8 results on '"Mulè, Flavia"'
Search Results
2. sj-docx-1-nmi-10.1177_11786388211012405 – Supplemental material for Obesogenic Diets Cause Alterations on Proteins and Theirs Post-Translational Modifications in Mouse Brains
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Siino, Valentina, Jensen, Pia, James, Peter, Vasto, Sonya, Amato, Antonella, Mulè, Flavia, Accardi, Giulia, and Larsen, Martin Røssel
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111199 Nutrition and Dietetics not elsewhere classified ,FOS: Health sciences - Abstract
Supplemental material, sj-docx-1-nmi-10.1177_11786388211012405 for Obesogenic Diets Cause Alterations on Proteins and Theirs Post-Translational Modifications in Mouse Brains by Valentina Siino, Pia Jensen, Peter James, Sonya Vasto, Antonella Amato, Flavia è, Giulia Accardi and Martin Røssel Larsen in Nutrition and Metabolic Insights
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- 2021
- Full Text
- View/download PDF
3. Spasmolytic Effects of Aphanizomenon Flos Aquae (AFA) Extract on the Human Colon Contractility
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Martina Martorana, Flavia Mulè, Antonella Amato, Pierenrico Marchesa, Angela Maffongelli, Simona Terzo, S. Scoglio, Amato A, Terzo S, Marchesa P, Maffongelli A, Martorana M, Scoglio S, and Mulè Flavia
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Male ,Colon ,motility discomfort ,Methysergide ,Gene Expression ,Pharmacology ,Article ,PEA ,Contractility ,TAAR1 ,medicine ,Serotonin receptor antagonist ,Aphanizomenon ,Humans ,TX341-641 ,Myenteric plexus ,Aged ,human colon contractility ,Aged, 80 and over ,Biological Products ,AFA extract ,Nutrition and Dietetics ,Dose-Response Relationship, Drug ,Chemistry ,Nutrition. Foods and food supply ,Parasympatholytics ,EPPTB ,Muscle, Smooth ,Klamin® ,Middle Aged ,Immunohistochemistry ,Mechanism of action ,Dietary Supplements ,Enteric nervous system ,Female ,Peristalsis ,medicine.symptom ,Biomarkers ,β-PEA ,Food Science ,medicine.drug ,Muscle Contraction - Abstract
The blue-green algae Aphanizomenon flos aquae (AFA), rich in beneficial nutrients, exerts various beneficial effects, acting in different organs including the gut. Klamin® is an AFA extract particularly rich in β-PEA, a trace-amine considered a neuromodulator in the central nervous system. To date, it is not clear if β-PEA exerts a role in the enteric nervous system. The aims of the present study were to investigate the effects induced by Klamin® on the human distal colon mechanical activity, to analyze the mechanism of action, and to verify a β-PEA involvement. The organ bath technique, RT-PCR, and immunohistochemistry (IHC) were used. Klamin® reduced, in a concentration-dependent manner, the amplitude of the spontaneous contractions. EPPTB, a trace-amine receptor (TAAR1) antagonist, significantly antagonized the inhibitory effects of both Klamin® and exogenous β-PEA, suggesting a trace-amine involvement in the Klamin® effects. Accordingly, AphaMax®, an AFA extract containing lesser amount of β-PEA, failed to modify colon contractility. Moreover, the Klamin® effects were abolished by tetrodotoxin, a neural blocker, but not by L-NAME, a nitric oxide-synthase inhibitor. On the contrary methysergide, a serotonin receptor antagonist, significantly antagonized the Klamin® effects, as well as the contractility reduction induced by 5-HT. The RT-PCR analysis revealed TAAR1 gene expression in the colon and the IHC experiments showed that 5-HT-positive neurons are co-expressed with TAAR1 positive neurons. In conclusion, the results of this study suggest that Klamin® exerts spasmolytic effects in human colon contractility through β-PEA, that, by activating neural TAAR1, induce serotonin release from serotoninergic neurons of the myenteric plexus.
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- 2021
4. Altered insulin pathway compromises mitochondrial function and quality control both in in vitro and in vivo model systems
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Flavia Mulè, Giacoma Galizzi, Luca Caruana, Alice Conigliaro, Riccardo Alessandro, Marta Di Carlo, Pasquale Massimo Picone, Laura Palumbo, Domenico Nuzzo, Simona Terzo, Antonella Amato, Galizzi G., Palumbo L., Amato A., Conigliaro A., Nuzzo D., Terzo S., Caruana L., Picone P., Alessandro R., Mulè Flavia., and Di Carlo M.
