6533b837fe1ef96bd12a274e

RESEARCH PRODUCT

Glucagon-like peptide-2 analog and inflammatory state in obese mice

Sara BaldassanoGaetano Felice CaldaraFlavia MulèSimona TerzoAntonella AmatoLaura Lentini

subject

medicine.medical_specialtybusiness.industryEndocrinology Diabetes and MetabolismGlucagon-like Peptide-2 AnalogMice Obesemedicine.diseaseSettore BIO/09 - FisiologiaGlucagon-Like Peptide-1 ReceptorPeptide FragmentsMiceEndocrinologyEndocrinologyGlucagon-Like Peptide 1Diabetes mellitusInternal medicineGlucagon like peptide-2 (GLP-2) obese high fat diet (HFD) mice inflammation insulin signaling.Glucagon-Like Peptide 2medicineAnimalsInsulinbusinessObese Mice

description

Obesity is characterized by chronic low grade of systemic inflammation that develops in response to nutrient excess and plays a key role in the pathogenesis of insulin resistance. It is characterized by macrophage infiltration into adipose tissue (AT) and abnormal cytokine production. These factors damage the metabolic homeostasis leading to alteration in the insulin signaling in specific tissues and organs such as AT and liver. Thus, obese subjects develop over the time resistance to the cellular actions of insulin. Glucagon like peptide-2 (GLP-2) is an intestinal proglucagon-derived hormone released together with GLP1, in response to the passage of food by the distal small intestine. Once released, GLP-2 acts through its specific GLP-2 receptor. GLP-2 quickly is degraded with formation of GLP-2 (3-33). In order to extend the GLP-2 half-life, the protease-resistant analog, Gly2-GLP-2 (teduglutide) has been synthetized. The GLP-2 mainly influences gastrointestinal functions, but it exhibits also anti-inflammatory activity in intestinal disease models, in the brain of obese high fat diet (HFD) mice and can mitigate metabolic dysfunctions associated with hyperadiposity. The aim of the present study was to investigate if Gly2-GLP-2 exerts anti-inflammatory effects in AT and liver of HFD mice, which present central and peripheral IR, and to verify a possible improvement in the insulin signaling.

yearjournalcountryeditionlanguage
2020-03-14Endocrine
https://doi.org/10.1007/s12020-020-02261-0