Vitamin E (α-tocopherol) supplementation in diabetic rats: effects on the proximal colon

<p>Abstract</p> <p>Background</p> <p>Neuropathy is one of the complications caused by diabetes mellitus which is directly related to the gastrointestinal manifestations of the disease. Antioxidant substances, such as vitamin E, may play an important role in the reduction of the neurological damage caused by diabetes mellitus. The aim of the present study was to determine whether vitamin E (α-tocopherol) at different concentrations induces any effects on the morphology of the intestinal wall and intrinsic innervation in the proximal colon of diabetic rats.</p> <p>Methods</p> <p>Thirty rats (90-day-old) were assigned to the following groups: N (normoglycemic), NE1 (normoglycemic supplemented with vitamin E 0.1%), NE2 (normoglycemic supplemented with vitamin E 2%), D (diabetic), DE1 (diabetic supplemented with vitamin E 0.1%), and DE2 (diabetic supplemented with vitamin E 2%). Animals received vitamin E supplementation for 120 days and were sacrificed when they were 210 days old. The proximal colon of each animal was subjected to histology to study the intestinal wall and goblet cells and processed for whole-mount preparations to morphoquantitatively determine the total myenteric population.</p> <p>Results</p> <p>Supplementation with vitamin E significantly reduced glycemia and glycated hemoglobin values and preserved the number of myenteric neurons in group DE2, without affecting intestinal area or thickness of the intestinal wall or muscular tunic.</p> <p>Conclusion</p> <p>Vitamin E (2%) influenced the glycemic parameters and had a neuroprotective effect on the total myenteric population, but the morphometric characteristics of the intestinal wall were unaffected.</p

Effect of l-glutamine on myenteric neuron and of the mucous of the ileum of diabetic rats

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

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

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 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%) promoted a neuroprotective effect on the myenteric neurons from the duodenum of rats, both in terms of natural aging and of diabetes mellitus