Diabetic Rats Supplemented with L-Glutamine: A Study of Immunoreactive Myosin-V Myenteric Neurons and the Proximal Colonic Mucosa

Tashima, Cristiano Massao; Tronchini, Eleandro Aparecido; Pereira, Renata Virginia Fernandes; Bazotte, Roberto Barbosa; Zanoni, Jacqueline Nelisis

doi:10.1007/s10620-006-9564-8

Cited by 22 publications

(27 citation statements)

References 47 publications

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“…Thus, we can infer that diabetes promoted a reduction of neuron metabolism, leading to the death of a portion of its neuronal population. We observed a reduction of more than half of these neurons, and diabetic neuropathy was observed, similar to studies that used other experimental models of diabetes and evaluated different regions of the gastrointestinal tract, including the stomach (Takahashi et al 1997;Fregonesi et al 2001), duodenum (Pereira et al 2006;Zanoni et al 2011;Lopes et al 2012), jejunum (Defani et al 2003;De Freitas et al 2008;Alves et al 2010;HermesUliana et al 2014), ileum Shotton and Lincoln 2006;Pereira et al 2011), cecum (Zanoni et al 1997;Zanoni et al 2011), and proximal colon (Tashima et al 2007;Roldi et al 2009). The development of neuropathy affects different types of enteric neurons, which are responsible for the control of important functions, such as motility, secretion, blood flow, and growth aspects of the local mucosal immune system (Furness 2012).…”

Section: Discussionsupporting

confidence: 84%

“…Among the chronic complications caused by diabetes, neurological manifestations are the most common, affecting both the autonomic and peripheral nervous systems and impairing the quality of life of patients (Chandrasekharan et al 2011). Our research group found that diabetes mellitus reduced the density of myenteric neurons and enteric neural plasticity in various segments of the digestive system (Takahashi et al 1997;Zanoni et al 1997;Fregonesi et al 2001;Defani et al 2003;Zanoni et al 2003;Pereira et al 2006;Tashima et al 2007;Zanoni et al 2007;De Freitas et al 2008;Roldi et al 2009;Alves et al 2010;Pereira et al 2011;Zanoni et al 2011;Lopes et al 2012;Hermes-Uliana et al 2014). These changes in enteric innervation that arise from diabetes are attributable to persistent hyperglycemia that produces numerous metabolic changes.…”

Section: Introductionmentioning

confidence: 78%

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Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

Zanoni

Hermes-Uliana

2015

Braz. arch. biol. technol.

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The present study evaluated the effects of supplementation with a combination of vitamin C and vitamin E on NADH-diaphorase-positive (NADH-d + ) and neuronal nitric oxide synthase (nNOS)-immunoreactive myenteric neurons in the duodenum and ileum in diabetic rats. Forty rats were distributed into the following groups: normoglycemic (N), normoglycemic supplemented with vitamin C and vitamin E (NS), diabetic (D), and diabetic supplemented with vitamin C and vitamin E (DS). Vitamin C was added to the drinking water, and vitamin E was incorporated in the diet (1%). After 120 days, the animals were euthanized, and the duodenum and ileum were subjected to NADH-d and nNOS staining. Quantitative and morphometric analyses of myenteric neurons were performed. Diabetes reduced NADH-d + neurons in the D group. The density of nitrergic neurons was not changed by diabetes or vitamin treatment. Hypertrophy of the cell body area of NADH-d + and nNOS-immunoreactive neurons was observed in both intestinal segments. Combined supplementation with vitamin C and vitamin E prevented the reduction of the density of NADH-d+ neurons and hypertrophy, demonstratred by both techniques. Supplementation with a combination of vitamin C and vitamin E promoted myenteric neuroprotection in the small intestine in diabetic rats.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 78%

Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

Zanoni

Hermes-Uliana

2015

Braz. arch. biol. technol.

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“…Similar results were found by Freitas et al (12) , who observed a significant 37.9% reduction in neuronal density in the jejunum in diabetic animals compared with non-diabetic animals. Other studies performed by our group have analyzed different segments of the gastrointestinal tract, including the ileum (3,22,46) , proximal colon (15,24,25,34,39) , and stomach (14) and showed similar results. This reduction in the number of myenteric neurons results from hyperglycemia, which initiates several biochemical events, such as disturbances in the polyol pathway, formation of AGEs, activation of the protein kinase C and hexosamine pathways, and glycolysis.…”

Section: Discussionsupporting

confidence: 64%

Supplementation with 0.1% and 2% vitamin e in diabetic rats: analysis of myenteric neurons immunostained for myosin-V and nNOS in the jejunum

Tronchini

Trevizan

Tashima

et al. 2012

Arq. Gastroenterol.

