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World J Gastroenterol. Published online Nov All rights reserved.
This article has been cited by other articles in PMC. Abstract AIM: To investigate the effect of ascorbic acid AA dietary supplementation on myenteric neurons and epithelial cell proliferation of the jejunum of adult rats with chronic diabetes mellitus. After d of treatment with AA the animals were killed.
The myenteric neurons were stained for myosin-V and analyzed quantitatively in an area of We further measured the cellular area of neurons per group.
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The data area was analyzed using the Olympus BX40 microscope. There were no significant differences in MI parameters, villi height or crypt depths among the groups.
There was no observation of alteration of the cellular proliferation of the jejunum mucosa layer of rats with chronic diabetes mellitus with or without supplementation with AA. Chronic hyperglycemia and the associated metabolic abnormalities are responsible for many disease complications, including damage to the blood vessels, eyes, kidneys and nervous system[ 1 ].
In diabetes mellitus, the mucosa of the small intestine undergoes morphological changes[ 2 , 3 ]. This impairs passage of food along the intestine, secretion of enteric juices and the absorption of the digestion products, all of which depend on the integrity of the epithelial lining.
It has been shown that the autonomic nervous system has a role in intestinal epithelium renewal, which can be assessed through the elimination of the parasympathetic[ 5 ], sympathetic[ 6 ] or myenteric innervation[ 7 ]. The enteric nervous system is a division of the autonomic nervous system in the gastrointestinal tract; it can mediate independent reflexes motility, absorption and secretion and is made up of sensory neurons, interneurons and interconnected motor neurons[ 8 ].
Diabetes mellitus causes a decrease in enteric innervation with a consequent onset of the diabetic neuropathy[ 9 - 11 ]. Several theories have been proposed to explain the neuropathy in diabetes mellitus.
They include: impaired metabolism of fatty acids, reduction in the blood supply to the nerves, advanced products of non enzymatic glycation, oxidative stress, inadequate trophic support and the activation of the polyol pathway[ 12 , 13 ].
Aldose reductase converts glucose excess into sorbitol[ 14 , 15 ] which is responsible for edema, neuronal lesions[ 14 , 16 , 17 ]. The sorbitol concentration can be reduced in the diabetes mellitus through the use of ascorbic acid AA , an inhibitor of the enzyme aldose reductase[ 18 , 19 ].
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Another factor that can be related to the paper neuroprotector of the AA is the antioxidant activity exercised by this vitamin, being of some importance in the diabetes mellitus seen that in this pathology the oxidative stress is intensified and the defense antioxidants are diminished. In this way, our aim was to verify the effect of supplementation with AA on the myosin-V immunoreactive myenteric neurons and on the intestinal mucosa of the jejunum of diabetic rats.
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Fisiologia Humana - Uma Abordagem Integrada, 5ª Edição (Artmed) - Dee Unglaub Silverthorn
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British Association of Critical Care Nurses, ; 17 6 :