Influence of glycine on intestinal ischemia‐reperfusion injury

Lee, Mark A.; Mccauley, Rosalie; Kong, Sung‐Eun; Hall, John C.

doi:10.1177/0148607102026002130

Cited by 42 publications

(34 citation statements)

References 27 publications

(29 reference statements)

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“…32) Glycine is an immunomodulatury agent, inhibits macrophage activation, reduces inflammation and inhibits apoptosis. 33) In the intestine, glycine limits the damage caused by intestinal reperfusion injury, [34][35][36][37][38][39] abdominal irradiation 40) and can prevent or reduce the severity of experimentally induced colitis. 41) As in other tissues, the protection appears to be at least bi-modal.…”

Section: Introductionmentioning

confidence: 99%

“…41) As in other tissues, the protection appears to be at least bi-modal. Tsune et al 41) demonstrated that dietary glycine was able to reduce intestinal inflammation in rats when given 2 d after administration of the damaging agent trinitrobenzenesulphonic acid (TNBS), whereas the work of Lee et al 37) showed a necessity for glycine administration before reperfusion to prevent ischemia/reperfusion injury.…”

Section: Introductionmentioning

confidence: 99%

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The Glycine Transporter GLYT1 in Human Intestine: Expression and Function

Howard

Hirst

2011

Biological & Pharmaceutical Bulletin

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Glycine is a well-documented cytoprotective agent and protects mammalian intestine against ischemiareperfusion injury, irradiation and experimentally induced colitis. The specific glycine transporter GLYT1 is found throughout the human intestine where it is responsible for some 30-50% of glycine uptake into intestinal epithelial cells across the basolateral membrane and appears to function to maintain glycine supply to enterocytes and colonocytes. This paper reviews current knowledge of GLYT1 and presents recent evidence supporting its essential role in glycine mediated cytoprotection in intestinal absorptive cells. Regulatory mechanisms involved in intestinal expression of GLYT1 are discussed and the potential of glycine for use as an anti-inflammatory, protective agent in the management of inflammatory bowel disease examined.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Glycine Transporter GLYT1 in Human Intestine: Expression and Function

Howard

Hirst

2011

Biological & Pharmaceutical Bulletin

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“…Such was the case of: glucagon 13 , 21-amino-steroids 14 , pentoxifylline 15 , somatostatin 16 and perfluorocarbons 17 . More recently, by using a model of HR in rats, glycine was put to the test as a protective agent of intestinal injuries stemming there from [18][19][20] . Glycine is a non-essential simple amino acid formed by a carbon molecule bonded to an amino group and to a carboxyl group.…”

mentioning

confidence: 99%

“…Glycine is a non-essential amino acid that protects the gut against lesions caused by the ischemia-reperfusion phenomenon [18][19][20]28 . It is considered an anti-inflammatory, immune modulator agent of direct cytoprotective function 21 .…”

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Glycine reduces tissue lipid peroxidation in hypoxia-reoxygenation-induced necrotizing enterocolitis in rats

et al. 2006

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Glycine reduces tissue lipid peroxidation in hypoxia-reoxygenation-induced necrotizing enterocolitis in rats 8 -ORIGINAL ARTICLE Glycine reduces tissue lipid peroxidation in hypoxia-reoxygenation-induced necrotizing enterocolitis in rats 1Glicina reduz a peroxidação lipídica tecidual em enterocolite necrosante induzida por hipóxia-reoxigenação em ratos ABSTRACT Purpose:To assess the protective effect of glycine in an experimental model of Neonatal Necrotizing Enterocolitis (NEC). Methods: Fifty (50) neonatal Wistar rats, from a litter of six female rats and weighing 4 to 6 grams, were used. Five animals were cannibalized and the 45 remaining were distributed into three groups: the G1 normal control group (n=12); the G2 Group (n=16), of animals that underwent hypoxia-reoxygenation (HR); the G3 Group of animals (n=17) that underwent HR following a 5% intraperitoneal glycine infusion. The animals underwent hypoxia in a CO 2 chamber receiving an air flow of 100% CO 2 for 5 minutes and reoxygenation receiving an O 2 flow at 100% for 5 minutes. One centimeter long small bowel and colon segments were prepared for histological analysis. The rest of the bowel was removed in a block and frozen at minus 80°C for homogenization and determination of tissue malondialdehyde (MDA). Tissue lesions were classified as Grade 0 to Grade 5, according to the level of damaged mucosa. Results: The animals in Group G1 had levels of small bowel and colon lesion significantly smaller as compared to the animals in Groups G2 and G3. The G2 group had mean MDA values significantly higher than the animals in the G1 (p = .015) and G3 (p=0.021) groups. MDA values did not differ significantly (p = 0.992) for the animals in groups G1 and G3. Conclusion: Glycine reduces tissue MDA levels (a measurement of lipid peroxidation) following HR in neonatal rats. Key words: Enterocolitis, Necrotizing. Glycine. Prevention & Control. RESUMO Objetivo:Avaliar o efeito protetor da glicina, num modelo experimental de ECN. Métodos: Foram utilizados 50 ratos Wistar recém-nascidos, com peso variando de 4 a 6 gramas, provenientes da ninhada de seis ratas. Cinco animais foram canibalizados e, os 45 restantes, foram distribuídos em três grupos: controle G1(n=12); G2(n=16), animais que foram submetidos à hipóxia-reoxigenação; G3(n=17), animais submetidos à hipóxia-reoxigenação após uma infusão intraperitoneal de glicina 5%. Os animais foram submetidos à hipóxia em uma câmara de CO 2 recebendo um fluxo de ar contendo 100% de CO 2, durante 5 minutos e à reoxigenação recebendo um fluxo de O 2 a 100% por 5 minutos. Segmentos de intestino delgado e cólon de 1 cm de extensão foram preparados para análise histológica. O restante do intestino foi removido em bloco e congelado a menos 80°C para homogeneização e dosagem de malondialdeído tecidual (MDA). Classificou-se as lesões teciduais de Grau 0 a Grau 5, de acordo com a extensão da lesão mucosa. Resultados: Os animais do Grupo G1 apresentaram graus de lesão de intestino delgado e cólon significantemente menores do que os anima...

