Iranian

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Angiotensin-converting enzyme (ACE) inhibitors appear to correct many of the abnormalities associated with the vascular dysfunction found in diabetic patients. In this respect, quinapril is a unique ACE inhibitor with multiple protective effects. The present study was carried out to investigate the effect of intraperitoneal administration of quinapril on the aortic reactivity of streptozotocin (STZ)-diabetic rats. For this purpose, male Wistar rats received one injection of streptozotocin (STZ), 60 mg/kg, to induce diabetes. Three days after STZ injection, rats were treated with quinapril (2 mg/kg/day) for 4 weeks, after that aortic reactivity to vasoactive agents were compared with those of untreated diabetic rats or non-diabetic control rats. For this purpose, contractile response to phenylephrine (PE) was obtained from aortic rings. Concentration-response curves from quinapril-treated diabetic rats to PE in the presence and absence of endothelium were attenuated as compared to vehicle-treated diabetics. Therefore, the 4-week treatment of diabetic rats with quinapril could prevent the functional changes in vascular reactivity in diabetic rats

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Insulin resistance syndrome, also referred to as the metabolic syndrome or syndrome X, refers to a constellation of common metabolic and cardiovascular disorders (e.g. obesity, type 2 diabetes mellitus, hypertension, and dyslipidemia), which are all cardiovascular risk factors. Insulin resistance can be induced by fructose-rich diet in rats. We investigated the effect of vanadyl sulfate (0.2 mg/ml in drinking water for 7 days) on glucose, triglyceride, and plasma insulin levels in male Wistar rats that were fed with fructose-rich diets. Control rats were fed with standard chow for 7 days. The animals were divided into three groups: fructose-fed rats, fructose fed-vanadyl sulfate treated rats, and control rats. Fasting plasma glucose levels of the three groups were comparable (p>0.05). Fasting plasma insulin increased in the fructose-fed rats (190 ± 6.3 pM vs. control rats 83.06 ± 3.3 pM, p<0.001), likewise, plasma triglyceride significantly increased in fructose-fed rats (394.0 ± 25.8 vs. control rats 98.63 ± 6.7, p<0001). Vanadyl sulfate treatment prevented the increase in plasma insulin levels in the fructose fed-vanadyl treated rats (78.9 ± 5.1 pM vs. fructose fed-groups, p<0.001). Also vanadyl sulfate treatment significantly decreased plasma triglyceride levels (116.43 ± 6.7 vs. fructose-fed rats, p<0.001). Furthermore, fructose-fed groups had higher fasting insulin resistance index (FIRI: p<0.001) than control rats. In contrast, vanadyl sulfate significantly decreased FIRI in the fructose fed- vanadyl treated groups (p<0.001) compared with fructose- fed animals. These results indicate that administration of low doses of vanadyl sulfate may be advantageous for preservation of the functional characteristics of pancreatic beta cells, probably by improving insulin action and thereby insulin resistance prevention

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Angiotensin-converting enzyme (ACE) inhibitors including quinapril could exert a protective effect on cardiovascular system through endothelial system in normoglycemic and diabetic rats. The present experimental work was designed to study the vascular reactivity of aortic ring segments isolated from streptozotocin (STZ)-diabetic rats treated for 4 weeks with nitro-L-arginine-methyl ester (L-NAME 50 mg/100 ml) or L-NAME plus quinapril (10 mg/100 ml) in drinking water. The results showed that quinapril treatment significantly attenuated the augmented contractile response to phenylephrine and KCl in diabetic rats. In addition, quinapril treatment partially restored the reduced contractile response in diabetic animals treated chronically with L-NAME. It can be concluded that quinapril could partly counteract the effect of long-term L-NAME administration on vascular reactivity in STZ-diabetic rats

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The present study was undertaken to determine whether two-month treatment of streptozotocin (STZ)-diabetic rats with aqueous leaf extract of Trigonella foenum-graecum (TFG 200 mg/kg i.p.) could improve thoracic aortic responsiveness and to evaluate its endothelium dependency. For this purpose, vascular responses to KCl and noradrenaline (NA) were measured. Diabetic state significantly increased contractile responses to KCl and NA in aortic rings in both endothelium-intact and -denuded rings. Extract-treated diabetic rats showed a significant lower maximal contractile response to KCl only in endothelium-intact rings as compared to diabetic rings. It is concluded that intraperitoneal administration of aqueous leaf extract of TFG for two months could improve some functional indices of the vascular system in diabetic state and the integrity of the endothelium is essential for its beneficial effects

