Abstract
The objective of this work was to investigate the effect of the L-glutamine supplementation to prevent - diabetes induced changes in myenteric neurons and also to verify the effect on the mucosa of the ileum of Wistar rats. The animals were divided in five groups (n = 5): untreated normoglycaemic (UN), normoglycaemic treated with L-glutamine (NG), untreated diabetics (UD), diabetics treated with L-glutamine, starting on the 4th (DG4) or 45th day following diabetes induction (DG45). The amino acid was added to the diet at 1%. The density and size of neurons, the metaphasic index in the crypt, the height of the villus, the depth of the crypt and the number of globet cells were determined. There was no difference in the neuronal density and in the cellular body area of the myosin-stained myenteric neurons of groups DG4 and DG45 when compared to group D. The metaphase index and the number of goblet cells showed no significant differences when all groups were compared (P > 0.05). The villi height of groups DG4 and DG45 were 45.5% (P < 0.05) and 32.4% (P > 0.05) higher than those in group UD, respectively. The analyzed crypts showed similar depth for all studied groups.
Highlights
Diabetes mellitus is a heterogeneous clinical syndrome characterized by endocrine-metabolic abnormalities that alter homeostasis
The rats were divided in five groups: untreated normoglycaemic (UN), normoglycaemic treated with L-glutamine (NG), untreated diabetics (UD), diabetics treated with L-glutamine, starting on the 4th (DG4) or 45th day following the onset of diabetes (DG45)
We verified in this study that the diabetic rats did not gain weight in the same proportion as the animals from the normoglycaemic groups (UN and NG) (P < 0.05) (Table I)
Summary
Diabetes mellitus is a heterogeneous clinical syndrome characterized by endocrine-metabolic abnormalities that alter homeostasis. An important factor related to the diabetic neuropathy is oxidative stress (Vinson et al 1989, Baynes 1991), which happens when there is an increase of reactive oxygen species (ROS) (Parthiban et al 1995, Kuyvenhoven and Meinders 1999) and/or a reduction on the efficiency of the endogenous antioxidants (Baynes 1991, Kuyvenhoven and Meinders 1999) Another factor that provokes neuronal dege neration is the intracellular increase of sorbitol and fructose, due to the increase of the aldose reductase enzyme activity in the polyol metabolic pathway as a consequence of hyperglycemia (Vinik 1999, Giugliano et al 1996, Afzaal and Saleem 2002). The L-glutamine supplementation is likely to present some neuroprotective effects, since it is a substrate for the production of glutathione (Amores-Sánchez and Medina 1999)
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