Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain

Sara Baldassano, Flavia Mule', Antonella Amato, Gaetano Felice Caldara, Domenico Nuzzo, Pasquale Picone, Giacoma Galizzi, Marta Di Carlo, Domenico Nuzzo, Marta Di Carlo, Pasquale Picone

Risultato della ricerca: Article

3 Citazioni (Scopus)

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.
Lingua originaleEnglish
pagine (da-a)296-304
Numero di pagine9
RivistaNeurobiology of Disease
Volume121
Stato di pubblicazionePublished - 2019

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Glucagon-Like Peptide 2
High Fat Diet
Encephalitis
Obesity
Brain
Amyloid beta-Protein Precursor
Glial Fibrillary Acidic Protein
In Situ Nick-End Labeling
Obese Mice
Gliosis
NF-kappa B
Sexually Transmitted Diseases
Heat-Shock Proteins
Interleukin-8
Interleukin-1
Fluorescent Antibody Technique
Interleukin-6
Reactive Oxygen Species
Oxidative Stress
Cell Count

All Science Journal Classification (ASJC) codes

  • Neurology

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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain. / Baldassano, Sara; Mule', Flavia; Amato, Antonella; Caldara, Gaetano Felice; Nuzzo, Domenico; Picone, Pasquale; Galizzi, Giacoma; Di Carlo, Marta; Nuzzo, Domenico; Di Carlo, Marta; Picone, Pasquale.

In: Neurobiology of Disease, Vol. 121, 2019, pag. 296-304.

Risultato della ricerca: Article

Baldassano, S, Mule', F, Amato, A, Caldara, GF, Nuzzo, D, Picone, P, Galizzi, G, Di Carlo, M, Nuzzo, D, Di Carlo, M & Picone, P 2019, 'Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain', Neurobiology of Disease, vol. 121, pagg. 296-304.
Baldassano, Sara ; Mule', Flavia ; Amato, Antonella ; Caldara, Gaetano Felice ; Nuzzo, Domenico ; Picone, Pasquale ; Galizzi, Giacoma ; Di Carlo, Marta ; Nuzzo, Domenico ; Di Carlo, Marta ; Picone, Pasquale. / Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain. In: Neurobiology of Disease. 2019 ; Vol. 121. pagg. 296-304.
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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.",
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AU - Mule', Flavia

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AU - Caldara, Gaetano Felice

AU - Nuzzo, Domenico

AU - Picone, Pasquale

AU - Galizzi, Giacoma

AU - Di Carlo, Marta

AU - Nuzzo, Domenico

AU - Di Carlo, Marta

AU - Picone, Pasquale

PY - 2019

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N2 - 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.

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