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It has been shown that nitric oxide is synthesized in the central nervous system as well as in vascular endothelial cells. Recently, it was reported that nitric oxide was involved in central cardiovascular regulation, baroreflex modulation, and involved in a reciprocal release with excitatory amino acids in the nucleus tractus solitarii of rats. The purpose of the present study was to investigate the possible interaction of nitric oxide and glucose in the nucleus tractus solitarii on blood pressure regulation. Male Wistar stereptozotocin induced diabetic rats were anesthetized with urethane. A cannula was inserted above the nucleus tractus solitarii and blood pressure was monitored intra-arterially. Unilateral microinjection of L-glutamate (2.3 nmol/60 nL) into the nucleus produced a decrease in blood pressure in diabetic rats. Microinjection of lidocaine (0.5 µl %2) increased blood pressure. Unilateral microinjection of sodium nitroprusside (100 mmol/60 nL) into the nucleus increased blood pressure in diabetic rats. After microinjection of sodium nitroprusside, the depressive responses to glutamate were significantly attenuated. These results demonstrated the probable role of glucose on blood pressure regulation in diabetic animals affecting on nitric oxidergic neurons and so it implicates an interaction between nitric oxide and glucose in central cardiovascular regulation. Iran. Biomed. J. 10 (1): 15-19, 2006

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Background: Diabetes is a major public health problem. The development of new therapies that are able to improve glycemia management and even to cure diabetes is of great interest. In this study, protective effects of sodium tungstate against STZ-induced beta-cell damages were investigated. Methods: Sixty rats were divided into six groups: control, diabetic, sodium tungstate treated diabetic rats from one week before STZ injection (TDB), food-restricted diabetic (FRD), tungstate treated control, sodium tungstate treated diabetic rats from one week after STZ administration (TDA). We evaluated serum insulin, glucose and glucose tolerance liver glycogen content, glucokinase (GK) activity blood and pancreas antioxidant power, lipid peroxidation and fuchsin-aldehyde histochemical staining of beta-cells. Results: Blood glucose levels of TDB group were lower than other diabetic groups (P<0.01). Blood insulin levels of all diabetic groups were lower than controls (P<0.01). Glucose intolerance improved in TDB animals. Blood and pancreas antioxidant power, liver glycogen contents and GK activities and granulated beta cells increased in TDB rats in comparison with other diabetic groups (P<0.01). Likewise, lipid peroxidation decreased significantly in TDB rats (P<0.01). Conclusions: Results suggested that sodium tungstate if administrated before STZ injection improves glycemic state by a direct effect on pancreatic beta-cells and preserves them by reducing the activity of these cells at the time of STZ injection, reducing STZ-induced oxidative stress, reducing insulin secretion, or all of the above mentioned.

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Background: Patients with diabetes mellitus type II suffer from hyperglycemia because they are not able to use the insulin that they produce, often due to inadequate function of insulin receptors. There are some evidences that this deficiency is inherited in a dominant autosomal manner and leads to the malfunction of the pancreatic beta cells resulting in insulin excretion disorders. In this study, we sought to identify mutations in the insulin receptor (INSR) gene, which can cause insulin resistance in type II diabetic patients. Methods: DNA was extracted from peripheral blood cells of the patients (n = 128) diagnosed with type II diabetes. All 22 exons of the INSR gene of the patients were analyzed for mutations running PCR, conformation-sensitive gel electrophoresis and DNA sequencing, consecutively. Results: Approximately 26% of the patients had genetic mutations however, most of them were not reported. These mutations include exon 2 (His171Asn, Ile172Ser, Cys196Ser and Ser210Arg), exon 3 (Gly227Asp and Gly232Ser), exon 8 (Thr543Ser), exon 9 (a heterozygote was observed with no change in phenylalanine at position 669), exon 13 (two heterozygotes: Arg890Pro with Asn865 remaining unchanged), exon 14 (Ala906Gly and Pro918Trp with Arg902 unchanged), exon 17 (Val1086Glu) and exon 19 (His1157Gln with Thr1172 unchanged). Conclusion: The lack of similar mutation records in literature and genetic data banks may suggest a geographic pattern for these INSR gene variants in our population.

