegenerative disorders are interrelated in deep, thus allowing the finding of successful preventive and therapeutic approaches. © 2016 Elsevier Ltd |
| author |
Bonaventura, María Marta |
| author_facet |
Bonaventura, María Marta |
| author_sort |
Bonaventura, María Marta |
| title |
Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| title_short |
Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| title_full |
Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| title_fullStr |
Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| title_full_unstemmed |
Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| title_sort |
juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity |
| publishDate |
2016 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064530_v72_n_p22_Vinuesa http://hdl.handle.net/20.500.12110/paper_03064530_v72_n_p22_Vinuesa |
| work_keys_str_mv |
AT bonaventuramariamarta juvenileexposuretoahighfatdietpromotesbehavioralandlimbicalterationsintheabsenceofobesity |
| _version_ |
1768544820479918080 |
| spelling |
paper:paper_03064530_v72_n_p22_Vinuesa2023-06-08T15:31:21Z Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity Bonaventura, María Marta Cognitive performance Emotionality High fat diet Hippocampal neuroinflammation Neurogenesis Periadolescence insulin receptor substrate 1 insulin receptor substrate 2 interleukin 1beta Ki 67 antigen phospholipase A2 protein c fos protein kinase B tumor necrosis factor alpha adult amygdala animal experiment animal model animal tissue anxiety Article behavior change cell proliferation controlled study dentate gyrus depression disease association dyslipidemia enzyme activity enzyme phosphorylation gene expression insulin resistance lipid composition lipid diet male memory disorder motivation mouse nervous system inflammation nonhuman obesity population exposure priority journal protein blood level protein expression protein phosphorylation short term memory spatial memory amygdala animal animal behavior C57BL mouse cognitive defect dyslipidemia hippocampus hyperinsulinism inflammation lipid diet metabolism nervous system development pathology pathophysiology physiology Amygdala Animals Behavior, Animal Cognitive Dysfunction Diet, High-Fat Dyslipidemias Hippocampus Hyperinsulinism Inflammation Male Mice Mice, Inbred C57BL Neurogenesis The incidence of metabolic disorders including obesity, type 2 diabetes and metabolic syndrome have seriously increased in the last decades. These diseases – with growing impact in modern societies – constitute major risk factors for neurodegenerative disorders such as Alzheimer's disease (AD), sharing insulin resistance, inflammation and associated cognitive impairment. However, cerebral cellular and molecular pathways involved are not yet clearly understood. Thus, our aim was to study the impact of a non-severe high fat diet (HFD) that resembles western-like alimentary habits, particularly involving juvenile stages where the brain physiology and connectivity are in plain maturation. To this end, one-month-old C57BL/6J male mice were given either a control diet or HFD during 4 months. Exposure to HFD produced metabolic alterations along with changes in behavioral and central parameters, in the absence of obesity. Two-month-old HFD mice showed increased glycemia and plasmatic IL1β but these values normalized at the end of the HFD protocol at 5 months of age, probably representing an acute response that is compensated at later stages. After four months of HFD exposure, mice presented dyslipidemia, increased Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity, hepatic insulin resistance and inflammation. Alterations in the behavioral profile of the HFD group were shown by the impediment in nest building behavior, deficiencies in short and mid-term spatial memories, anxious and depressive- like behavior. Regarding the latter disruptions in emotional processing, we found an increased neural activity in the amygdala, shown by a greater number of c-Fos+ nuclei. We found that hippocampal adult neurogenesis was decreased in HFD mice, showing diminished cell proliferation measured as Ki67+ cells and neuronal differentiation in SGZ by doublecortin labeling. These phenomena were accompanied by a neuroinflammatory and insulin-resistant state in the hippocampus, depicted by a reactive phenotype in Iba1+ microglia cells (increased in number and soma size) and an impaired response to insulin given by decreased phosphorylated Akt levels and increased levels of inhibitory phosphorylation of IRS1. Our data portray a set of alterations in behavioral and neural parameters as a consequence of an early-life exposure to a quite moderate high fat diet, many of which can resemble AD-related features. These results highly emphasize the need to study how metabolic and neurodegenerative disorders are interrelated in deep, thus allowing the finding of successful preventive and therapeutic approaches. © 2016 Elsevier Ltd Fil:Bonaventura, M.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2016 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064530_v72_n_p22_Vinuesa http://hdl.handle.net/20.500.12110/paper_03064530_v72_n_p22_Vinuesa |