Abstract:Diabetes mellitus (DM) is a chronic progressive metabolic disorder associated with several gastrointestinal complications, affecting up to 75% of patients. Knowing that Angiotensin II (AngII) also regulates intestinal contraction, we decided to evaluate changes in ileum and colon histomorphometry and AngII reactivity in a rat model of DM. Streptozotocin (STZ, 55 mg/kg) was administered to induce DM to 24 adult male Wistar rats. Diabetic rats displayed all the characteristic signs of type 1 DM (T1DM) and fecal … Show more
“…Thus, the neuron alteration in the muscular plexus may explain the sensory-motor function changes. Intestinal function alteration in the strepto zotocin-induced diabetic rat is also associated with a declined level of Angiotensin II, which controls small intestine contraction [4]. Necrotic features of neurons in the Meissner plexus were lesser than degenerated form in the T2DM group (Figure 1-3: F) and may be addressed to neuro degenerative complications in the diabetic patient [24].…”
Section: Discussionmentioning
confidence: 95%
“…Histological alteration in the Auerbach plexus correlates to their function in controlling muscular contraction and intestine motility. It also may be associated with most cases in T2DM patients that manifest, abdominal pain, bloating, constipation, or diarrhea [4,5]. Damaged ENS by prolonged hyperglicemia and oxidative stress in T2DM denotes diabetes-associatedintestinal motility alteration [6].…”
Section: Discussionmentioning
confidence: 99%
“…Beta cell dysfunction and insulin resistance lead to persistent hyperglycemia, which characterizes T2DM [3]. Gastrointestinal motility disorder is a common complication in around 75% of cases found in each segment of the digestive system and manifests as nausea, vomitus, abdominal pain, bloating, constipation, or diarrhea [4,5]. However, information about the intestine histological features of T2DM patients is still lacking.…”
<p class="MDPI17abstract"><strong>Objective: </strong>This study marked<strong> </strong>histological features of small intestine neurons in the type-2 diabetes mellitus (T2DM) rat model treated with ethanolic extract red betel leaf nanoparticle (EERbLNp)</p><p class="MDPI17abstract"><strong>Methods: </strong>Thirty male Wistar rats were allotted into five groups (six rats each). Group I is nondiabetic control; group II is streptozotocin-nicotinamide (STZ-NA)-induced T2DM; group III-V are the STZ-NA-induced T2DM treated daily per oral with EERbL-Np at the doses 30, 60, and 90 mg/kg, respectively, within 28days. The duodenum, jejunum, and ileum were collected for routine histological staining and cresyl violet special staining to evaluate the feature of neurons in the Meissner (submucosa) and Auerbach (muscular) plexus. Descriptive statistical analysis ANOVA and Tukey HSD were used to compare neuron indexes among groups.<strong></strong></p><p class="MDPI17abstract"><strong>Results: </strong>The necrotic neuron index in the duodenal and ileal Auerbach plexus, including the degenerative neuron index in the jejunal Auerbach plexus, were significantly decreased with the EERbL-Np treatment at the dosages 60 and 90mg/kg.<strong></strong></p><p><strong>Conclusions: </strong>The 60 mg/kg EERbL-Np administration in the T2DM model may provide a neuroprotectant candidate in duodenal and ileal neuropathy. Dosage of 90mg/kg EERbL-Np is also promising in jejunal neuropathy treatment.</p>
“…Thus, the neuron alteration in the muscular plexus may explain the sensory-motor function changes. Intestinal function alteration in the strepto zotocin-induced diabetic rat is also associated with a declined level of Angiotensin II, which controls small intestine contraction [4]. Necrotic features of neurons in the Meissner plexus were lesser than degenerated form in the T2DM group (Figure 1-3: F) and may be addressed to neuro degenerative complications in the diabetic patient [24].…”
Section: Discussionmentioning
confidence: 95%
