Ghrelin improves burn-induced delayed gastrointestinal transit in rats

Sallam, Hanaa S.; Oliveira, Hermes M.; Gan, Hua; Herndon, David N.; Chen, Jiande

doi:10.1152/ajpregu.00100.2006

Cited by 53 publications

(82 citation statements)

References 35 publications

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“…Severe cutaneous burn injury significantly delayed non-nutrient liquid gastric emptying, intestinal transit, and colonic transit compared with sham injury, whereas intraperitoneal application of acyl ghrelin normalized both non-nutrient liquid gastric emptying and intestinal transit, but not the colonic transit in rats (Sallam et al, 2007). Subcutaneous atropine blocked the prokinetic effects of acyl ghrelin on gastric emptying and intestinal transit, suggesting that the prokinetic effects of acyl ghrelin are exerted via the cholinergic pathway (Sallam et al, 2007). Therefore, acyl ghrelin may have a therapeutic potential for clinical burn patients with delayed upper gastrointestinal transit.…”

Section: Normal Physiology and Pathophysiology Of Ghrelin Gene mentioning

confidence: 89%

Ghrelin Gene Products and the Regulation of Food Intake and Gut Motility

et al. 2009

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Section: Normal Physiology and Pathophysiology Of Ghrelin Gene mentioning

confidence: 89%

Ghrelin Gene Products and the Regulation of Food Intake and Gut Motility

et al. 2009

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“…Given the widespread anatomic and cellular distribution of the GR, a variety of endocrine and paracrine functions likely exist (Wu et al, 2009). For example, ghrelin has been shown to improve intestinal motility and gastric emptying following abdominal operations and large body surface area burns (Sallam et al, 2007). More recently, ghrelin has been shown to have potent anti-inflammatory properties.…”

Section: Discussionmentioning

confidence: 99%

The Hormone Ghrelin Prevents Traumatic Brain Injury Induced Intestinal Dysfunction

Bansal

Ryu

Blow

et al. 2010

Journal of Neurotrauma

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Intestinal barrier breakdown following traumatic brain injury (TBI) is characterized by increased intestinal permeability, leading to bacterial translocation, and inflammation. The hormone ghrelin may prevent intestinal injury and have anti-inflammatory properties. We hypothesized that exogenous ghrelin prevents intestinal injury following TBI. A weight-drop model created severe TBI in three groups of anesthetized Balb/c mice. Group TBI: animals underwent TBI only; Group TBI/ghrelin: animals were given 10 mg of ghrelin intraperitoneally prior and 1 h following TBI; Group sham: no TBI or ghrelin injection. Intestinal permeability was measured 6 h following TBI by detecting serum levels of FITC-Dextran after injection into the intact ileum. The terminal ileum was harvested for histology, expression of the tight junction protein MLCK and inflammatory cytokine TNF-a. Permeability increased in the TBI group compared to the sham group (109.7 AE 21.8 mg/mL vs. 32.2 AE 10.1 mg/mL; p < 0.002). Ghrelin prevented TBI-induced permeability (28.3 AE 4.2 mg/mL vs. 109.7 AE 21.8 mg/mL; p < 0.001). The intestines of the TBI group showed blunting and necrosis of villi compared to the sham group, while ghrelin injection preserved intestinal architecture. Intestinal MLCK increased 73% compared to the sham group ( p < 0.03). Ghrelin prevented TBI-induced MLCK expression to sham levels. Intestinal TNF-a increased following TBI compared to the sham group (46.2 AE 7.1 pg/mL vs. 24.4 AE 2.2 pg/mL p < 0.001). Ghrelin reduced TNF-a to sham levels (29.2 AE 5.0 pg/mL; p ¼ NS). We therefore conclude that ghrelin prevents TBI-induced injury, as determined by intestinal permeability, histology, and intestinal levels of TNF-a. The mechanism for ghrelin mediating intestinal protection is likely multifactorial, and further studies are needed to delineate these possibilities.

