Intestinotrophic Glucagon-Like Peptide-2 (GLP-2) Activates Intestinal Gene Expression and Growth Factor-Dependent Pathways Independent of the Vasoactive Intestinal Peptide Gene in Mice

Yusta, Bernardo; Holland, Diane T.; Waschek, James A.; Drucker, Daniel J.

doi:10.1210/en.2012-1069

Cited by 34 publications

(24 citation statements)

References 43 publications

(55 reference statements)

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“…Treatment with GLP-2 increased the abundance of and activated VIP-expressing neurons in healthy and inflamed rat colon through a PI3Kg/Akt-mediated pathway [67][68][69]. Noticeably, GLP-2's proliferative effects on the intestinal crypts and small intestinal mucosa do not require VIP [70]. In addition to reducing inflammation, GLP-2 exhibits antioxidant activity, reduces inflammation-induced oxidative stress in intestinal tissues [71], and provides protection from gut ischemia and reperfusion injury [72]; although the mechanisms of these actions have not been fully investigated to date.…”

Section: Physiological Effects Of Glp-2 On Intestinal Tissuesmentioning

confidence: 96%

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Connor

Evock‐Clover

Wall³

et al. 2016

Domestic Animal Endocrinology

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Numerous endocrine cell subtypes exist within the intestinal mucosa and produce peptides contributing to the regulation of critical physiological processes including appetite, energy metabolism, gut function, and gut health. The mechanisms of action and the extent of the physiological effects of these enteric peptides are only beginning to be uncovered. One peptide in particular, glucagon-like peptide 2 (GLP-2) produced by enteroendocrine L cells, has been fairly well characterized in rodent and swine models in terms of its ability to improve nutrient absorption and healing of the gut after injury. In fact, a long-acting form of GLP-2 recently has been approved for the management and treatment of human conditions like inflammatory bowel disease and short bowel syndrome. However, novel functions of GLP-2 within the gut continue to be demonstrated, including its beneficial effects on intestinal barrier function and reducing intestinal inflammation. As knowledge continues to grow about GLP-2's effects on the gut and its mechanisms of release, the potential to use GLP-2 to improve gut function and health of food animals becomes increasingly more apparent. Thus, the purpose of this review is to summarize: (1) the current understanding of GLP-2's functions and mechanisms of action within the gut; (2) novel applications of GLP-2 (or stimulators of its release) to improve general health and production performance of food animals; and (3) recent findings, using dairy calves as a model, that suggest the therapeutic potential of GLP-2 to reduce the pathogenesis of intestinal protozoan infections.

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Section: Physiological Effects Of Glp-2 On Intestinal Tissuesmentioning

confidence: 96%

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Connor

Evock‐Clover

Wall³

et al. 2016

Domestic Animal Endocrinology

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“…Interestingly, GLP2 is also known to increase disaccharide absorption by increasing the expression and activity of SGLT1 (Cheeseman, 1997;Cheeseman and Tsang, 1996). In addition, GLP2R activation enhanced KGF production (Yusta et al, 2012). Whether the increase of KGF expression in the SuperEGF group is via the up-regulation of GLP2 by EGF is to be further explored.…”

Section: Egfmentioning

confidence: 99%

Epidermal growth factor containing culture supernatant enhances intestine development of early-weaned pigs in vivo: Potential mechanisms involved

Bedford

Chen

Huynh

et al. 2015

Journal of Biotechnology

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“…For example, we have demonstrated that mice deficient in VIP (VIP KO) exhibit ameliorated responses to experimental autoimmune encephalomyelitis (EAE) and to lipopolysaccharide (LPS)-induced endotoxemia [33,34]. In addition, VIP KO mice displayed a milder weight loss and intestinal damage than WT mice in a dextran sodium sulphate (DSS) murine model of disease [35]. These reports hint that long term lack of VIP is somehow protective in the development of this disease or that VIP is necessary for the development of certain inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Vasoactive Intestinal Peptide-Deficient Mice Exhibit Reduced Pathology in Trinitrobenzene Sulfonic Acid-Induced Colitis

Cheung-Lau¹,

Coûté-Monvoisin²,

Waschek³

2014

Neuroimmunomodulation

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Objectives: Vasoactive intestinal peptide (VIP) is an immunomodulatory neuropeptide with therapeutic properties in multiple murine models of inflammatory disease including the trinitrobenzene-sulfonic acid (TNBS)-colitis model of Crohn's disease. Understanding the spectrum of biological actions of endogenously produced VIP may help us dissect the complex and multifactorial pathogenesis of such inflammatory diseases. Our goal was to determine the contribution of endogenously produced VIP to TNBS-colitis by using VIP knockout (KO) mice. Methods: TNBS was intracolonically administered to wild-type (WT) and VIP KO mice, and weight loss and colitis were assessed over time. Colon histopathological changes and myeloperoxidase activities were analyzed and the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in colon and serum quantified. The proliferative response in vitro of splenocytes from TNBS WT and VIP KO administered mice to anti-CD3 and anti-CD28 was determined. Results: VIP KO mice did not exhibit the predicted exacerbated response to TNBS. Instead, they developed a milder clinical profile than WT mice, with lower TNF-α and IL-6 levels. Such potential defects seem selective, because other parameters such as the histopathological scores and the cytokine levels in the colon did not differ between the two strains of mice. Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro. Conclusion: Chronic loss of VIP in mice leads to a disruption of certain but not all immunological compartments, corroborating recent findings that VIP KO mice exhibit reduced mortality in the lipopolysaccharide-induced endotoxemia model and attenuated clinical development of experimental autoimmune encephalomyelitis while developing robust T-cell responses.

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Intestinotrophic Glucagon-Like Peptide-2 (GLP-2) Activates Intestinal Gene Expression and Growth Factor-Dependent Pathways Independent of the Vasoactive Intestinal Peptide Gene in Mice

Cited by 34 publications

References 43 publications

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Epidermal growth factor containing culture supernatant enhances intestine development of early-weaned pigs in vivo: Potential mechanisms involved

Vasoactive Intestinal Peptide-Deficient Mice Exhibit Reduced Pathology in Trinitrobenzene Sulfonic Acid-Induced Colitis

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