No abstract

The purpose of this work was to study the neurons of the myenteric plexus of the cecum of rats with chronic streptozotocin-induced diabetes. We used four experimental groups of animals. In groups D2 and D8 animals were killed two and eight months, respectively, after diabetes induction and groups C2 and C8 were used as controls. We carried out whole-mount preparations stained with Giemsa and NADH-diaphorase. We verified that the diabetes did not alter the shape and disposition of the myenteric ganglia; it provoked decrease on the neuronal density and increase on the incidence of weakly basophilic neurons. The effects of streptozotocin caused dilatation of the cecum still evidenced two months after induction, but no more observed on the eight months after induction. The smaller incidence of neurons in group D8 relative to group C8 was due to the early loss related to the drug toxicity and later to the aging in diabetic condition.

We concluded that 2% L: -glutamine had neuroprotective effects directly on myenteric neurons and indirectly through glial cells, which had gliatrophic effects.

-The purpose of the present study was to investigate the morphological and quantitative alterations of the myenteric plexus neurons of the stomach of rats with streptozotocin-induced chronic diabetes and compare them to those of non-diabetic animals. Samples from the body of the stomach were used for wholemount preparations stained with NADH-diaphorase and for histological sections stained with hematoxylineosin. It was observed that diabetes cause a significant decrease on the number of neurons.KEY WORDS: myenteric plexus, diabetes, rat.Estudo quantitativo do plexo mientérico do estômago de ratos com diabetes induzido por estreptozootocina RESUMO -A proposta deste trabalho foi estudar as alterações morfológicas e quantitativas dos neurônios do plexo mientérico do estômago de ratos com diabetes induzido por estreptozootocina e estabelecer uma comparação com animais não diabéticos. Amostras do corpo do estômago foram submetidas a preparados de membrana corados pelo método da NADH-diaforase e a cortes histológicos corados por hematoxilinaeosina. Observou-se que o diabetes provoca significante redução no número de neurônios. Diabetes mellitus is a pathological condition in which several physiological abnormalities are observed, such as neuropathies that affect the central nervous system, the peripheral nerves and the autonomic nervous system 1 . Streptozotocin-induced diabetes causes a cycle of events in the nerve cells of the myenteric plexus that begins within one to three days, with the development of chromatolysis followed by regenerative changes over the next six weeks, with some continuous, albeit occasional, ganglionic degeneration 2 ; changes in the innervation of the ileum and colon 3 are reported, as well as a decrease on the neuronal activity 4 . Studies on streptozotocininduced diabetic rats have emphasized the alterations that occur in the small and large intestines. However, it should be remembered that alterations in the neurons of the myenteric plexus, in addition to changing intestinal peristalsis, can affect stomach motility, leading to dilation and retarded gastric emptying, interfering with the coordination between stomach and duodenum and impairing the digestive process 5 . PALAVRAS-CHAVEIn a diabetic ketonuric Chinese hamsters examination of the gastrointestinal tract was observed that the animals had distention and atony of the stomach and intestines when compared with control animals 6 . In humans, among the clinical manifestations of autonomic neuropathy, there is motor impairment of the stomach, which can lead to anorexia, nausea, vomiting and persisting fullness, characterizing gastric debilitation 1,5 . It is also noteworthy that diabetic gastric atony is similar to that observed after vagotomy 5 .Considering the extensive development of the myenteric plexus and its importance for the control of gastric and intestinal functions, and suspecting that diabetes may affect these neurons, in this way contributing to the gastric disturbances, we undertook the present study to determine ...

Supplementation with L-glutathione exerted a better neuroprotective effect than L-glutamine and may prevent the development of enteric diabetic neuropathy.

The effect of vitamin E (1 g/kg body weight) supplementation on myosin-V and neuronal nitric oxide synthase (nNOS) immunoreactive myenteric neurons from the ileum of diabetic rats was investigated in the present study. Forty animals were divided into the following groups: normoglycemics (N), normoglycemics treated with vitamin E (NE), diabetics (D), and diabetics treated with vitamin E (DE). Quantitative and morphometric analyses were performed. The area of the tertiary plexus was also determined. Diabetes produced a 24% reduction in the number of myosin-V neurons in group D compared with group N, an effect that was accompanied by an increase in the tertiary plexus area (P < 0.05). Neuronal density was 27% higher in group NE than group N (P < 0.05). Nitrergic neuronal density was not altered as a consequence of either diabetes or vitamin E treatment. Myosin-V and nNOS immunoreactive neuronal cell body area increased significantly in group NE. The area of myosin-V and nNOS myenteric neurons also increased in group D. Vitamin E treatment (group DE) increased only the size of nitrergic neurons. The present results suggest that vitamin E elicited a neuroprotective and neurotrophic effect on the natural aging process, but with regard to diabetes, vitamin E supplementation exerted a neurotrophic effect only on nitrergic neurons.

