Role of Alcohol Intake on Lipid Profiles and Nutrients Intake in Type 2 Diabetes Mellitus

2008 ◽  
Vol 9 (4) ◽  
pp. 329
Author(s):  
Hyun Ju Yoen ◽  
Mi Young Lee ◽  
Soo Min Nam ◽  
Song Yi Kim ◽  
Jang Hyun Koh ◽  
...  
2015 ◽  
Vol 12 (4) ◽  
pp. 715-723
Author(s):  
Baghdad Science Journal

Coronary artery disease (CAD) is a major health concern and leading of death in individuals with type 2 diabetes mellitus (T2DM). Glutathione S – Transferase(GST) are known for their broad range of detoxification and in the metabolism of xenobiotics . The role of functional variants of these genes in the development of various disorder is proven. We investigated the possible role of these variants in the development of CAD in T2DM patients. In this case – control study a total of 60 patients (T2DM = 30 ; T2DM – CAD = 30) and 30 controls were included. Serum lipid profiles were measured and DNA was extracted from the blood samples. Multiplex PCR for GSTT1/M1 (present / null) polymorphism, were performed for genotyping of study participants. Gene frequency and lipid profiles were statistically analyzed for disease association. Regression analysis showed that, there was no significant difference of the frequency of GSTT1 (positive /null) genotype and GSTM1 (positive /null) genotype in the 3 study groups . GSTT1 – positive genotype is associated with a 0.51 fold increased ( OR = 0.51 ; 95%CI = 2- 0.1 ;P = 0.321 ) , while the GSTM1 – positive genotype was associated with a 3 fold increase ( OR = 3.06 ; 95%CI=1- 9.7 ; P = 0.055) .We conclude GSTT1 positive genotype considered to be a protective risk from CAD in T2DM patients . The GSTM1 – positive genotype it was considered to be a risk factor of the CAD in T2DM patients.


Author(s):  
Nermien Abd El Rahman Ibraheim ◽  
Fatema El Zahraa Sayed Bukhary ◽  
Yehia Zakareia Mahmoud ◽  
Mahmoud Ragab Mohamed ◽  
Salama Rabei Abdel-Rahim

2018 ◽  
Vol 15 (1) ◽  
pp. 31-43 ◽  
Author(s):  
Sayantan Nath ◽  
Sambuddha Das ◽  
Aditi Bhowmik ◽  
Sankar Kumar Ghosh ◽  
Yashmin Choudhury

Background:Studies pertaining to association of GSTM1 and GSTT1 null genotypes with risk of T2DM and its complications were often inconclusive, thus spurring the present study.Methods:Meta-analysis of 25 studies for evaluating the role of GSTM1/GSTT1 null polymorphisms in determining the risk for T2DM and 17 studies for evaluating the role of GSTM1/GSTT1 null polymorphisms in development of T2DM related complications were conducted.Results:Our study revealed an association between GSTM1 and GSTT1 null polymorphism with T2DM (GSTM1; OR=1.37;95% CI =1.10-1.70 and GSTT1; OR=1.29;95% CI =1.04-1.61) with an amplified risk of 2.02 fold for combined GSTM1-GSTT1 null genotypes. Furthermore, the GSTT1 null (OR=1.56;95%CI=1.38-1.77) and combined GSTM1-GSTT1 null genotypes (OR=1.91;95%CI=1.25- 2.94) increased the risk for development of T2DM related complications, but not the GSTM1 null genotype. Stratified analyses based on ethnicity revealed GSTM1 and GSTT1 null genotypes increase the risk for T2DM in both Caucasians and Asians, with Asians showing much higher risk of T2DM complications than Caucasians for the same. </P><P> Discussion: GSTM1, GSTT1 and combined GSTM1-GSTT1 null polymorphism may be associated with increased risk for T2DM; while GSTT1 and combined GSTM1-GSTT1 null polymorphism may increase the risk of subsequent development of T2DM complications with Asian population carrying an amplified risk for the polymorphism.Conclusion:Thus GSTM1 and GSTT1 null genotypes increases the risk for Type 2 diabetes mellitus alone, in combination or with regards to ethnicity.


Epigenomics ◽  
2021 ◽  
Author(s):  
Marwa Matboli ◽  
Doaa Ibrahim ◽  
Amany H Hasanin ◽  
Mohamed Kamel Hassan ◽  
Eman K Habib ◽  
...  

Aim: To assess isorhamnetin efficacy for diabetic kidney disease in a Type 2 diabetes mellitus rat model, through investigating its effect at the epigenetic, mRNA and protein levels. Materials & methods: Type 2 diabetes mellitus was induced in rats by streptozotocin and high-fat diet. Rats were treated with isorhamnetin (50 mg/kg/d) for 4 or 8 weeks. Fasting blood glucose, renal and lipid profiles were evaluated. Renal tissues were examined by light and electron microscopy. Autophagy genes ( FYCO1, ULK, TECPR1 and  WIPI2) and miR-15b, miR-34a and miR-633 were assessed by qRT-PCR, and LC3A/B by immunoblotting. Results: Isorhamnetin improved fasting blood glucose, renal and lipid profiles with increased autophagosomes in renal tissues. It suppressed miRNA regulation of autophagy genes Conclusion: We propose a molecular mechanism for the isorhamnetin renoprotective effect by modulation of autophagy epigenetic regulators.


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