Terminal ileum submucous plexus: Study of the VIP-ergic neurons of diabetic rats treated with ascorbic acid

Tronchini

Moure

et al. 2011

Arq. Gastroenterol.

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-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%. 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 mm 2 in the cecum and 3.6 mm 2 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%) promoted a neuroprotective effect on the myenteric neurons from the duodenum of rats, both in terms of natural aging and of diabetes mellitus.

Section: Discussionsupporting

confidence: 91%

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

Tronchini

Moure

et al. 2011

Arq. Gastroenterol.

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“…An increase (p<0.05) of the glycemia and blood glucose was observed in group D, confirming that these animals had the diabetic syndrome, similar to what was observed by Zanoni et al 15 . The ALC supplementation did not act immediately in the metabolic control of DM, as evidenced by the similar levels of blood glucose between groups D and DC.…”

Section: Discussionsupporting

confidence: 89%

“…The expressive increase of the area verified in groups D and DC could be related not only to the increment of the synthesis machinery but also to its accumulation and expression difficulties. We observed an increase in the immunoreactivity to VIP associated to an increase of the area, thus indicating that the accumulation of this substance within the neurons was similar to what was previously observed in VIP-ergic neurons of the terminal ileum of diabetic rats 15 . See et al 19 analyzed the submucous VIP neurons of the jejunum of rats after chemical denervation and verified that the area of these neurons increases once the myenteric and extrinsic pulse is removed from the jejunum.…”

Section: Groupsupporting

confidence: 88%

Effect of acetyl-L-carnitine on Vip-ergic neurons in jejunum submucous plexus of diabetic rats

Defani

Natali

et al. 2003

Arq. Neuro-Psiquiatr.

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-The effect of the treatment with acetyl-L-carnitine (ALC) on neurons releasing the vasoactive intestinal polypeptide (VIP) of the submucous plexus in the jejunum of diabetic rats was the purpose of our investigation. Diabetes (DM) was induced by injecting streptozotocin endovenously (35mg/kg). After sacrificing the animals, the jejunum was collected and processed for VIP detection. Four groups were used: C (nondiabetic), CC (non-diabetic treated with ALC), D (diabetic), DC (diabetes treated with ALC). We analyzed the immunoreactivity and the cellular profile of 126 cell bodies. The treatment with ALC improved some aspects of DM. However, it promoted a small increase in the area of neurons from group CC, suggesting a possible neurotrophic effect. Neurons from groups D and DC showed a large increase in their cellular profile and immunoreactivity when compared to C and CC, suggesting a larger concentration of this neurotransmitter within the neurons that produce it. This observation constitutes a recurrent finding in diabetic animals, suggesting that ALC doesnot interfere in the pathophysiological mechanisms that unchain a higher production and/or neurotransmitter accumulation and increase the profile of the VIP-ergic neurons.KEY WORDS: acetyl-L-carnitine, submucous plexus, VIP, diabetes, jejunum, rat. Efeito da acetil-L-carnitina sobre neurônios Vip-érgicos do plexo submucoso do jejuno de ratos diabéticosRESUMO -Investigamos o efeito da acetil-L-carnitina (ALC) sobre os neurônios que expressam o peptídeo intestinal vasoativo (VIP) do plexo submucoso no jejuno de ratos diabéticos. O diabetes (DM) foi induzido pela administração endovenosa de estreptozootocina (35mg/kg). Após o sacrifício dos animais, o jejuno foi coletado e processado para a detecção de VIP. Utilizou-se quatro grupos: C (não diabéticos), CC (não diabéticos suplementados com ALC), D (diabéticos) e DC (diabéticos suplementados com ALC). Analisou-se a imunoreatividade e o perfil celular de 126 corpos celulares. O tratamento com ALC melhorou alguns aspectos do DM. Porém, promoveu pequeno aumento na área dos neurônios do grupo CC, indicando possível efeito neurotrófico. Neurônios dos grupos D e DC apresentaram grande aumento do perfil celular e na imunoreatividade em relação a C e CC, sugerindo maior concentração deste neurotransmissor nestes neurônios. Esta observação é constante em animais diabéticos, sugerindo que a ALC não interfere nos mecanismos fisiopatológicos que desencadeiam a maior produção e/ou acúmulo de neurotransmissor e aumento do perfil dos neurônios VIP-érgicos. PALAVRAS-CHAVE: acetil-L-carnitina, plexo submucoso, VIP, diabetes, jejuno, rato. Diabetes mellitus (DM) main chronic complications are, among others, vascular changes and peripheral neuropathies, which lead to gastrointestinal dysfunctions. Several hypotheses have been reported concerning the main causes for the origin of the diabetic neuropathy. Recent reports have described that the carnitine abnormal metabolism may be one of the reasons that triggers neural damage...

“…Zanoni et al (2003) when used the myosin-V technique for staining the total population of myenteric neurons, did not observe significant differences between the number of neurons when comparing the groups of diabetic animals and the ascorbic acid supplemented. On the other hand, Zanoni et al (2002) and Zanoni et al (2003) reported that the ascorbic acid supplementation was positive on the VIP-ergic submucous and nitrergic neurons (NADPHdiaphorase histochemistry technique) of the ileum of diabetic rats, respectively. The ascorbic acid supplementation is beneficial for diabetics since, according to Garg and Bansal (2000), it reduces the levels of lipidic and plasmatic peroxidation, regulates the plasmatic levels of vitamin C and increases the levels of vitamin E, besides increasing the glutathione peroxidase activity.…”

Section: Discussionmentioning

confidence: 99%

“…The reduction in the number of neurons demonstrates that the diabetes mellitus causes the death of these cells. Besides, alterations had also been observed in its morphology, in cases of chronic diabetes, in different intestinal segments (Romano et al, 1996;Zanoni et al, 1997;Hernandes et al, 2000;Fregonesi et al, 2001;Zanoni et al, 2002;Zanoni et al, 2003). The ascorbic acid is a substance that acts as antioxidant and also promotes the reduction on sorbitol plasmic concentration, inhibiting the aldose reductase (Vinson et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Effect of the ascorbic acid treatment on the NADHd-positive myenteric neurons of diabetic rats proximal colon

Braz. arch. biol. technol.

Pereira

Freitas

2007

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The aim of this work was to study the effect of the ascorbic acid on the myenteric neurons of diabetic rats proximal colon. Fifteen rats (90 days old) were divided into three groups: control, untreated diabetic and treated diabetic with ascorbic acid (DA). After 120 days of daily treatment with ascorbic acid, the intestinal segments were submitted to the NADH-diaphorase (NADHd) histochemistry technique to expose the myenteric neurons. The group DA showed a higher neuronal density (33.4 %) when compared to the untreated diabetic animals (p < 0.05). Cellular body area of neurons was significantly larger in group DA (17.3 %) when compared to the untreated diabetics (p < 0.05). It could be concluded that the ascorbic acid promoted a neuroprotective effect on the NADHd myenteric neurons of the proximal colon of diabetic rats.