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“…Colonic transit was measured by the geometric center method as described previously (34,40). A Silastic catheter (1 mm inside diameter and 2.1 mm outside diameter) was implanted under general anesthesia (2% isoflurane inhalation) into the proximal colon, with its tip resting ϳ2 cm distal to the cecum.…”

Section: Methodsmentioning

confidence: 99%

Gene plasticity in colonic circular smooth muscle cells underlies motility dysfunction in a model of postinfective IBS

Choudhury

Shi²,

Sarna³

2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Choudhury BK, Shi X-Z, Sarna SK. Gene plasticity in colonic circular smooth muscle cells underlies motility dysfunction in a model of postinfective IBS. Am J Physiol Gastrointest Liver Physiol 296: G632-G642, 2009. First published January 8, 2009 doi:10.1152/ajpgi.90673.2008.-The cellular mechanisms of motility dysfunction in postinfectious irritable bowel syndrome (PI-IBS) are not known. We used a rat model of neonatal inflammation to test the hypothesis that gene plasticity in colonic circular smooth muscle cells underlies motility dysfunction in PI-IBS. Mild/moderate or severe inflammation was induced in neonatal and adult rats. Experiments were performed in tissues obtained at 7 days (short term) and 6 -8 wk (long term) after the induction of inflammation. Severe inflammation in neonatal rats induced persistent long-term smooth muscle hyperreactivity to acetylcholine (ACh), whereas that in adult rat caused smooth muscle hyporeactivity that showed partial recovery in the long term. Mild/moderate inflammation had no effect in neonatal rats, but it induced smooth muscle hyporeactivity to ACh in adult rats, which recovered fully in the long term. Smooth muscle hyperreactivity to ACh resulted in accelerated colonic transit and increase in defecation rate, whereas hyporeactivity had opposite effects. Smooth muscle hyperreactivity to ACh was associated with increase in transcription rate of key cell-signaling proteins of the excitation-contraction coupling ␣1C subunit of Cav1.2 (L-type) calcium channels, G␣q, and 20-kDa myosin light chain (MLC20), whereas hyporeactivity was associated with their suppression. Inflammation in adult rats induced classical inflammatory response, which was absent in neonatal rats. Severe neonatal inflammation enhanced plasma norepinephrine and muscularis propria vasoactive intestinal polypeptide in the long term. We conclude that severe, but not mild/moderate, inflammation in a state of immature or impaired stress and immune response systems alters the transcription rate of key cell-signaling proteins of excitationcontraction coupling in colonic circular smooth muscle cells to enhance their contractility and accelerate colonic transit and defecation rate.irritable bowel syndrome; enteric nervous system; gastrointestinal motility; neurotransmitters; gene expression MOTILITY DYSFUNCTION RESULTING in diarrhea, constipation, or alternating diarrhea and constipation and visceral hypersensitivity are the defining symptoms of irritable bowel syndrome (IBS). Motility dysfunction in IBS is thought to be attributable to defects in smooth muscle and/or enteric neuronal regulatory systems. However, the cellular and molecular mechanisms of these defects in the absence of an organic disease, infection, or structural abnormality are not known.Clinical observations indicate that a subset (about 10 -25%) of the subjects exposed to enteric infections in an individual or a community setting go on to develop predominantly the symptoms of diarrhea-predominant IBS (IBS-D) (8, 15-17, 23, 28, 30). Why only l...

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Ghrelin improves burn-induced delayed gastrointestinal transit in rats

Cited by 53 publications

References 35 publications

Ghrelin Gene Products and the Regulation of Food Intake and Gut Motility

Ghrelin Gene Products and the Regulation of Food Intake and Gut Motility

The Hormone Ghrelin Prevents Traumatic Brain Injury Induced Intestinal Dysfunction

Gene plasticity in colonic circular smooth muscle cells underlies motility dysfunction in a model of postinfective IBS

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