Early ultra- and microstructural alterations in rat pancreas in alloxan-induced diabetes mellitus

Titova, Angelina; Мавликеев, М. О.; Калигин, М. С.; Süleymanova, Dilara; Chekmaryeva, I A; Kiyasov, Andrey P.; Деев, Р. В.

doi:10.1080/01913123.2019.1710313

Cited by 8 publications

(7 citation statements)

References 14 publications

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“…The diabetes models showed that CD34 has the potential to be used as a biomarker for monitoring β-cell failure in the progression of diabetes, i.e., a strong linear and negative correlation exists between the loss of β-cells and increase of CD34 cells during disease progression. Furthermore, the proportion of CD34 and GLU in islet α-cells was significantly higher than that in the control, and changes in the islet α-cells observed in the present study is consistent with previous reports (Plesner et al, 2014;Titova et al, 2020), suggesting that some islet β-cells did not undergo apoptosis but lost the function of INS secretion and differentiated into GLU-positive islet α-cells, these transdifferentiated islet β-cells could be labeled by CD34. Interestingly, our experimental on the relationship between islet α-cells and β-cells during diabetes also suggested that transdifferentiation of islet β-cells into α-cells may be occur during diabetes.…”

Section: Discussionsupporting

confidence: 93%

“…The monitoring of changes in the β-cells in pancreatic islets is required for the early diagnosis and treatment of diabetes. At present, the common diagnostic methods, including the diagnostic index of type 1 diabetes 60, oral glucose tolerance test, glycosylated hemoglobin, and some biomarkers for the risk prediction and clinical diagnosis of β-cell autoantigen such as Glutamate Decarboxylase 65 (Schlosser et al, 2008), C-peptide (Sims et al, 2019), and proinsulin (Titova et al, 2020), always diagnose diabetes after most β-cells are injured. Therefore, it is important to explore a biomarker for monitoring early β-cell changes in the clinical diagnosis and intervention of diabetes (Sims et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Islet β-cell apoptosis is the major form of β-cell failure in diabetes (Cnop et al, 2005;Moin and Butler, 2019). In recent years, attention has been paid to the relationship between β-cell dedifferentiation and trans-differentiation in diabetes (Moin and Butler, 2019), in which the percentage of INS-positive cells in the islet structure is decreased and the corresponding percentage of GLU-positive cells is increased (Titova et al, 2020). The β-cells lose the characteristics of mature cells and subsequently lose the ability to secrete INS because of gene regulation (Bensellam et al, 2018;Moin and Butler, 2019).…”

Section: Introductionmentioning

confidence: 99%

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Increased CD34 in pancreatic islet negatively predict islet β-cell decrease in type1 diabetes model

Huang¹,

Li²,

Sun³

et al. 2022

Front. Physiol.

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Islet β-cell biomarkers can reflect changes in the number and function of islet β-cells in the prediabetes or early diabetes stage. CD34 is a commonly used stem cell biomarker; however, its expression and function in pancreatic islets remain unclear. In the present study, double immunofluorescence staining, proteomic bioinformatics analysis, and correlation analysis were used to explore the potential of CD34 as an islet β-cell biomarker. Bioinformatics analysis revealed that the amino acid sequence of CD34 was conserved among multiple species and abundantly expressed on mouse and human pancreatic tissues. Immunofluorescence demonstrated that in the control rat pancreas, CD34 was expressed on glucagon-labeled islet α-cells but not on insulin-labeled islet β-cells. Furthermore, the proportion of CD34-positive cells, which were also positive for glucagon, was significantly increased in alloxan-induced diabetes models. Statistical analysis revealed that the expression of CD34 was negatively correlated with the number of insulin-labeled islet β-cells during diabetes progression in dose-dependent fashion in alloxan-induced diabetes models. Furthermore, the results suggested that the transdifferentiation of islet β-cells into islet α-cells may occur in the process of diabetes. Thus, the present study demonstrated that CD34 is expressed on islet α-cells, and its number is linearly and negatively correlated with the number of islet β-cells, suggesting that CD34 can be used as a prospective biomarker for islet β-cells in the early diagnosis of diabetes. The study also suggests the transformation of β-cells to α-cells in diabetes which provide a potential to be applied towards diabetes mechanism research.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Increased CD34 in pancreatic islet negatively predict islet β-cell decrease in type1 diabetes model

Huang¹,

Li²,

Sun³

et al. 2022

Front. Physiol.