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-Context -Diabetes mellitus is a disease characterized by hyperglycemia that, when allowed to progress long-term untreated, develops vascular and neurological complications, which are responsible for the development of alterations in the enteric nervous system in diabetic patients. In the gastrointestinal tract, diabetes mellitus promotes motor and sensory changes, and in the reflex function of this system, causing gastroparesis, diarrhea, constipation, megacolon, slow gastrointestinal transit, gastric stasis and dilation with decreased or increased peristaltic contractions. Several studies have shown that oxidative stress is the main responsible for the vascular and neurological complications affecting the enteric nervous system of diabetics. Objective -The effects of 0.1% and 2% vitamin E on myosin-V-and nNOS-immunoreactive neurons in the jejunum of diabetic rats were investigated. Methods -Thirty rats were divided into the groups: normoglycemic, normoglycemic treated with 0.1% vitamin E, normoglycemic treated with 2% vitamin E, diabetic, diabetic treated with 0.1% vitamin E, and diabetic treated with 2% vitamin E. The neuronal density and areas of neuron cell bodies were determined. Results -Diabetes (diabetic group) significantly reduced the number of myosin-V-immunoreactive neurons compared with the normoglycemic group. The diabetic treated with 0.1% vitamin E and diabetic treated with 2% vitamin E groups did not exhibit a greater density than the D group (P>0.05). Nitrergic density did not change with diabetes (P>0.05). The areas of myosin-V-and nNOS-immunoreactive neurons significantly increased in the normoglycemic treated with 2% vitamin E and diabetic groups compared with the normoglycemic group. Conclusion -Supplementation with 2% vitamin E had a neurotrophic effect only in the area of myosin-V-immunoreactive neurons compared with the diabetic group. HEADINGS -Vitamin E. Diabetes mellitus, experimental. Jejunum. Neurons. Myosin type V. Nitric oxide sinthase. Rats.

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“…Several authors have shown that autonomic neuropathy caused chronically by diabetes mellitus is related to quantitative and morphometric changes in the enteric neurons in various GI segments [22,77,155,156] . However, studies on the number and area of glial cells in diabetes mellitus are scarce.…”

Section: Enteric Gliamentioning

confidence: 99%

Diabetes-related alterations in the enteric nervous system and its microenvironment

Bagyánszki

Bódi²

2012

WJD

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Gastric intestinal symptoms common among diabetic patients are often caused by intestinal motility abnormalities related to enteric neuropathy. It has recently been demonstrated that the nitrergic subpopulation of myenteric neurons are especially susceptible to the development of diabetic neuropathy. Additionally, different susceptibility of nitrergic neurons located in different intestinal segments to diabetic damage and their different levels of responsiveness to insulin treatment have been revealed. These findings indicate the importance of the neuronal microenvironment in the pathogenesis of diabetic nitrergic neuropathy. The main focus of this review therefore was to summarize recent advances related to the diabetes-related selective nitrergic neuropathy and associated motility disturbances. Special attention was given to the findings on capillary endothelium and enteric glial cells. Growing evidence indicates that capillary endothelium adjacent to the myenteric ganglia and enteric glial cells surrounding them are determinative in establishing the ganglionic microenvironment. Additionally, recent advances in the development of new strategies to improve glycemic control in type 1 and type 2 diabetes mellitus are also considered in this review. Finally, looking to the future, the recent and promising results of metagenomics for the characterization of the gut microbiome in health and disease such as diabetes are highlighted.

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Diabetic Rats Supplemented with L-Glutamine: A Study of Immunoreactive Myosin-V Myenteric Neurons and the Proximal Colonic Mucosa

Cited by 22 publications

References 47 publications

Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

Supplementation with 0.1% and 2% vitamin e in diabetic rats: analysis of myenteric neurons immunostained for myosin-V and nNOS in the jejunum

Diabetes-related alterations in the enteric nervous system and its microenvironment

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