l-Glutamine Supplementation Prevents Myenteric Neuron Loss and Has Gliatrophic Effects in the Ileum of Diabetic Rats

Abstract

We concluded that 2% L: -glutamine had neuroprotective effects directly on myenteric neurons and indirectly through glial cells, which had gliatrophic effects.

Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

“…In addition to the reduction of neuronal density, hypertrophy of the cell body area occurred of NADH-d + neurons in the duodenum (37.8%) and in the ileum (35.8%), possibly in an attempt to maintain physiological conditions of the neurons that survived. Similar results were reported in previous studies in diabetic rats (Pereira et al 2011;Lopes et al 2012;Hermes-Uliana et al 2014). Adaptive mechanisms of the remaining neurons attempt to compensate for neuronal loss by increasing protein synthesis to maintain their function and target tissue (Zanoni et al 2002;Hermes-Uliana et al 2014).…”

“…Thus, we can infer that diabetes promoted a reduction of neuron metabolism, leading to the death of a portion of its neuronal population. We observed a reduction of more than half of these neurons, and diabetic neuropathy was observed, similar to studies that used other experimental models of diabetes and evaluated different regions of the gastrointestinal tract, including the stomach (Takahashi et al 1997;Fregonesi et al 2001), duodenum (Pereira et al 2006;Zanoni et al 2011;Lopes et al 2012), jejunum (Defani et al 2003;De Freitas et al 2008;Alves et al 2010;HermesUliana et al 2014), ileum Shotton and Lincoln 2006;Pereira et al 2011), cecum (Zanoni et al 1997;Zanoni et al 2011), and proximal colon (Tashima et al 2007;Roldi et al 2009). The development of neuropathy affects different types of enteric neurons, which are responsible for the control of important functions, such as motility, secretion, blood flow, and growth aspects of the local mucosal immune system (Furness 2012).…”

“…Among the chronic complications caused by diabetes, neurological manifestations are the most common, affecting both the autonomic and peripheral nervous systems and impairing the quality of life of patients (Chandrasekharan et al 2011). Our research group found that diabetes mellitus reduced the density of myenteric neurons and enteric neural plasticity in various segments of the digestive system (Takahashi et al 1997;Zanoni et al 1997;Fregonesi et al 2001;Defani et al 2003;Zanoni et al 2003;Pereira et al 2006;Tashima et al 2007;Zanoni et al 2007;De Freitas et al 2008;Roldi et al 2009;Alves et al 2010;Pereira et al 2011;Zanoni et al 2011;Lopes et al 2012;Hermes-Uliana et al 2014). These changes in enteric innervation that arise from diabetes are attributable to persistent hyperglycemia that produces numerous metabolic changes.…”

Effects of Quercetin-Supplementation in NADH-Diaphorase Positive Neurons Subpopulations in the Ileum of Rats with Experimental Diabetes Mellitus

“…Other antioxidant compounds have been evaluated in addition to quercetin and the literature shows conflicting results regarding their effects on fasting glucose levels of diabetic rats. There are reports of hypoglycemic effects by supplementation with vitamin E (Wan Nazaimoon & Khalid, 2002), ascorbic acid (Adeneye et al, 2007) a-lipoic acid (Maritim et al, 2003), whereas the l-glutamine had no action on glycaemia in a study by Pereira et al (2011).…”

“…Many studies have assessed the effects of several antioxidants on the enteric neurons of diabetic rats such as: Glutamine as an important precursor of glutathione and, therefore, it could have an action mechanism similar to quercetina (Pereira et al, 2011); vitamin C together with vitamin E neutralizes free radicals; vitamin E, which donates electrons to neutralize free radicals, transforms itself into a potent free radical and needs electrons donated by vitamin C to recompose and start acting as an antioxidant while the radical formed by vitamin C is eliminated (Veit & Zanoni, 2012). In general, all the authors who have studied antioxidants found neuroprotective effect evidenced by lower neuronal loss or prevention of morphological changes in the neurons of diabetics.…”