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“…Rag1 −/− islets compared to NOD.ALRc8(D8Mit293-D8Mit137) islets. As this regulates mitochondrial protein it may affect the Chr2-Chr8-mt-Nd2 interaction to prevent ALinduced mitochondrial damage through control of translation of genes encoded on the mitochondrial genome, including mt-Nd2 (Titova et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Intergenomic and epistatic interactions control free radical mediated pancreatic β-cell damage

Chen

Li²,

Knapp³

et al. 2022

Front. Genet.

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Alloxan (AL)-generated Reactive Oxygen Species (ROS) selectively destroy insulin-producing pancreatic β-cells. A previous genome-wide scan (GWS) using a cohort of 296 F2 hybrids between NOD (AL-sensitive) and ALR (AL-resistant) mice identified linkages contributing to β-cell susceptibility or resistance to AL-induced diabetes on Chromosomes (Chr) 2, 3, 8, and a single nucleotide polymorphism in mt-Nd2 of the mitochondrial genome (mtDNA). AL treatment of congenic and consomic NOD mouse stocks confirmed resistance linked to both the mtDNA and the Chr 8 locus from ALR [NOD.mtALR.ALR-(D8Mit293-D8Mit137)]. To identify possible epistatic interactions, the GWS analysis was expanded to 678 F2 mice. ALR-derived diabetes-resistance linkages on Chr 8 as well as the mt-Nd2a allele were confirmed and novel additional linkages on Chr 4, 5, 6, 7, and 13 were identified. Epistasis was observed between the linkages on Chr 8 and 2 and Chr 8 and 6. Furthermore, the mt-Nd2 genotype affected the epistatic interactions between Chr 8 and 2. These results demonstrate that a combination of nuclear-cytoplasmic genome interactions regulates β-cell sensitivity to ROS-mediated ALD.

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“…In the presence of glutathione and other intracellular thiols, alloxan undergoes cyclic redox reaction to generate reactive oxygen species (ROS) and dialuric acid [12]. Auto-oxidation of dialuric acid generates superoxide radicals, hydrogen peroxide and hydroxyl radicals with fatty degeneration, signs of mitochondrial damage, perivascular edema and leukocytic infiltration [13]. The hydroxyl radicals generated ultimately destroy the beta cells, cause a significant deficit in pancreatic β-cell mass, selectively inhibit glucose-induced insulin secretion, leading to insulin dependent diabetes mellitus [14].…”

mentioning

confidence: 99%

Potentials of Aqueous Extract ofBambusa vulgaristo Reactivate β-Cells of Pancreas in Alloxan-Induced Diabetic Wistar Rats

Akiibinu

Folawuyo

Oyekan

et al. 2020

Preprint

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Ability of the damaged pancreas to generate new β-cells when activated with external stimuli has been documented. This study assessed the potentials of aqueous extract of bambusa vulgaris leaf to reactivate damaged β-cells in insulin dependent diabetes mellitus (IDDM). Eighteen healthy male Wistar rats (12 weeks old; weight= between 150 and 200g) were used for this study. The rats were randomly divided into three groups (six per group); group A (un-induced); group B (untreated alloxan-induced diabetics); group C (alloxan-induced diabetics treated with 200mg/kg body weight of freshly prepared extract of bambusa vulgaris leaf). Fasting blood sugar (FBS) and plasma insulin levels were determined in all animals using glucometer and enzyme linked immunosorbent assay methods respectively. Sections of pancreas tissues were prepared for histology. IDDM was confirmed in groups B and C (FBS increased significantly=p<0.05) after 2 days of alloxan administration). The FBS remained significantly (p>0.05) higher in group B, compared to group A, but reduced significantly (p<0.05) in group C after 7 days of treatment with bambusa vulgaris leaf extract. On the 7th day, plasma insulin level decreased significantly (p<0.05) in group B, but no significant difference observed in group C compared with group A.Histology reports showed damaged pancreas in group B, while Group C showed normal islet cells after 7 days of oral administration of bambusa vulgaris extract. In conclusion, aqueous extract of Bambusa vulgaris could restore the activities of alloxan-damaged pancreas. The extract could be a reliable alternative to synthetic pharmaceuticals in the treatment IDDM.

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Early ultra- and microstructural alterations in rat pancreas in alloxan-induced diabetes mellitus

Cited by 8 publications

References 14 publications

Increased CD34 in pancreatic islet negatively predict islet β-cell decrease in type1 diabetes model

Increased CD34 in pancreatic islet negatively predict islet β-cell decrease in type1 diabetes model

Intergenomic and epistatic interactions control free radical mediated pancreatic β-cell damage

Potentials of Aqueous Extract ofBambusa vulgaristo Reactivate β-Cells of Pancreas in Alloxan-Induced Diabetic Wistar Rats

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