The Content of Blood Leptin and Activity of Systemic Inflammatory Response in Patients with Type 2 Diabetes Mellitus depending on Weight and Length of the Process

Author(s):  
Boris Mankovsky ◽  
Alina Urbanovych
2020 ◽  
Vol 11 ◽  
Author(s):  
Xiaomeng Liu ◽  
Yusong Zhang ◽  
Hongwei Liang ◽  
Yanchao Xu

Background: Type 2 diabetes mellitus (T2DM) is a chronic, hyperglycemia-associated, metabolic disorder. Heart disease is a major complication of T2DM. The present study aimed to explore the effects of miR-216a-3p on cardiomyocyte proliferation, apoptosis, and inflammation in T2DM through the Toll-like receptor (TLR) pathway involving interferon-α2 (IFN-α2) mediation.Methods: T2DM was induced in rats by a high-fat diet, in combination with an intraperitoneal injection of low-dose streptozotocin. ELISAs were conducted to measure inflammatory-related factors in serum. Next, isolated cardiomyocytes were used in loss- and gain-of-function experiments, followed by MTT and flow cytometry assays, conducted to evaluate cell proliferation, cell cycle, and apoptosis.Results: Our results revealed an increase in the inflammatory response in T2DM rat models, accompanied by significantly increased expression of miR-216a-3p and TLR pathway-related genes. However, a decrease in the expression of IFN-α2 was observed. Moreover, the presence of an miR-216a-3p inhibitor and si-IFN-α2 increased the expression of TLR pathway-related genes and cell apoptosis, whereas cell proliferation was significantly decreased in the cardiomyocytes.Conclusion: We found that in T2DM, miR-216a-3p inhibited the proliferation and enhanced the apoptosis of cardiomyocytes and generated an inflammatory response through activation of the TLR pathway and targeting of IFN-α2.


2021 ◽  
Vol 6 (4) ◽  
pp. 253-255
Author(s):  
Sujeet Raina ◽  
Sayan Malakar ◽  
Bhagwan Dass Negi ◽  
Katyayani Dutt ◽  
Krishna Bharath

We report a case of acute pulmonary embolism (PE) following short term exposure to smoke in an enclosed area. The patient was obese and had type 2 diabetes mellitus. He developed PE as a consequence of acute systemic inflammatory response to short term exposure to smoke and an underlying chronic inflammatory milieu.


e-CliniC ◽  
2016 ◽  
Vol 4 (2) ◽  
Author(s):  
. Guntur ◽  
Jeffrey Ongkowijaya ◽  
Frans E. Wantania

Abstrak: Diabetes mellitus is a metabolic disorder with characteristics of hyperglycemia that occurs due to abnormalities in insulin secretion, action or both. Uric acid is the end product of purine metabolism. Uric acid has been identified as a marker for a metabolic number and hemodynamic abnormalities. In diabetic patients, there is biochemical interaction between serum glucose and purine metabolism, with increased excretion of uric acid during hyperglycemia and glycosuria. Another theory explained that the increase of inflammatory response on diabetes mellitus may have a direct protective effect toward incidences of gout and hyperuricemia which directly produces an intense inflammatory response on uric crystallines containing antioxidant effects and free radical. HbA1C is a bond between glucose and hemoglobin. HbA1c examination is a standard for measuring the long-term glycemic value in diabetic patients. This study was aimed to determine the correlation of uric acid and HbA1C in patients with type 2 diabetes mellitus. The study was an analytical cross sectional. Sample selection was done by simple random sampling method. Data sources were secondary data from medical records of patients with type 2 diabetes mellitus who are hospitalized. The result of Spearman correlation analysis on the correlation of uric acidand HbA1C showed r value = -0.211 and p = 0.263 (p>α). Conclusion: There was no correlation between uric acid and HbA1C in patients with type 2 diabetes mellitus.Keywords: Type 2 diabetes mellitus, uric acid, HbA1C Abstrak: Diabetes melitus merupakan suatu kelompok metabolik dengan karakteristik hiperglikemia yang terjadi karena kelainan sekresi insulin, kerja insulin atau keduanya. Asam urat merupakan produk akhir metabolisme purin. Asam urat telah diidentifikasi sebagai penanda dari beberapa abnormalitas metabolik dan hemodinamik. Pada pasien diabetes melitus, dijumpai interaksi biokimiawi antara glukosa serum dan metabolisme purin, dengan peningkatan ekskresi asam urat selama hiperglikemia dan glikosuria. Teori lain menjelaskan bahwa meningkatnya respons inflamasi pada DM mungkin secara langsung justru memiliki efek protektif terhadap kejadian gout dan hiperurisemia yang secara langsung menghasilkan respons inflamasi yang intens terhadap kristal urat yang memiliki efek anti oksidan dan radikal bebas. HbA1C merupakan ikatan antara glukosa dengan hemoglobin. Pemeriksaan HbA1C merupakan standard dalam pemeriksaan kadar gula darah jangka panjang pada penyandang diabetes. Penelitian ini bertujuan untuk mengetahui hubungan asam urat dan HbA1C pada penderita diabetes melitus tipe 2. Jenis penelitian ialah analitik dengan desain potong lintang. Pemilihan sampel dilakukan dengan metode simple random sampling. Sumber data merupakan data sekunder dari data rekam medik pasien diabetes melitus tipe 2 yang dirawat inap. Hasil analisis korelasi spearman pada hubungan asam urat dengan HbA1c memperoleh nilai r = -0,211dan p = 0,263 (p > α). Simpulan: Tidak terdapat hubungan asam urat dengan HbA1C pada penderita diabetes melitus tipe2. Kata kunci: diabetes melitus tipe 2, asam urat, HbA1C


2020 ◽  
Vol 4 (1) ◽  
pp. 1
Author(s):  
Rona Kartika ◽  
Heri Wibowo

Pathogenesis of type 2 Diabetes Mellitus (DM) is often associated with chronic low-grade inflammation. This kind of inflammation is characterized by an increased level of pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-6 and IL-1β. From an immunological point of view, an inflammatory response is always followed by an anti-inflammatory response as negative feedback to avoid excessive tissue damages. Regulatory T cells are a subset of cluster of differentiation (CD)4+ T cells that have the function to maintain peripheral tolerance and suppress immune response. This review would discuss the impaired function of regulatory T cells in type 2 DM. DM is a group of metabolic diseases characterized by hyperglycemia due to a defect of insulin secretion or a combination of insulin resistance and relative insulin deficiency. Chronic low-grade inflammation has been known as a key factor in the development of insulin resistance. Regulatory T cells (Treg cells) action through contact and non-contact inhibition could suppress inflammatory response in innate and adaptive immune systems. In type 2 DM, the proportion and function of CD4+CD25+Foxp3+ and CD4+CD25+ regulatory T cell decreases due to the reduced number of Treg cells and the Treg cells depletion contributes to metabolic conditions such as insulin resistance. Moreover, Treg cells are more susceptible to apoptosis, the ability of Treg cells to produce anti-inflammatory cytokines such as transforming growth factor β (TGF-β) and IL-10 decreases, and there is an imbalance between the proportion of Th1/Th17 cells and Treg cells. This inadequate anti-inflammatory response gives rise to the chronic low-grade inflammatory condition in type 2 DM.Keywords: type 2 diabetes mellitus, inflammation, regulatory T cell


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