Effects of Insulin Treatment on HuC/HuD, NADH Diaphorase, and nNOS-Positive Myoenteric Neurons of the Duodenum of Adult Rats with Acute Diabetes

Mello, Sônia Trannin de; Neto, Marcílio Hübner de Miranda; Zanoni, Jacqueline Nelisis; Furlan, Maria Montserrat Diaz Pedrosa

doi:10.1007/s10620-008-0430-8

Cited by 14 publications

(16 citation statements)

References 30 publications

(52 reference statements)

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“…RENATA V.F. PEREIRA, DAVID R. LINDEN, MARCÍLIO H. MIRANDA-NETO and JACQUELINE N. ZANONI Previous studies from our laboratory showed that the number of nNOS-IR neurons present per unit area does not change with diabetes in the stomach (Fregonesi et al 2005), duodenum (de Mello et al 2009), jejunum (Tronchini et al 2012) and ileum (Pereira et al 2008, Zanoni et al 2003. In the present study, when nNOS neurons were quantified per ganglion, which was not completed in the previous studies, a significantly 24.5% reduction induced by diabetes was found.…”

Section: Discussionmentioning

confidence: 91%

Differential effects in CGRPergic, nitrergic, and VIPergic myenteric innervation in diabetic rats supplemented with 2% L-glutamine

Pereira

Linden

Miranda-Neto

et al. 2016

An. Acad. Bras. Ciênc.

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The objective of this study was to investigate the effects of 2% L-glutamine supplementation on myenteric innervation in the ileum of diabetic rats, grouped as follows: normoglycemic (N); normoglycemic supplemented with L-glutamine (NG); diabetic (D); and diabetic supplemented with L-glutamine (DG). The ileums were subjected to immunohistochemical techniques to localize neurons immunoreactive to HuC/D protein (HuC/D-IR) and neuronal nitric oxide synthase enzyme (nNOS-IR) and to analyze varicosities immunoreactive to vasoactive intestinal polypeptide (VIP-IR) and calcitonin gene-related peptide (CGRP-IR). L-Glutamine in the DG group (i) prevented the increase in the cell body area of nNOS-IR neurons, (ii) prevented the increase in the area of VIP-IR varicosities, (iii) did not prevent the loss of HuC/D-IR and nNOS-IR neurons per ganglion, and (iv) reduced the size of CGRP-IR varicosities. L-Glutamine in the NG group reduced (i) the number of HuC/D-IR and nNOS-IR neurons per ganglion, (ii) the cell body area of nNOS-IR neurons, and (iii) the size of VIP-IR and CGRP-IR varicosities. 2% L-glutamine supplementation exerted differential neuroprotective effects in experimental diabetes neuropathy that depended on the type of neurotransmitter analyzed. However, the effects of this dose of L-glutamine on normoglycemic animals suggests there are additional actions of this beyond its antioxidant capacity.

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Section: Discussionmentioning

confidence: 91%

Differential effects in CGRPergic, nitrergic, and VIPergic myenteric innervation in diabetic rats supplemented with 2% L-glutamine

Pereira

Linden

Miranda-Neto

et al. 2016

An. Acad. Bras. Ciênc.

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“…Similar results were found by Pereira et al (22) in the ileum of rats using the same experimental model. Other studies did not find significant results with regard to the number of nNOS-immunoreactive neurons in different segments of the gastrointestinal tract, such as stomach (14) , distal colon (44) , and duodenum (13) . According to Pereira et al (22) , this subpopulation of neurons is highly resistant to the action of free radicals produced by DM-induced hyperglycemia, explaining the results described above, including our study of enteric neurons.…”

Section: Discussionmentioning

confidence: 78%

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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“…Izbeki et al [496] also found that in the jejunum, ileum and colon of rats with streptozotocin-induced diabetes, both the total and the nitrergic neuronal cell number decreased significantly, while in the duodenum only the number of nitrergic neurons decreased. De Mello et al [495] also demonstrated a significant reduction in density of the duodenal myenteric neurons stained with HuC/HuD compared with controls (18.6 and 19.77%, respectively, p<0.001). The density of nNOS neurons was also lower than that of controls (8.62 and 7.30%, respectively), but the difference did not attain statistical significance, which may suggest that the nitrergic neurons are less sensitive to acute diabetes induced by streptozotocin [495].…”

Section: Gt Segment Motility Disorders Referencesmentioning

confidence: 85%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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Effects of Insulin Treatment on HuC/HuD, NADH Diaphorase, and nNOS-Positive Myoenteric Neurons of the Duodenum of Adult Rats with Acute Diabetes

Cited by 14 publications

References 30 publications

Differential effects in CGRPergic, nitrergic, and VIPergic myenteric innervation in diabetic rats supplemented with 2% L-glutamine

Differential effects in CGRPergic, nitrergic, and VIPergic myenteric innervation in diabetic rats supplemented with 2% L-glutamine

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

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

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