Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats / Efeitos da suplementação com L-glutamina sobre os neurônios mioentéricos do duodeno e jejuno de ratos diabéticos

CONTEXT: Peripheral neuropathy is one of the chronic complications of diabetes mellitus and is directly related to gastrointestinal consequences of the disease. Myenteric neurons are affected in some pathological conditions such as diabetic neuropathy. The imbalance between cellular antioxidants and free radicals, leading to an increase in oxidative stress, is considered one of the main factors responsible for neuronal damages in diabetes. Drugs that reduce the oxidative stress may play a significant role in the treatment of neurological complications of diabetes mellitus. OBJECTIVE: To evaluate the effect of L-glutamine supplementation on the myenteric neurons from the cecum and duodenum of Wistar rats with streptozotocin-induced diabetes mellitus. METHODS: The animals were divided in four groups (n = 5): non-treated normoglycemics, normoglycemics treated with L-glutamine, non-treated diabetics and diabetics treated with L-glutamine from the 4th day of diabetes induction on. The amino acid L-glutamine was added to their diet at 1 percent. Giemsa's technique was employed to stain the myenteric neurons. We determined the cell body area of 500 neurons in each group studied. The quantitative analysis was performed by sampling in an area of 16.6 mm² in the cecum and 3.6 mm² in the duodenum of each animal. RESULTS: After the supplementation with L-glutamine in the duodenum, we observed a preservation of neuronal density in groups normoglycemic and diabetic (P<0.05). We also observed a preservation of the cell bodies area in diabetic animals (group treated with L-glutamine) (P<0.05). In the cecum, that preservation was not evident. CONCLUSION: Supplementation with L-glutamine (1 percent) promoted a neuroprotective effect on the myenteric neurons from the duodenum of rats, both in terms of natural aging and of diabetes mellitus.

CONTEXTO: Os neurônios entéricos são afetados em condições patológicas, como a neuropatia diabética. A neuropatia periférica é uma das complicações crônicas do diabetes mellitus e está diretamente relacionada com as manifestações gastrointestinais da doença. O desequilíbrio entre antioxidantes celulares e radicais livres, com o consequente aumento do estresse oxidativo, é considerado um dos principais responsáveis pelas alterações neuronais provocadas pelo diabetes. Drogas que reduzem o estresse oxidativo podem ter papel relevante no tratamento das complicações neurológicas do diabetes mellitus. OBJETIVO: Avaliar os efeitos da suplementação com L-glutamina sobre os neurônios mioentéricos do ceco e duodeno de ratos Wistar com diabetes mellitus induzido pela estreptozootocina. MÉTODOS: Os animais foram divididos em quatro grupos (n = 5): normoglicêmicos, normoglicêmicos suplementados com L-glutamina, diabéticos, diabéticos suplementados com L-glutamina a partir do 4º dia da indução do diabetes. O aminoácido L-glutamina foi adicionado à ração na quantidade de 1 por cento. A técnica de Giemsa foi utilizada para evidenciar os neurônios mioentéricos. Foram avaliadas as áreas de corpos celulares de 500 neurônios em cada grupo estudado. A análise quantitativa foi realizada em uma área de 16,6 mm² no ceco e 3,6 mm² no duodeno de cada animal. RESULTADOS: Após suplementação com L-glutamina verificou-se no duodeno a preservação da densidade neuronal tanto nos animais normoglicêmicos quanto nos animais diabéticos (P<0,05), e também o restabelecimento da área do corpo celular nos animais diabéticos (P<0,05). No ceco esta preservação e restabelecimento não foram evidenciados. CONCLUSÃO: A suplementação com L-glutamina (1 por cento) teve efeito neuroprotetor sobre os neurônios mioentéricos do duodeno tanto em condições de envelhecimento natural como no diabetes mellitus.

Analysis of myenteric neurons of the cecum of diabetic rats after supplementation with ascorbic acid / Análisis de neuronas mientéricas del ciego de ratas diabéticas después de suplementación con ácido ascórbico

The objective of this work was to investigate the neuroprotective action of the ascorbic acid over the myenteric neurons in the cecum of Wistar rats, four months after induction of the diabetes mellitus experimental with streptozotocin. Three groups with five rats each were used: C- controls, D- diabetic, DA- diabetic treated with ascorbic acid. For evidentiation of the myenteric neurons was carried out to Giemsa's technique. Were evaluated the areas of cell bodies of 500 neurons in each group studied. The quantitative analysis was carried out in an area of 16.6 mm2 in each cecum studied. In the animals diabetic observed elevation of the glycemia and glycated hemoglobin. The supplementation with ascorbic acid was effective under the myenteric neurons of the cecum of diabetics rays, since was presented the effect neuroprotective and neurotrofic.

El objetivo de este trabajo fue verificar el efecto neuroprotector del ácido ascórbico sobre las neuronas mientéricas en el ciego de Rattus Wistar, cuatro meses después de la inducción de diabetes mellitus experimental con estreptozotocina. Utilizamos tres grupos de animales: C- control, D- diabético, DA- diabético tratado con ácido ascórbico. Para la observación de las neuronas mientéricas fue llevado a cabo la técnica de Giemsa. Fueron evaluadas las áreas del soma de 500 neuronas, en cada grupo estudiado. El análisis cuantitativo fue llevado a cabo, en cada ciego, en un área de 16,6 mm². En los animales diabéticos, se observó la elevación de la glicemia y de la hemoglobina glicosilada. La suplementación con ácido ascórbico fue efectiva en las neuronas mientéricas del ciego de animales diabéticos, ya que se produjeron los efectos neuroprotetor y neurotrófico.

Morhological and quantitative analysis of the neurons of myenteric plexus of the cecum of streptozotocin-induced diabetic rats

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 neuron 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.