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Rashidi H.,Joundi Shapour University of Medical science | Salesi M.,Isfahan University of Medical Sciences | Fatahi F.,Endocrine Clinic
Iranian Journal of Diabetes and Lipid Disorders

Background: Recent studies revealed that smoking causes metabolic syndrome and insulin resistance which are characterized by increased postprandial triglyceride in smokers compared with nonsmoker people. This study aimed to evaluate the effects of smoking on postprandial triglyceride in healthy smokers. Methods: In a case-control study 78 participants aged 30-60 years (35 female and 43 male) who referred to the clinics of Khatam-Al-Anbia Hospital, Zahedan and had normal lipid levels and fasting blood sugar were recruited. Of 78 total subjects 39 were smokers and the remaining were non-smokers. Their body mass indices were between 19 to 29.9 kg/m2. Each of these patients consumed 60 g butter (containing 716 kcal energy per 100 grams and 81.06% fat). Then blood triglyceride levels were evaluated one and six hours after consumption. The results were statistically analyzed using T- test and ANOVA. Results: Triglyceride levels among men and women showed no significant differences (P = 0.403). In both smokers and non-smokers, fasting triglyceride levels were not significantly different, but was significantly different one and six hours after butter consumption (P <0.001). Furthermore, triglyceride levels significantly increased from fasting than one hour and six hours after the butter consumption between smokers and nonsmokers (P <0.001.( Conclusion: In this study it was shown that in smokers postprandial triglyceride levels increased more than non-smokers, triglycerides after a meal remained longer in blood and triglyceride clearance delayed as well. The increase in triglyceride levels after a meal and smoking may consider as an important factor in the development of cardiovascular diseases. Source

Kanazirev B.,Medical University-Varna | Hristozov K.,Endocrine Clinic | Bachvarova M.,Medical University-Varna | Georgieva G.,Medical University-Varna | Dimova M.,Medical University-Varna

The cardiovascular signs and symptoms of thyroid disease are some of the most profound and clinically relevant findings that accompany hyperthyroidism. On the basis of the understanding of the cellular mechanisms of thyroid hormone action on the heart and cardiovascular system, it is possible to explain the changes in cardiac output, cardiac contractility, blood pressure, vascular resistance, and rhythm disturbances that result from thyroid dysfunction. The importance of the recognition of the effects of thyroid disease on the heart also derives from the observation that restoration of normal thyroid function most often reverses the abnormal cardiovascular hemodynamics. Source

Gershoni M.,Ben - Gurion University of the Negev | Levin L.,Ben - Gurion University of the Negev | Ovadia O.,Ben - Gurion University of the Negev | Toiw Y.,Ben - Gurion University of the Negev | And 10 more authors.
Genome biology and evolution

The mutation rate of the mitochondrial DNA (mtDNA), which is higher by an order of magnitude as compared with the nuclear genome, enforces tight mitonuclear coevolution to maintain mitochondrial activities. Interruption of such coevolution plays a role in interpopulation hybrid breakdown, speciation events, and disease susceptibility. Previously, we found an elevated amino acid replacement rate and positive selection in the nuclear DNA-encoded oxidative phosphorylation (OXPHOS) complex I subunit NDUFC2, a phenomenon important for the direct interaction of NDUFC2 with the mtDNA-encoded complex I subunit ND4. This finding underlines the importance of mitonuclear coevolution to physical interactions between mtDNA and nuclear DNA-encoded factors. Nevertheless, it remains unclear whether this interaction is important for the stability and activity of complex I. Here, we show that siRNA silencing of NDUFC2 reduced growth of human D-407 retinal pigment epithelial cells, significantly diminished mitochondrial membrane potential, and interfered with complex I integrity. Moreover, site-directed mutagenesis of a positively selected amino acid in NDUFC2 significantly interfered with the interaction of NDUFC2 with its mtDNA-encoded partner ND4. Finally, we show that a genotype combination involving this amino acid (NDUFC2 residue 46) and the mtDNA haplogroup HV likely altered susceptibility to type 2 diabetes mellitus in Ashkenazi Jews. Therefore, mitonuclear coevolution is important for maintaining mitonuclear factor interactions, OXPHOS, and for human health. © The Author(s) 2014. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. Source

Blech I.,Hebrew University of Jerusalem | Katzenellenbogen M.,Bar - Ilan University | Katzenellenbogen A.,The Central Bureau of Statistics | Wainstein J.,Diabetes Unit | And 5 more authors.

