Absence of the interstitial cells of cajal in patients with gastroparesis and correlation with clinical findings

Forster, Jameson; Damjanov, Ivan; Lin, Zhiyue; Sarosiek, Irene; Wetzel, Paul A.; McCallum, Richard W.

doi:10.1016/s0016-5085(03)83982-3

Cited by 49 publications

(71 citation statements)

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“…A patchy disruption of ICC networks may result in re-entrant tachyarrhythmias as well as loss of generation of the slow waves, resulting in bradyarrhythmias. A recent study reported severe ICC loss in 12 out of 34 patients with refractory diabetic gastroparesis and correlated loss of ICCs with an abnormal electrogastrogram (EGG) showing tachygastria 59. Similar findings have also been reported in idiopathic gastroparesis with loss of ICCs, suggesting that abnormal function is a result of loss of ICCs rather than an effect of diabetes.…”

Section: Pathogenesissupporting

confidence: 55%

Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years: Figure 1

Kashyap

Farrugia

2010

Gut

163

127

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Diabetic gastroparesis is a disorder that occurs in both type 1 and type 2 diabetes. It is associated with considerable morbidity among these patients and resultant economic burden on the health system. It is primarily a disease seen in middle aged women though the increased predisposition in women still remains unexplained. Patients often present with nausea, vomiting, bloating, early satiety, and abdominal pain. The pathogenesis of this complex disorder is still not well understood but involves abnormalities in multiple interacting cell types including the extrinsic nervous system, enteric nervous system, Interstitial Cells of Cajal (ICC), smooth muscles and immune cells. The primary diagnostic test remains gastric scintigraphy though other modalities such as breath test, capsule, ultrasound, MRI and SPECT imaging show promise as alternative diagnostic modalities. The mainstay of treatment for diabetic gastroparesis has been antiemetics, prokinetics, nutritional support and pain control. In recent years, gastric stimulation has been used in refractory cases with nausea and vomiting. As we better understand the pathophysiology, newer treatment modalities are emerging which aim to correct the underlying defect. In this review we highlight what has been learned about diabetic gastroparesis in the past 5 years. We review the epidemiology, pathogenesis, diagnosis and treatment of diabetic gastroparesis focusing on the areas that are still controversial and those that require more studies. We also focus on advances in our understanding of the cellular changes that underlie development of diabetic gastroparesis highlighting new opportunities for targeted therapy. Keywords

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Section: Pathogenesissupporting

confidence: 55%

Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years: Figure 1

Kashyap

Farrugia

2010

Gut

163

127

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“…Oxidative stress mediates many of the deleterious effects of diabetes on organ function, and induces not only gastric mucosal injury, but also gastric motility dysfunction, such as diabetic gastroparesis [7]. Gastroparesis is thought to be caused by ROS-induced damage to the networks formed by ICCs [27]. Moreover, antioxidants can reverse diabetic gastroparesis in NOD mice [6].…”

Section: Discussionmentioning

confidence: 99%

Curcumin improves expression of SCF/c-kit through attenuating oxidative stress and NF-κB activation in gastric tissues of diabetic gastroparesis rats

Jin

Shen

Wang

et al. 2013

Diabetol Metab Syndr

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BackgroundDiabetes mellitus is associated with many kinds of complications. Recent studies have shown that oxidative stress and inflammatory reactions have critical roles in the pathogenesis of diabetic gastroparesis. Curcumin is known to have antioxidant and anti-inflammatory properties. In the present study, we investigated the effect of curcumin on diabetic gastric motility in a Sprague Dawley rat model of type 1 diabetes mellitus.MethodsMale SD rats were divided into a control group, a control group receiving curcumin, a diabetic group, and a diabetic group receiving curcumin. Diabetes was induced by intraperitoneal injection of streptozotocin. Curcumin (150 mg/kg) was given intragastrically for 6 weeks, and blood glucose levels and body weights were measured. Stomachs were excised for analysis of gastric emptying rates, and levels of oxidative stress. NF-κB, I-κB, and stem cell factor (SCF)/c-kit protein levels were assessed by western blot analysis, while the apoptosis of interstitial cells of Cajal (ICCs) was assessed by TUNEL staining.ResultsCurcumin-treated diabetic rats showed significantly improved gastric emptying rates [(59.4 ± 7.5)%] compared with diabetic rats [(44.3 ± 5.7)%], as well as decreased levels of MDA [21.4 ± 1.8 (nmol/mg) vs 27.9 ± 2.1 (nmol/mg)], and increased SOD activity [126.2 ± 8.8 (units/mg) vs 107.9 ± 7.5 (units/mg)]. On the other hand, the gastric emptying level in the control group was not significantly different from that in the control group receiving curcumin treatment. In addition, curcumin-treated diabetic rats showed significantly increased levels of SCF/c-kit protein in stomach tissues, inhibited I-κB degradation and NF-κB activation, and reduced ICC apoptosis index [(26.2 ± 4.1)% vs (47.5 ± 6.2)%], compared with the diabetic group.ConclusionCurcumin treatment improved gastric emptying by blocking the production of oxidative stress, abolishing NF-κB signal transduction and enhancing expression of SCF/c-kit in rats with diabetic gastroparesis.

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“…Gastroparesis are thought to be caused by ROS-induced damage of the networks of the interstitial cells of Cajal. (38) The authors reported that the plasma ghrelin levels and gastric preproghrelin mRNA expression levels are increased in rats with streptozotocin-induced diabetes, that is known for hyperphagia. (39) In a human study, however, the fasting plasma ghrelin level was significantly lower in diabetes mellitus with diabetic gastroparesis than in healthy controls.…”

Section: Gastric Motility Dysfunction and Ghrelinmentioning

confidence: 99%

Ghrelin and oxidative stress in gastrointestinal tract

Suzuki

Matsuzaki

Hibi

2010

J. Clin. Biochem. Nutr.

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Oxidative stress is a major cause of the gastrointestinal damage under physical or psychological stress. Ghrelin exhibits gastroprotective effects and they are supposed to be derived from antioxidant effects. In gastroduodenal mucosal injury, the plasma ghrelin levels increase in response to the demand for gastroduodenal cytoprotection. However, in the condition of Helicobacter pylori-induced gastric mucosal severe atrophy, the plasma ghrelin concentration shifted to lower levels. In diabetic gastroparesis, the regulation of ghrelin secretion is impaired with vagal nerve dysfunction. Selective ghrelin agonist is expected to represent a new class of prokinetic agent. In addition, the plasma ghrelin levels are also enhanced by systemic oxidative stress, and ghrelin exhibits antioxidant effects in many organs, such as heart, pancreas, and lung. This suggests that ghrelin would be an important player as a sensor of systemic oxidative stress.

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Absence of the interstitial cells of cajal in patients with gastroparesis and correlation with clinical findings

Cited by 49 publications

References 0 publications

Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years: Figure 1

Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years: Figure 1

Curcumin improves expression of SCF/c-kit through attenuating oxidative stress and NF-κB activation in gastric tissues of diabetic gastroparesis rats

Ghrelin and oxidative stress in gastrointestinal tract

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