Obesogenic Diets Cause Alterations on Proteins and Theirs Post-Translational Modifications in Mouse Brains
| Autor: | Martin R. Larsen, Giulia Accardi, Pia Jensen, Peter James, Antonella Amato, Flavia Mulè, Valentina Siino, Sonya Vasto |
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| Přispěvatelé: | Siino Valentina, James Peter, Vasto Sonya, Amato Antonella, Mulè Flavia, Accardi Giulia, Rossel Larsen Martin |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty RC620-627 Endocrinology Diabetes and Metabolism medicine.medical_treatment Tau protein Obesity nutrition brain impairment proteomics post-translational modifications Brain damage Mitochondrion Proteomics medicine.disease_cause Settore BIO/09 - Fisiologia 03 medical and health sciences proteomics 0302 clinical medicine Internal medicine post-translational modifications medicine TX341-641 Obesity Nutritional diseases. Deficiency diseases Original Research Settore MED/04 - Patologia Generale Nutrition and Dietetics biology Nutrition. Foods and food supply Insulin Neurodegeneration medicine.disease brain impairment Insulin receptor nutrition 030104 developmental biology Endocrinology biology.protein medicine.symptom 030217 neurology & neurosurgery Oxidative stress Food Science |
| Zdroj: | Nutrition and Metabolic Insights Nutrition and Metabolic Insights, Vol 14 (2021) |
| ISSN: | 1178-6388 |
| DOI: | 10.1177/11786388211012405 |
| Popis: | Obesity constitutes a major global health threat and is associated with a variety of diseases ranging from metabolic and cardiovascular disease, cancer to neurodegeneration. The hallmarks of neurodegeneration include oxidative stress, proteasome impairment, mitochondrial dysfunction and accumulation of abnormal protein aggregates as well as metabolic alterations. As an example, in post-mortem brain of patients with Alzheimer’s disease (AD), several studies have reported reduction of insulin, insulin-like growth factor 1 and insulin receptor and an increase in tau protein and glycogen-synthase kinase-3β compared to healthy controls suggesting an impairment of metabolism in the AD patient’s brain. Given these lines of evidence, in the present study we investigated brains of mice treated with 2 obesogenic diets, high-fat diet (HFD) and high-glycaemic diet (HGD), compared to mice fed with a standard diet (SD) employing a quantitative mass spectrometry-based approach. Moreover, post-translational modified proteins (phosphorylated and N-linked glycosylated) were studied. The aim of the study was to identify proteins present in the brain that are changing their expression based on the diet given to the mice. We believed that some of these changes would highlight pathways and molecular mechanisms that could link obesity to brain impairment. The results showed in this study suggest that, together with cytoskeletal proteins, mitochondria and metabolic proteins are changing their post-translational status in brains of obese mice. Specifically, proteins involved in metabolic pathways and in mitochondrial functions are mainly downregulated in mice fed with obesogenic diets compared to SD. These changes suggest a reduced metabolism and a lower activity of mitochondria in obese mice. Some of these proteins, such as PGM1 and MCT1 have been shown to be involved in brain impairment as well. These results might shed light on the well-studied correlation between obesity and brain damage. The results presented here are in agreement with previous findings and aim to open new perspectives on the connection between diet-induced obesity and brain impairment. |
| Databáze: | OpenAIRE |
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