GLP-2 Receptor Localizes to Enteric Neurons and Endocrine Cells Expressing Vasoactive Peptides and Mediates Increased Blood Flow

Guan, Xiaofei; Karpen, Heidi; Stephens, John; Bukowski, John; Niu, Sanyong; Zhang, Guangcheng; Stoll, Barbara J.; Finegold, Milton J.; Holst, Jens J.; Hadsell, Darry L.; Nichols, Buford L.; Burrin, Douglas G.

doi:10.1053/j.gastro.2005.11.005

Cited by 220 publications

(239 citation statements)

References 42 publications

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“…Activation of GLP2 receptors regulates epithelial cell growth (Tsai et al 1997, Bjerknes & Cheng 2001, reduces intestinal permeability, enhances the barrier function (Benjamin et al 2000, Moran et al 2012, Drucker & Yusta 2014, increases mesenteric blood flow (Guan et al 2006, Bremholm et al 2009) and inhibits gastrointestinal motility, thus providing another mechanism to increase digestion and absorption of nutrient (Wøjdemann et al 1998, McDonagh et al 2007, Amato et al 2009, Cinci et al 2011.…”

Section: Overview On Glp2mentioning

confidence: 99%

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Amato¹,

Baldassano²,

Mulè³

2016

Journal of Endocrinology

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Glucagon-like peptide 2 (GLP2) is a proglucagon-derived peptide produced by intestinal enteroendocrine L-cells and by a discrete population of neurons in the brainstem, which projects mainly to the hypothalamus. The main biological actions of GLP2 are related to the regulation of energy absorption and maintenance of mucosal morphology, function and integrity of the intestine; however, recent experimental data suggest that GLP2 exerts beneficial effects on glucose metabolism, especially in conditions related to increased uptake of energy, such as obesity, at least in the animal model. Indeed, mice lacking GLP2 receptor selectively in hypothalamic neurons that express proopiomelanocortin show impaired postprandial glucose tolerance and hepatic insulin resistance (by increased gluconeogenesis). Moreover, GLP2 acts as a beneficial factor for glucose metabolism in mice with high-fat diet-induced obesity. Thus, the aim of this review is to update and summarize current knowledge about the role of GLP2 in the control of glucose homeostasis and to discuss how this molecule could exert protective effects against the onset of related obesity type 2 diabetes.

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Section: Overview On Glp2mentioning

confidence: 99%

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Amato¹,

Baldassano²,

Mulè³

2016

Journal of Endocrinology

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“…Instead, GLP-2Rs are expressed in the enteroendocrine cells of the proximal small intestine (jejunum). In porcine intestine, in addition to expression in enteroendocrine cells, GLP-2Rs are also expressed in endothelial nitric oxide synthase-expressing neurons and vasoactive intestinal polypeptide-positive enteric neurons (78). GLP-2 infusion upregulated endothelial nitric oxide synthase expression and activity and stimulated intestinal blood flow in pigs (78).…”

Section: Glp-2 Stimulates "Preformed" Intestinal Lipoprotein Particlementioning

confidence: 99%

“…In porcine intestine, in addition to expression in enteroendocrine cells, GLP-2Rs are also expressed in endothelial nitric oxide synthase-expressing neurons and vasoactive intestinal polypeptide-positive enteric neurons (78). GLP-2 infusion upregulated endothelial nitric oxide synthase expression and activity and stimulated intestinal blood flow in pigs (78). In humans, GLP-2 increased blood flow primarily in the superior mesenteric artery (79).…”

Section: Glp-2 Stimulates "Preformed" Intestinal Lipoprotein Particlementioning

confidence: 99%

Gut Peptides Are Novel Regulators of Intestinal Lipoprotein Secretion: Experimental and Pharmacological Manipulation of Lipoprotein Metabolism

et al. 2015

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Individuals with metabolic syndrome and frank type 2 diabetes are at increased risk of atherosclerotic cardiovascular disease, partially due to the presence of lipid and lipoprotein abnormalities. In these conditions, the liver and intestine overproduce lipoprotein particles, exacerbating the hyperlipidemia of fasting and postprandial states. Incretin-based, antidiabetes therapies (i.e., glucagon-like peptide [GLP]-1 receptor agonists and dipeptidyl peptidase-4 inhibitors) have proven efficacy for the treatment of hyperglycemia. Evidence is accumulating that these agents also improve fasting and postprandial lipemia, the latter more significantly than the former. In contrast, the gut-derived peptide GLP-2, cosecreted from intestinal L cells with GLP-1, has recently been demonstrated to enhance intestinal lipoprotein release. Understanding the roles of these emerging regulators of intestinal lipoprotein secretion may offer new insights into the regulation of intestinal lipoprotein assembly and secretion and provide new opportunities for devising novel strategies to attenuate hyperlipidemia, with the potential for cardiovascular disease reduction.

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“…Finally, Glp-2 increases hexose transportation and inhibits apoptosis by decreasing intestinal motility and permeability. Externally administered Glp-2 has many effects on the intestinal system, such as increasing intestinal blood flow (6)(7)(8)(9) and intestinal barrier function (10,11). In other studies, Glp-2 has also been found to have an antiinflammatory effect (12,13).…”

Section: Introductionmentioning

confidence: 95%

Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?

Topaloğlu¹,

Memi²,

Kaner³

et al. 2015

Turk J Med Sci

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Background/aim: To investigate the neuroprotective effects of glucagon-like peptide 2 (Glp-2), which increases cerebral blood flow, on the hippocampal complex after cerebral ischemia/reperfusion (I/R) injury in rats.Materials and methods: Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2. Cerebral ischemia was performed via the occlusion of the bilateral internal carotid artery for 40 min and continued with a reperfusion process. At the end of 6 h of reperfusion, animals were decapitated in all groups and brain tissues were removed. Malondialdehyde (MDA) and natural intracellular antioxidant glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured in the left hippocampal tissue. The right hippocampal tissues of all group members were taken for histopathologic study.Results: MDA levels and MPO activities increased from Group I to Group II and decreased from Group II to Groups III and IV. On the other hand, GSH levels were not significantly different among the groups. The number of apoptotic hippocampal tissue cells increased from Group I to Group II and decreased from Group II to Groups III and IV. Conclusion:Our preliminary study revealed that Glp-2 treatment may decrease oxidative damage from I/R in cerebral tissue.

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GLP-2 Receptor Localizes to Enteric Neurons and Endocrine Cells Expressing Vasoactive Peptides and Mediates Increased Blood Flow

Cited by 220 publications

References 42 publications

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Gut Peptides Are Novel Regulators of Intestinal Lipoprotein Secretion: Experimental and Pharmacological Manipulation of Lipoprotein Metabolism

Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?

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