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Abnormalities in metabolic pathways in celiac disease investigated by the metabolic profiling of small intestinal mucosa, blood plasma and urine by NMR spectroscopy

et al. 2020

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Celiac disease (CeD) is an autoimmune enteropathy caused by gluten intake in genetically predisposed individuals. We investigated the metabolism of CeD by metabolic profiling of intestinal mucosa, blood plasma and urine using NMR spectroscopy and multivariate analysis. The metabolic profile of the small intestinal mucosa was compared between patients with CeD (n = 64) and disease controls (DCs, n = 30). The blood plasma and urinary metabolomes of CeD patients were compared with healthy controls (HCs, n = 39). Twelve metabolites (proline (Pro), arginine (Arg), glycine (Gly), histidine (His), glutamate (Glu), aspartate, tryptophan (Trp), fumarate, formate, succinate (Succ), glycerophosphocholine (GPC) and allantoin (Alln)) of intestinal mucosa differentiated CeD from controls. The metabolome of blood plasma with 18 metabolites (Pro, Arg, Gly, alanine, Glu, glutamine, glucose (Glc), lactate (Lac), acetate (Ace), acetoacetate (AcAc), β‐hydroxybutyrate (β‐OHB), pyruvate (Pyr), Succ, citrate (Cit), choline (Cho), creatine (Cr), phosphocreatine (PCr) and creatinine) and 9 metabolites of urine (Pro, Trp, β‐OHB, Pyr, Succ, N‐methylnicotinamide (NMN), aminohippurate (AHA), indoxyl sulfate (IS) and Alln) distinguished CeD from HCs. Our data demonstrated changes in nine metabolic pathways. The altered metabolites were associated with increased oxidative stress (Alln), impaired healing and repair mechanisms (Pro, Arg), compromised anti‐inflammatory and cytoprotective processes (Gly, His, NMN), altered energy metabolism (Glc, Lac, β‐OHB, Ace, AcAc, Pyr, Succ, Cit, Cho, Cr and PCr), impaired membrane metabolism (GPC and Cho) and intestinal dysbiosis (AHA and IS). An orthogonal partial least square discriminant analysis model provided clear differentiation between patients with CeD and controls in all three specimens. A classification model built by combining the distinguishing metabolites of blood plasma and urine samples gave an AUC of 0.99 with 97.7% sensitivity, 93.3% specificity and a predictive accuracy of 95.1%, which was higher than for the models built separately using small intestinal mucosa, blood plasma and urine. In conclusion, a panel of metabolic biomarkers in intestinal biopsies, plasma and urine samples has potential to differentiate CeD from controls and may complement traditional tests to improve the diagnosis of CeD.

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Influence of glycine on intestinal ischemia‐reperfusion injury

Abstract: Local perfusion with 20% glycine can diminish warm ischemia-reperfusion injury to the rat small intestine in an in vivo model. The role of glycine supplementation should be evaluated in situations where hemodynamic instability may be responsible for breakdown in the gut barrier.

Cited by 42 publications

References 27 publications

The Glycine Transporter GLYT1 in Human Intestine: Expression and Function

The Glycine Transporter GLYT1 in Human Intestine: Expression and Function

Glycine reduces tissue lipid peroxidation in hypoxia-reoxygenation-induced necrotizing enterocolitis in rats

Abnormalities in metabolic pathways in celiac disease investigated by the metabolic profiling of small intestinal mucosa, blood plasma and urine by NMR spectroscopy

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