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Male ,Aging ,Amyloid beta-Peptide ,medicine.medical_treatment ,Metabolic disease ,PINK1 ,Insulin pathway, Neurodegeneration, Metabolic diseases, Mitochondrion, Mitophagy, Aging ,Mitochondrion ,Diet, High-Fat ,Parkin ,NO ,Mice ,Insulin resistance ,Metabolic Diseases ,Cell Line, Tumor ,Mitophagy ,medicine ,Animals ,Humans ,Insulin ,Neurodegeneration ,Molecular Biology ,Amyloid beta-Peptides ,biology ,Animal ,Chemistry ,Cell Biology ,medicine.disease ,Cell biology ,Mitochondria ,Mice, Inbred C57BL ,Insulin receptor ,Mitochondrial permeability transition pore ,biology.protein ,Molecular Medicine ,Insulin Resistance ,Insulin pathway ,Human ,Signal Transduction - Abstract
Altered insulin signaling and insulin resistance are considered the link between Alzheimer's disease (AD) and metabolic syndrome. Here, by using an in vitro and an in vivo model, we investigated the relationship between these disorders focusing on neuronal mitochondrial dysfunction and mitophagy. In vitro Aβ insult induced the opening of mitochondrial permeability transition pore (mPTP), mitochondrial membrane potential (ΔΨm) loss, and apoptosis while insulin addition ameliorated these dysfunctions. The same alterations were detected in a 16 weeks of age mouse model of diet-induced obesity and insulin resistance. In addition, we detected an increase of fission related proteins and activation of mitophagy, proved by the rise of PINK1 and Parkin proteins. Nevertheless, in vitro, the increase of p62 and LC3 indicated an alteration in autophagy, while, in vivo decreased expression of p62 and increase of LC3 suggested removing of damaged mitochondria. Finally, in aged mice (28 and 48 weeks), the data indicated impairment of mitophagy and suggested the accumulation of damaged mitochondria. Taken together these outcomes indicate that alteration of the insulin pathway affects mitochondrial integrity, and effective mitophagy is age-dependent.
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- 2021
5. From obesity to Alzheimer's disease through insulin resistance
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Flavia Mulè, Antonella Amato, Simona Terzo, Terzo S., Amato A., and Mulè Flavia.
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medicine.medical_specialty ,Endocrinology, Diabetes and Metabolism ,Type 2 diabetes ,medicine.disease_cause ,Endocrinology ,Insulin resistance ,Downregulation and upregulation ,Alzheimer Disease ,Internal medicine ,Diabetes mellitus ,Internal Medicine ,medicine ,Humans ,Dementia ,Obesity ,Neurodegeneration ,Inflammation ,business.industry ,Brain ,Alzheimer's disease ,medicine.disease ,Diabetes Mellitus, Type 2 ,Lipotoxicity ,business ,Oxidative stress - Abstract
Alzheimer's disease is one of the most frequent forms of dementia. It is a progressive neurodegenerative disease, characterized by presence of amyloid plaques and neurofibrillary tangles in the brain. Obesity is regarded as abnormal fat accumulation with deleterious impact on human health. There is full scientific evidence that obesity and the metabolic comorbidities (e.g., insulin resistance, hyperglycaemia, and type 2 diabetes) are related to Alzheimer's disease and likely in the causative pathway. Numerous studies have identified several overlapping neurodegenerative mechanisms, including oxidative stress, mitochondrial dysfunction, and inflammation. In this review, we present how obesity and the associated lipotoxicity as well as chronic inflammation initiate a state of insulin resistance that in turn, may have a role in causing the characteristic cerebral alterations of AD. In particular, we focus on the molecular mechanisms linking the obesity-induced impairment in insulin signalling to the upregulation of Aβ aggregation, tau hyper-phosphorylation, inflammation, oxidative stress and mitochondrial dysfunction.
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- 2021
6. Obesogenic Diets Cause Alterations on Proteins and Theirs Post-Translational Modifications in Mouse Brains
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Martin R. Larsen, Giulia Accardi, Pia Jensen, Peter James, Antonella Amato, Flavia Mulè, Valentina Siino, Sonya Vasto, and Siino Valentina, James Peter, Vasto Sonya, Amato Antonella, Mulè Flavia, Accardi Giulia, Rossel Larsen Martin
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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 - Abstract
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.
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- 2021
7. Honey and obesity-related dysfunctions: a summary on health benefits
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Flavia Mulè, Simona Terzo, Antonella Amato, and Terzo Simona, Mulè Flavia, Amato Antonella.
