Clinical and pathogenetic features of intestinal lesions in patients with type 2 diabetes mellitus

Author(s):  
Y. Z. Dynia

Objective — to study the incidence and clinical and pathogenetic features of intestinal injury in patients with type 2 diabetes mellitus. Materials and methods. Examinations involved 138 patients with type 2 diabetes mellitus (DM 2), aged from 39 to 67 years (mean age 53 ± 5 years), including 82 women (59 %) and 56 men (41 %). In addition to general clinical methods, investigations included plasma levels of the transforming growth factor‑b1 (TGF‑b1) and vascular endothelial growth factor (VEGF), the hydrogen breath test with lactulose, endoscopic examination of the intestine with biopsy followed by staining with hematoxylin‑eosin, immunohistochemical determining of claudin‑1 and VEGF, and conduction of PAS‑reaction. Results. Diabetic enterocolopathy (DECP) was diagnosed in 72 (52.2 %) patients with DM 2. Clinical manifestations were nonspecific and similar to those of irritable bowel syndrome (IBS). It has been found that DECP correlates with the duration of the DM 2 course and was diagnosed more often in middle‑aged patients (52.1 ± 4.1 years). In patients with DECP, the increase in the proinflammatory cytokines TGF‑b1 and VEGF significantly exceeded those in IBS patients. Histologically the inflammatory cell infiltration in patients with DECP was more intense and diverse, there were signs of subatrophy of the glands with a relative decrease in the number of vacuoles in the goblet cells. The immunohistochemical study revealed that VEGF in the colon mucosa was visualized mainly in patients with DECP. Moreover, a tendency to a decrease in the claudin‑1 levels was established in these patients. Conclusions. Intestinal damage was revealed in 67.4 % of patients with type 2 diabetes mellitus, and DECP was diagnosed in more than half of patients. Diabetic enterocolopathy had nonspecific clinical symptoms, required differential diagnosis with IBS, and was not always accompanied with abdominal pain. The presence of DECP more often correlated with the bacterial overgrowth syndrome, and levels of proinflammatory cytokines in the blood plasma and intestinal mucosa of these patients was raised.  

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Karina Braga Gomes ◽  
Kathryna Fontana Rodrigues ◽  
Ana Paula Fernandes

Several studies have demonstrated that chronic and low-grade inflammation is closely linked to type 2 diabetes mellitus. The associated mechanisms are related to synthesis and release of proinflammatory and anti-inflammatory cytokines, mainly by the adipose tissue. Moreover, there are evidences that cytokines and adhesion molecules are important for development of diabetic nephropathy. Among the cytokines associated with inflammatory responses in type 2 diabetes mellitus, the transforming growth factor-β (TGF-β) has been recognized as a central player in the diabetic nephropathy being involved in the development of glomerulosclerosis and interstitial fibrosis, as observed in the course of end-stage renal disease. Although TGF-β1 is classically an anti-inflammatory immune mediator it has been shown that in the presence of IL-6, which increases before the onset of T2D, TGF-β1 favors the differentiation of T helper 17 (Th17) cells that are activated in many pro-inflammatory conditions. Since TGF-β1 mRNA and consequently serum TGF-β1 levels are under genetic control, this review aims to discuss the relationship of TGF-β1 levels and polymorphisms in the development of nephropathy in type 2 diabetes mellitus.


2021 ◽  
Vol 5 (2) ◽  

Objectives: To assess the association between Transforming Growth Factor β1 gene polymorphism (T869C) and type 2 diabetes mellitus with and without nephropathy complications with endogenous antioxidant reduced glutathione levels in type 2 diabetic patients with/without nephropathy complications of Kerbala province: Iraq. Methods: A case-control study was performed at which 100 patients with diabetic nephropathy, 100 patients with only type 2 diabetic and another 100 apparently healthy individuals as control were recruited. Fasting blood glucose, HbA1c%, urea, creatinine and glutathione were measured by spectrophotometric methods using enzymatic procedures. Transforming growth factor β1 gene was genotyped for the T>C (T869C) SNP by PCR-ARMS technique. Results: The genotype and allele frequencies of TGFβ1 gene polymorphism in type 2 diabetes mellitus, type 2 diabetic nephropathy, and control were examined. The transforming growth factor β1 (T869C) C allele, TC and TC + CC genotypes were significantly higher in patients; the T allele and TT genotype were significantly higher in controls (P ≤ 0.001). Glutathione give also a significant result in diabetic patients with and without nephropathy in when compared with controls. Conclusion: The observed data indicated that TGFβ1 (T869C) codon 10, allele C, and C allele-containing genotypes may be susceptible, and the T allele / TT genotype may be protective factors for type 2diabetic nephropathy complications. The results of glutathione showed that it may be one of the causes of presence high oxidants compounds, which is lead to the damage and destruction of mutations in the DNA of the cell.


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