Zanoni Jacqueline Nelisis, Tronchini Eleandro Aparecido, Moure Sheila Alves, Souza Ivan Domicio da Silva
Department of Morphological Sciences, Universidade Estadual de Maringá, Maringá, PR, Brazil.
Arq Gastroenterol. 2011 Jan-Mar;48(1):66-71. doi: 10.1590/s0004-28032011000100014.
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.
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.
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 mm² in the cecum and 3.6 mm² in the duodenum of each animal.
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.
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.
周围神经病变是糖尿病的慢性并发症之一，与该疾病的胃肠道后果直接相关。在某些病理状况如糖尿病性神经病变中，肠肌间神经元会受到影响。细胞抗氧化剂和自由基之间的失衡导致氧化应激增加，被认为是糖尿病中神经元损伤的主要因素之一。降低氧化应激的药物可能在糖尿病神经并发症的治疗中发挥重要作用。
评估补充L-谷氨酰胺对链脲佐菌素诱导的糖尿病Wistar大鼠盲肠和十二指肠肠肌间神经元的影响。
将动物分为四组（n = 5）：未治疗的血糖正常组、用L-谷氨酰胺治疗的血糖正常组、未治疗的糖尿病组以及从糖尿病诱导第4天起用L-谷氨酰胺治疗的糖尿病组。在它们的饮食中添加1%的氨基酸L-谷氨酰胺。采用吉姆萨技术对肠肌间神经元进行染色。我们测定了每组研究中500个神经元的细胞体面积。通过在每只动物盲肠16.6 mm²区域和十二指肠3.6 mm²区域取样进行定量分析。
在十二指肠补充L-谷氨酰胺后，我们观察到血糖正常组和糖尿病组的神经元密度得以保留（P<0.05）。我们还观察到糖尿病动物（用L-谷氨酰胺治疗的组）的细胞体面积得以保留（P<0.05）。在盲肠中，这种保留并不明显。
补充L-谷氨酰胺（1%）对大鼠十二指肠的肠肌间神经元具有神经保护作用，无论是在自然衰老还是糖尿病方面。