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0301 basic medicine ,Health Status ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Anti-Inflammatory Agents ,Adipose tissue ,Glycemic Control ,medicine.disease_cause ,Bioinformatics ,Biochemistry ,Antioxidants ,03 medical and health sciences ,0302 clinical medicine ,Hydroxybenzoates ,Animals ,Humans ,Medicine ,Obesity ,Neurodegeneration ,Molecular Biology ,Glycemic ,Flavonoids ,Inflammation ,Metabolic Syndrome ,Hyperplasia ,Nutrition and Dietetics ,medicine.diagnostic_test ,business.industry ,fungi ,Metabolic disorder ,Polyphenols ,food and beverages ,Neurodegenerative Diseases ,Honey ,medicine.disease ,Oxidative Stress ,030104 developmental biology ,Diabetes Mellitus, Type 2 ,Hypertension ,Oxidative stre ,Insulin Resistance ,Metabolic syndrome ,business ,Lipid profile ,030217 neurology & neurosurgery ,Oxidative stress - Abstract
Honey is a natural product, containing flavonoids and phenolic acids, appreciated for its therapeutic abilities since ancient times. Although the bioactive potential is linked to the composition, that is variable depending on mainly the botanical origin, honey has antioxidant and anti-inflammatory properties. Therefore, honey, administered alone or in combination with conventional therapy, might result useful in the management of chronic diseases that are commonly associated with oxidative stress and inflammation state. Obesity is a metabolic disorder characterized by visceral adiposity. The adipose tissue becomes hypertrophic and undergoes hyperplasia, resulting in a hypoxic environment, oxidative stress and production of pro-inflammatory mediators that can be responsible for other disorders, such as metabolic syndrome and neurodegeneration. Experimental evidence from animals have shown that honey improves glycemic control and lipid profile with consequent protection from endothelial dysfunction and neurodegeneration. The purpose of the present review is to summarize the current literature concerning the beneficial effects of honey in the management of the obesity-related dysfunctions, including neurodegeneration. Based on the key constituents of honey, the paper also highlights polyphenols to be potentially responsible for the health benefits of honey. Further well-designed and controlled studies are necessary to validate these benefits in humans.
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- 2020
8. Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain
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Sara Baldassano, Pasquale Picone, Marta Di Carlo, Flavia Mulè, Giacoma Galizzi, Domenico Nuzzo, Gaetano Felice Caldara, Antonella Amato, Nuzzo, Domenico, Baldassano, Sara, Amato, Antonella, Picone, Pasquale, Galizzi, Giacoma, Caldara, Gaetano Felice, Di Carlo, Marta, and Mulè, Flavia
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0301 basic medicine ,Male ,medicine.medical_specialty ,Inflammation ,medicine.disease_cause ,Diet, High-Fat ,Settore BIO/09 - Fisiologia ,Neuroprotection ,lcsh:RC321-571 ,03 medical and health sciences ,0302 clinical medicine ,Neuroinflammation ,Internal medicine ,medicine ,Glucagon-Like Peptide 2 ,Animals ,Obesity ,Neurodegeneration ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,TUNEL assay ,Glial fibrillary acidic protein ,biology ,Chemistry ,digestive, oral, and skin physiology ,Brain ,medicine.disease ,Mice, Inbred C57BL ,030104 developmental biology ,Endocrinology ,Neuroprotective Agents ,Neurology ,Gliosis ,Oxidative stress ,Astrocytes ,biology.protein ,Glucagon-Like Peptide-2 Receptor ,Oxidative stre ,Encephalitis ,medicine.symptom ,Inflammation Mediators ,GLP-2 ,030217 neurology & neurosurgery ,hormones, hormone substitutes, and hormone antagonists - Abstract
Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodegeneration, stress marker proteins (p-ERK, Hsp60 and i-NOS), amyloid-β precursor protein (APP). [Gly2]-GLP-2 treatment significantly attenuated the HFD-induced increased expression of the various markers, as well as the higher levels of reactive oxygen species found in brains of untreated-HFD mice. Immunofluorescence confirmed that the increase of GFAP or APP in the brain cortex of HFD mice were less prominent in the [Gly2]-GLP-2 treated group. TUNEL-positive cell number in brain sections of [Gly2]-GLP-2-treated HFD-fed mice was significantly lesser in comparison with untreated-HFD animals and similar to STD fed mice. In conclusion, the results of the present study suggest that GLP-2 stable analogue improves the obesity-associated neuroinflammation and the central stress conditions, it reduces the neuronal apoptotic death, providing evidence for a neuroprotective role of the peptide.
- Published
- 2018
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