L-Glutamine Supplementation Prevents Myenteric Neuron Loss and Has Gliatrophic Effects in the Ileum of Diabetic Rats
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Renata Virginia Fernandes Pereira Eleandro Aparecido Tronchini Cristiano Massao Tashima Eder Paulo Belato Alves Mariana Machado Lima Jacquel
- چاپ و سال / کشور: 2011
Description
Background Peripheral neuropathy caused chronically by diabetes mellitus is related to exacerbation of oxidative stress and a significant reduction in important endogenous antioxidants. L-Glutamine is an amino acid involved in defense mechanisms and is a substrate for the formation of glutathione, the major endogenous cellular antioxidant. Aim This study investigated the effects of 2% L-glutamine supplementation on peripheral diabetic neuropathy and enteric glia in the ileum in rats. Methods Male Wistar rats were divided into four groups: normoglycemics (N), normoglycemics supplemented with L-glutamine (NG), diabetics (D), and diabetics supplemented with L-glutamine (DG). After 120 days, the ileums were processed for HuC/D and S100 immunohistochemistry. Quantitative and morphometric analysis was performed. Results Diabetes significantly reduced the number of HuC/D-immunoreactive myenteric neurons per unit area and per ganglion in group D compared with normoglycemic animals (group N). L-Glutamine (2%) prevented neuronal death induced by diabetes (group DG) compared with group D. The glial density per unit area did not change with diabetes (group D) but was significantly reduced after L-glutamine supplementation (groups NG and DG). Ganglionic glial density was similar among the four groups. The neuronal area was not altered in groups D and DG. Glial size was reduced in group D; this was reversed by L-glutamine supplementation (group DG). Conclusions We concluded that 2% L-glutamine had neuroprotective effects directly on myenteric neurons and indirectly through glial cells, which had gliatrophic effects.
Dig Dis Sci DOI 10.1007/s10620-011-1806-8 Received: 25 April 2011 / Accepted: 14 June 2011