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Background: The leaves of Eucalyptus globulus (eucalyptus) are used for treatment of diabetes mellitus in traditional medicine. The aim of this study was to evaluate the effects of eucalyptus in treatment of established systemic infection with Candida albicans in normal and streptozotocin-induced diabetic rats. Methods: Sixty normoglycemic male Wistar rats, weighing 200-250 g, were selected and randomly divided into six groups (n= 10): normal control, control + C. albicans, control + eucalyptus + C. albicans, diabetic control, diabetic + C. albicans, diabetic + eucalyptus + C. albicans. Diabetes was induced after a single intraperitoneal injection of streptozotocin (60 mg/kg body weight) and eucalyptus was added to the diet (62.5 g/kg) and drinking water (2.5 g/L) of treated animals for 4 weeks. The concerned groups were inoculated with C. albicans 15 days after diabetes induction. At the end of one month experiment, fasted rats were killed by cervical decapitation. Blood was collected from neck vein for estimation of glucose. C. albicans concentrations were estimated in liver and kidneys using serial dilution culture of tissue homogenates. Results: Eucalyptus administration significantly improved the hyperglycemia, polydipsia, polyphagia, and it also compensated weight loss of diabetic rats (P<0.05). Moreover, eucalyptus caused a significant reduction in C. albicans concentration in liver and kidney homogenates (P<0.01). Conclusion: The results revealed that eucalyptus improves Candidia infection in normal and diabetic rats that in some ways validates the traditional use of this plant in treatment of diabetic patients.

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Background: Metabolic derangements in type 2 diabetes mellitus (T2DM) are likely to affect skeletal muscle contractile functions adversely. Levo-carnitine improves muscle contractile functions in healthy humans and rats and corrects metabolic derangements in T2DM. Therefore, it is likely to improve muscle contractile functions in T2DM as well. This study was designed to determine the effect of levo-carnitine on serum levo-carnitine levels, oxidative stress and contractile parameters of fast muscle in T2DM. Methods: Ninety Sprague-Dawley rats were randomly divided into three equal groups. Healthy rats served as the controls, while T2DM was induced in diabetic and carnitine groups. The carnitine group was administered levo-carnitine 200 mg/kg/day intraperitoneally for 6 days. At 28th day, extensor digitorum longus muscles were removed and their functions were assessed using iWorx data acquisition unit (AHK/214). Blood obtained by intra-cardiac sampling at 28th day was used for estimation of serum malondialdehyde (MDA) and levo-carnitine levels. Results: Maximum isometric twitch tension, time-to-peak twitch tension and time-to-relax to 50% of the peak twitch tension were not significantly different amongst the groups. Carnitine group showed significant improvement in maximum fused tetanic tension, maximum fused tetanic tension after fatigue protocol and recovery from fatigue after 5 minutes of rest period compared to the diabetic group. Serum MDA levels were reduced, while serum levo-carnitine levels were elevated significantly in carnitine group as compared to the diabetic group. Conclusion: Levo-carnitine supplementation increases serum levo-carnitine levels which decreases oxidative stress. This action improves contractile force but delays fatigue in fast muscles of diabetic rats.

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Introduction: Hemoglobin A1C (HbA1c) reflects patient’s glycemic status over the previous 3 months. Previous studies have reported that iron deficiency may elevate A1C concentrations, independent of glycemia. This study is aimed to analyze the effect of iron deficiency anemia on HbA1c levels in diabetic population having plasma glucose levels in control. Methods: Totally, 120 diabetic, iron-deficient anemic individuals (70 females and 50 males) having controlled plasma glucose levels with same number of iron-sufficient non-anemic individuals were streamlined for the study. Their data of HbA1c (Bio-Rad D-10 HPLC analyzer), ferritin (cobas e411 ECLIA hormone analyzer), fasting plasma glucose (FPG, Roche Hitachi P800/917 chemistry analyzer), hemoglobin (Beckman Coulter LH780), peripheral smear examination, red cell indices, and medical history were recorded. Statistical analysis was carried out by student’s t-test, Chi-square test, and Pearson’s coefficient of regression. Results: We found elevated HbA1c (6.8 ± 1.4%) in iron-deficient individuals as compared to controls, and elevation was more in women (7.02 ± 1.58%). On further classification on the basis of FPG levels, A1C was elevated more in group having fasting glucose levels between 100-126 mg/dl (7.33 ± 1.55%) compared to the those with normal plasma glucose levels (<100 mg/dl). No significant correlation was found between HbA1c and ferritin and hemoglobin. Conclusion: This study found a positive correlation between iron deficiency anemia and increased A1C levels, especially in the controlled diabetic women and individuals having FPG between 100-126 mg/dl. Hence, before altering the treatment regimen for diabetic patient, presence of iron deficiency anemia should be considered.