Aims: The tendency to develop diabetic nephropathy is, in part, genetically determined, however this genetic risk is largely undefined. In this proof-of-concept study, we tested the hypothesis that combined analysis of multiple genetic variants can improve prediction. Methods: Based on previous reports, we selected 27 SNPs in 15 genes from metabolic pathways involved in the pathogenesis of diabetic nephropathy and genotyped them in 1274 Ashkenazi or Sephardic Jewish patients with Type 1 or Type 2 diabetes of >10 years duration. A logistic regression model was built using a backward selection algorithm and SNPs nominally associated with nephropathy in our population. The model was validated by using random "training" (75%) and "test" (25%) subgroups of the original population and by applying the model to an independent dataset of 848 Ashkenazi patients. Results: The logistic model based on 5 SNPs in 5 genes (HSPG2, NOS3, ADIPOR2, AGER, and CCL5) and 5 conventional variables (age, sex, ethnicity, diabetes type and duration), and allowing for all possible two-way interactions, predicted nephropathy in our initial population (C-statistic = 0.672) better than a model based on conventional variables only (C = 0.569). In the independent replication dataset, although the C-statistic of the genetic model decreased (0.576), it remained highly associated with diabetic nephropathy (χ2 = 17.79, p<0.0001). In the replication dataset, the model based on conventional variables only was not associated with nephropathy (χ2 = 3.2673, p = 0.07). Conclusion: In this proof-of-concept study, we developed and validated a genetic model in the Ashkenazi/Sephardic population predicting nephropathy more effectively than a similarly constructed non-genetic model. Further testing is required to determine if this modeling approach, using an optimally selected panel of genetic markers, can provide clinically useful prediction and if generic models can be developed for use across multiple ethnic groups or if population-specific models are required. © 2011 Blech et al. Source

Karl D.,Endocrine Clinic | Zhou R.,Medpace Inc. | Vlajnic A.,Sanofi S.A. | Riddle M.,Oregon Health And Science University
Diabetic Medicine

Aims To evaluate whether fasting plasma glucose values measured early during insulin therapy can identify patients with Type2 diabetes who may not achieve adequate glycaemic control after 6months and will require additional treatment. Methods Patient-level data from seven prospective, randomized, controlled studies using treat-to-target methods were pooled to evaluate the efficacy of insulin glargine. Fasting plasma glucose was measured at baseline, week6 or 8 (6/8) and week12. HbA1c was measured at week24 to assess glycaemic control. Results One thousand and thirty-six patients (56% male, 81% white) were included in the analysis (mean age 56.3years; duration of diabetes 8.4years). Baseline mean fasting plasma glucose was 11.2mmol/l and mean HbA1c was 73mmol/mol (8.8%). After 24weeks of treatment, mean HbA1c decreased to 53mmol/mol (7.0%); 56% of patients reached a target HbA1c≤53mmol/mol (7.0%). Significant correlations with week24 HbA1c were obtained for fasting plasma glucose measured at week6/8 and week12 (r=0.32; P<0.0001 for both). Patients with fasting plasma glucose >10mmol/l at week6/8 or week12 were significantly less likely to achieve the HbA1c target at the end of treatment than patients with fasting plasma glucose <8.9mmol/l (P<0.0001 for both). If fasting plasma glucose was >10mmol/l at week 6/8 or week12, patients had only a 27% chance of reaching the HbA1c goal. Conclusions Fasting plasma glucose remaining >10mmol/l after 6-12weeks of glargine therapy indicates that reaching target HbA1c≤53mmol/mol (7.0%) is unlikely and calls for individualized attention to consider further therapeutic options. © 2012 The Authors. Diabetic Medicine © 2012 Diabetes UK. Source

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