The purpose of this work was to study the area of the varicosities of nerve fibers of myenteric neurons immunoreactive to vasoactive intestinal peptide (VIP-IR) and of the cell bodies of VIP-IR submucosal neurons of the jejunum of diabetic rats supplemented with 2% L-glutamine. Twenty male rats were divided into the following groups: normoglycemic (N), normoglycemic supplemented with L-glutamine (NG), diabetic (D) and diabetic supplemented with L-glutamine (DG). Whole-mounts of the muscle tunica and the submucosal layer were subjected to the immunohistochemical technique for neurotransmitter VIP identification. Morphometric analyses were carried out in 500 VIP-IR cell bodies of submucosal neurons and 2000 VIP-IR varicosities from each group. L-Glutamine supplementation to the normoglycemic animals caused an increase in the areas of the cell bodies (8.49%) and varicosities (21.3%) relative to the controls (P < 0.05). On the other hand, there was a decrease in the areas of the cell bodies (4.55%) and varicosities (28.9%) of group DG compared to those of group D (P < 0.05). It is concluded that L-glutamine supplementation was positive both to normoglycemic and diabetic animals.

-The aim of this study was to evaluate the effect of the ascorbic acid (AA) supplementation on the neurons that produce the vasoactive intestinal peptide (VIP) in the submucous plexus of the ileum of rat, four months after the induction of experimental diabetes mellitus with streptozotocin. Three groups of rats were used: C -control, D -diabetic, DA -diabetic receiving AA. We have measured the immunoreactivity and area of 80 cellular bodies of VIP-ergic neurons from each studied group. In the diabetic animals, we have observed hyperphagia, polydipsia, and an increase of glycemia and glycated hemoglobin. The VIP-ergic neurons have presented an increase of their immunoreactivity and the highest profiles when compared to the other groups. In the diabetic animals supplemented with AA it has been observed a small reduction in the glycemia and the water and food intake. We have also noticed smaller immunoreactivity in their VIP-ergic neurons, similar to what we have observed in the control group animals (group C).KEY WORDS: ascorbic acid, diabetes mellitus, streptozotocin, ileum, vasoactive intestinal peptide, submucous plexus, rats.Plexo submucoso de íleo terminal: estudo dos neurônios VIP Plexo submucoso de íleo terminal: estudo dos neurônios VIP Plexo submucoso de íleo terminal: estudo dos neurônios VIP Plexo submucoso de íleo terminal: estudo dos neurônios VIP Plexo submucoso de íleo terminal: estudo dos neurônios VIP-érgicos de ratos diabéticos tratados com -érgicos de ratos diabéticos tratados com -érgicos de ratos diabéticos tratados com -érgicos de ratos diabéticos tratados com -érgicos de ratos diabéticos tratados com ácido ascórbico ácido ascórbico ácido ascórbico ácido ascórbico ácido ascórbico RESUMO -O objetivo deste estudo foi avaliar o efeito da suplementação com ácido ascórbico (AA) sobre os neurônios que expressam o peptídeo intestinal vasoativo (VIP) no plexo submucoso do íleo de ratos, quatro meses após a indução do diabetes mellitus experimental com estreptozootocina. Três grupos de ratos foram usados: C-controles, D-diabéticos, DA-diabéticos recebendo AA. Foram avaliadas a imunoreatividade e a área de 80 corpos celulares de neurônios VIP-érgicos de cada grupo estudado. Nos animais diabéticos ocorreram hirperfagia, polidipsia, elevação da glicemia e hemoglobina glicada. Os neurônios VIP-érgicos apresentaram aumento da imunorreatividade e os maiores perfis, quando comparados aos demais grupos. Nos animais diabéticos suplementados com AA observou-se pequena redução na glicemia, ingesta de água e de alimento, verificando-se também menor imunorreatividade nos neurônios VIP-érgicos, o que foi semelhante ao observado nos animais do grupo controle (grupo C). PALAVRAS-CHAVE: acido ascórbico, diabetes mellitus, estreptozootocina, íleo, peptídeo intestinal vasoativo, plexo submucoso, ratos.