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Background: Data shows vanadium protects pancreatic beta cells (BC) from diabetic animals. Whether this effect is direct or through the relief of glucose toxicity is not clear. This study evaluated the potential effect of oral vanadyl sulfate (vanadium) on glycemic status and pancreatic BC of normal and diabetic rats. Methods: Rats were divided into five groups of normal and diabetic. Diabetes was induced with streptozocin (40 mg/kg, i.v.). Normal rats used water (CN) or vanadium (1 mg/ml VOSO4, VTN). Diabetic rats used water (CD), water plus daily neutral protamine Hagedorn insulin injection (80 U/kg, ITD) or vanadium (VTD). Blood samples were taken for blood glucose (BG, mg/dL) and insulin (ng/dL) measurements. After two months, the pancreata of sacrificed rats were prepared for islet staining. Results: Pre-treated normal BG was 88 ± 2, and diabetic BG was 395 ± 9. The final BG in CD, VTD, and ITD was 509 ± 22, 138 ± 14, and 141 ± 14, respectively. Insulin in VTN (0.75 ± 0.01) and VTD (0.78 ± 0.01) was similar, higher than CD (0.51 ± 0.07) but lower than CN (2.51 ± 0.02). VTN islets compared to CN had larger size and denser central core insulin immunoreactivity with plentiful BC. CD and ITD islets were atrophied and had scattered insulin immunoreactivity spots and low BC mass. VTD islets were almost similar to CN. Conclusion: Besides insulin-like activity, vanadium protected pancreatic islet BC, and the relief of glucose toxicity happening with vanadium had a little role in this action.

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Background: Defects in endoplasmic reticulum homeostasis are common occurrences in different diseases, such as diabetes, in which the function of endoplasmic reticulum is disrupted. It is now well established that ion channels of endoplasmic reticulum membrane have a critical role in endoplasmic reticulum luminal homeostasis. Our previous studies showed the presence of an ATP-sensitive cationic channel in endoplasmic reticulum. Therefore, in this study, we examined and compared the activities of this channel in control and diabetic rats using single-channel recording techniques. Method: Male Wistar rats were made diabetic for 2 weeks with a single dose injection of streptozotocin (45 mg/kg). Ion channel incorporation of rough endoplasmic reticulum of diabetic hepatocytes into the bilayer lipid membrane allowed the characterization of K+ channel. Results: Ion channel incorporation of rough endoplasmic reticulum vesicles into the bilayer lipid revealed that the channel current-voltage (I-V) relation with a mean slope conductance of 520 ± 19 pS was unaffected in diabetes. Interestingly, the channel Po-voltage relation was significantly lower in diabetic rats at voltages above +30 mV. Conclusion: We concluded that the endoplasmic reticulum cationic channel is involved in diabetes. Also, this finding could be considered as a goal for further therapeutic plans.

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Background: Hypertension is considered an independent risk factor for cardiovascular mortality in diabetic patients. The present study was designed to determine the role of gamma amino butyric acid B (GABAB) receptor and L-arginine (L-Arg) in GABA-induced vasorelaxation in normal and streptozotocin-induced diabetic rat vessels. Methods: Diabetes was induced by a single i.p. injection of streptozotocin (STZ, 60 mg/kg). Eight weeks later, superior mesenteric arteries of all groups were isolated and perfused according to the McGregor method. Results: Baseline perfusion pressure of STZ diabetic rats was significantly higher than non-diabetic rats in both intact and denuded endothelium. In the presence of faclofen, a selective GABAB receptor blocker, GABA-induced relaxation in intact and denuded endothelium mesenteric beds of STZ diabetic rats was suppressed, but this response in non-diabetic rats was not suppressed. Our results showed that in the presence of L-Arg, a nitric oxide precursor, GABA induced vasorelaxation in both diabetic and non-diabetic vessels. Conclusion: From the results of this study, it may be concluded that the vasorelaxatory effect of GABA in diabetic vessel is mediated by the GABAB receptor and nitric oxide, but it seems that in non-diabetic vessel GABAB receptor does not play any role in GABA-induced vasorelaxation, but nitric oxide induced GABA relaxation in non-diabetic vessel.