“…Histological alteration in the Auerbach plexus correlates to their function in controlling muscular contraction and intestine motility. It also may be associated with most cases in T2DM patients that manifest, abdominal pain, bloating, constipation, or diarrhea [4,5]. Damaged ENS by prolonged hyperglicemia and oxidative stress in T2DM denotes diabetes-associatedintestinal motility alteration [6].…”
Section: Discussionmentioning
confidence: 99%
“…Beta cell dysfunction and insulin resistance lead to persistent hyperglycemia, which characterizes T2DM [3]. Gastrointestinal motility disorder is a common complication in around 75% of cases found in each segment of the digestive system and manifests as nausea, vomitus, abdominal pain, bloating, constipation, or diarrhea [4,5]. However, information about the intestine histological features of T2DM patients is still lacking.…”
<p class="MDPI17abstract"><strong>Objective: </strong>This study marked<strong> </strong>histological features of small intestine neurons in the type-2 diabetes mellitus (T2DM) rat model treated with ethanolic extract red betel leaf nanoparticle (EERbLNp)</p><p class="MDPI17abstract"><strong>Methods: </strong>Thirty male Wistar rats were allotted into five groups (six rats each). Group I is nondiabetic control; group II is streptozotocin-nicotinamide (STZ-NA)-induced T2DM; group III-V are the STZ-NA-induced T2DM treated daily per oral with EERbL-Np at the doses 30, 60, and 90 mg/kg, respectively, within 28days. The duodenum, jejunum, and ileum were collected for routine histological staining and cresyl violet special staining to evaluate the feature of neurons in the Meissner (submucosa) and Auerbach (muscular) plexus. Descriptive statistical analysis ANOVA and Tukey HSD were used to compare neuron indexes among groups.<strong></strong></p><p class="MDPI17abstract"><strong>Results: </strong>The necrotic neuron index in the duodenal and ileal Auerbach plexus, including the degenerative neuron index in the jejunal Auerbach plexus, were significantly decreased with the EERbL-Np treatment at the dosages 60 and 90mg/kg.<strong></strong></p><p><strong>Conclusions: </strong>The 60 mg/kg EERbL-Np administration in the T2DM model may provide a neuroprotectant candidate in duodenal and ileal neuropathy. Dosage of 90mg/kg EERbL-Np is also promising in jejunal neuropathy treatment.</p>
“…It has been demonstrated that the histomorphological and biomechanical remodeling of gastrointestinal tract including small intestine and colon occurred during the development of diabetes in several diabetic animals [ 2 ]. In STZ-induced diabetic rat models, both small intestine [ 15 , [18] , [19] , [20] , 36 ] and colon [ 14 , 20 , 21 , 36 ] expressed as increasing in wet weight per unit length, total wall and layered wall thickness, and wall area. Collagen increasing in colonic mucosa has been reported [ 37 ].…”
“…SD rats aged 8 weeks were purchased from experimental Animal Center of Chongqing Medical University. The streptozotocin had toxic effects on pancreatic islet β-cells specially, causing almost all pancreatic β-cell necrosis [ 36 ]. Then STZ was dissolved into a sodium citrate buffer (50 mM, pH = 4.5) at a final concentration of 100 mg/mL.…”
Diabetes-associated bone complications lead to fragile bone mechanical strength and osteoporosis, aggravating the disease burden of patients. Advanced evidence shows that chronic hyperglycemia and metabolic intermediates, such as inflammatory factor, reactive oxygen species (ROS), and advanced glycation end products (AGEs), are regarded as dominant hazardous factors of bone complications, whereas the pathophysiological mechanisms are complex and controversial. By establishing a diabetic Sprague-Dawley (SD) rat model and diabetic bone loss cell model in vitro, we confirmed that diabetes impaired primary cilia and led to bone loss, while adding Icariin (ICA) could relieve the inhibitions. Mechanistically, ICA could scavenge ROS to maintain the mitochondrial and primary cilia homeostasis of osteoblasts. Intact primary cilia acted as anchoring and modifying sites of Gli2, thereby activating the primary cilia/Gli2/osteocalcin signaling pathway to promote osteoblast differentiation. All results suggest that ICA has potential as a therapeutic drug targeting bone loss induced by diabetes.
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