Search results for "GLP-2"
showing 10 items of 24 documents
Activation of the Glucagon-Like Peptide-2 Receptor Inhibits Neurally-Evoked Mucosal Chloride Secretion in the Guinea Pig Ileum In Vitro.
2009
Role of Endogenous GLP-2 in the Intestinal Adaptation to a Chronic High Fat Diet
2013
Does GLP-2 receptor expression change dynamically in fed and fasted states?
2009
Peripheral Glucagon-like peptide 2 administration inhibits food intake in mice: Analysis of the mechanism of action.
2012
OBJECTIVE: Previously we showed that, in mice, peripheral administration of glucagon-like peptide 2 (GLP-2) or [Gly2]GLP-2, the degradation-resistant analogue of GLP-2, reduces food intake in the short term. The purposes of the present study were to compare the influence of [Gly2]GLP-2 with the anorectic effect induced by glucagon-like peptide 1 (GLP-1) and to analyze the mechanism of action responsible for GLP-2-induced effects. METHODS: Food intake was measured in mice, fasted for 16-18 h, at the first hour following peptide or vehicle intraperitoneally (i.p.) administration. The effects of GLP-2 (3-33), GLP-2 receptor (GLP-2R) antagonist, and exendin (9-39), GLP-1R antagonist were also e…
Ruolo del peptide glucagone simile-2 nell'adattamento intestinale ad una dieta iperlipidica
2013
Glucagon-like peptide-2 treatment improves glucose dysmetabolism in mice fed a high fat diet
2016
Previous studies suggested that endogenous glucagon-like peptide 2 (GLP-2) is dispensable for the regulation of glucose homeostasis under normal conditions, while it can play a beneficial role in obesity conditions. The purpose of the present study was to investigate whether chronic treatment with Gly2-GLP-2, a stable analogue of GLP-2, can have an impact on glycaemic and lipid control in mice fed a high-fat diet (HFD), an animal model of human obesity and insulin resistance. HFD mice were treated once a day with Gly2-GLP-2 for 4 weeks. Body weight, food intake, fasting glucose, intraperitoneal glucose tolerance, insulin-induced glucose clearance, glucose-stimulated insulin secretion, β-cel…
Gastric relaxation induced by glucagon-like peptide-2 in mice fed a high-fat diet or fasted.
2011
Glucagon-like peptide-2 (GLP-2) is a nutrient-responsive gut hormone that increases the intestinal absorption. Exogenous GLP-2 also induces gastric fundus relaxation with possible implications for emptying rate or feeling of satiety. GLP-2 actions are mediated by GLP-2 receptor (GLP-2R), located on enteric neurons and myofibroblasts in murine gastrointestinal tract. Because it is not known whether changes in the endogenous GLP-2R levels occur in different nutritional states, we examined the GLP-2R gene and protein expression in gastric fundus from standard diet (STD)-fed, 12-h and 24-h fasted and re-fed, or high-fat diet (HFD)-fed mice and we analyzed the mechanical responses to exogenous G…
Food intake in lean and obese mice after peripheral administration of glucagon-like peptide 2
2012
We investigated the potential anorectic action of peripherally administered glucagon-like peptide 2 (GLP2) in lean and diet-induced obese (DIO) mice. Mice, fasted for 16 h, were injected i.p. with native GLP2 or [Gly2]GLP2, stable analog of GLP2, before or after GLP2 (3–33), a GLP2 receptor (GLP2R) antagonist, or exendin (9–39), a GLP1R antagonist. Food intake was measured at intervals 1, 2, 4, 8, and 24 h postinjection. In addition, we tested in lean mice the influence of [Gly2]GLP2 on gastric emptying and the effects of GLP1 alone or in combination with [Gly2]GLP2 on food intake. [Gly2]GLP2 dose dependently and significantly inhibited food intake in lean and DIO mice. The reduction of foo…
Protective potential of glucagon like peptide 2 (GLP-2) against the neurodegeneration
2019
Neurodegeneration consists in loss of neuron specific types, pattern and distribution, leading to progressive dysfunctions of the central nervous system. Neurodegenerative diseases include diverse pathological conditions, among which Alzheimer’s and Parkinson’s diseases are the most prevalent ones. Alzheimer’s disease is known as a growing dementia, characterized by progressive language, memory, and cognitive loss, while Parkinson’s disease is primarily characterized as a motor disorder. Senile plaques, caused by amyloid β peptide, hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal pathological hallmarks of Alzheimer’s disease. Amyloid β oligomer forma…
Review article: a comparison of glucagon-like peptides 1 and 2.
2013
Summary Background Recent advancements in understanding the roles and functions of glucagon-like peptide 1 (GLP-1) and 2 (GLP-2) have provided a basis for targeting these peptides in therapeutic strategies. Aim To summarise the preclinical and clinical research supporting the discovery of new therapeutic molecules targeting GLP-1 and GLP-2. Methods This review is based on a comprehensive PubMed search, representing literature published during the past 30 years related to GLP-1 and GLP-2. Results Although produced and secreted together primarily from L cells of the intestine in response to ingestion of nutrients, GLP-1 and GLP-2 exhibit distinctive biological functions that are governed by t…