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Background: Hyperlipidemia and oxidized-low-density lipoproteins (Ox-LDL) are important independent cardiovascular risk factors that have been shown to stimulate vascular smooth muscle cell (VSMC) proliferation. The purpose of the present study was to investigate the effect of vitamin E on Ox-LDL, lipid profile, C-reactive protein (CRP), and VSMC proliferation of rat aorta. Methods: Male Wistar rats (n = 32) were divided into four groups namely: sham (SH), control (C), non-treated diabetic, and vitamin E-treated diabetic (VETD) groups. Ox-LDL, lipid profile, CRP and VSMC proliferation of aorta were measured after 42 days. Results: The results revealed that along with a significant increase in VSMC proliferation, the amount of CRP, Ox-LDL, and lipid profiles in diabetic rats. VSMC proliferation was significantly ameliorated, and elevated CRP, Ox-LDL, and lipid profiles were also restored to those of shams in VETD. Conclusions: These findings strongly support the idea that diabetes induces Ox-LDL-mediated oxidative stress and VSMC proliferation in aorta of rat and imply that vitamin E has a strong protective effect as an antioxidant.

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Background: Adiponectin, an adipocyte-secreted hormone, is known to have anti-atherogenic, anti-inflammatory, and anti-diabetic properties. In the present study, the association between two common single nucleotide polymorphisms (SNPs) (+45T/G and +276G/T) of ADIOPQ gene and coronary artery disease (CAD) was assessed in the subjects with type 2 diabetes (T2DM). Methods: Genotypes of two SNPs were determined by polymerase chain reaction-restriction fragment length polymorphism in 200 subjects with T2DM (100 subjects with CAD and 100 without CAD). Results: The frequency of TT genotype of +276G/T was significantly elevated in CAD compared to controls (χ²=7.967, P=0.019). A similar difference was found in the allele frequency of +276G/T between two groups (χ²=3.895, P=0.048). The increased risk of CAD was associated with +276 TT genotype when compared to reference GG genotype (OR=5.158; 95% CI=1.016-26.182, P=0.048). However, no similar difference was found in genotype and allele frequencies of SNP +45T/G between two groups. There was a CAD protective haplotype combination of +276 wild-type and +45 mutant-type allele (276G-45G) (OR=0.37, 95% CI=0.16-0.86, P=0.022) in the subject population. Conclusion: Our findings indicated that T allele of SNP +276G/T is more associated with the increased risk of CAD in subjects with T2DM. Also, a haplotype combination of +45G/+276G of these two SNPs has a protective effect on the risk of CAD.

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Background: Islet transplantation could be an ideal alternative treatment to insulin therapy for type 1 diabetes Mellitus (T1DM). This clinical and experimental field requires a model that covers problems such as requiring a large number of functional and viable islets, the optimal transplantation site, and the prevention of islet dispersion. Hence, the methods of choice for isolation of functional islets and transplantation are crucial. Methods: The present study has introduced an experimental model that overcomes some critical issues in islet transplantation, including in situ pancreas perfusion by digestive enzymes through common bile duct. In comparison with conventional methods, we inflated the pancreas in Petri dishes with only 1 ml collagenase type XI solution, which was followed by hand-picking isolation or Ficoll gradient separation to purify the islets. Then we used a hydrogel composite in which the islets were embedded and transplanted into the peritoneal cavity of the streptozotocin-induced diabetic C57BL/6. Results: As compared to the yield of the classical methods, in our modified technique, the mean yield of isolation was about 130-200 viable islets/mouse pancreas. In vitro glucose-mediated insulin secretion assay indicated an appropriate response in isolated islets. In addition, data from in vivo experiments revealed that the allograft remarkably maintained blood glucose levels under 400 mg/dl and hydrogel composite prevents the passage of immune cells. Conclusion: In the model presented here, the rapid islet isolation technique and the application of biomimetic hydrogel wrapping of islets could facilitate islet transplantation procedures.

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Background: Increasing the prevalence of type 2 diabetes has given rise to a global health burden and a concern among health service providers and health administrators. The current study aimed at developing and comparing some statistical models to identify the risk factors associated with type 2 diabetes. In this light, artificial neural network (ANN), support vector machines (SVMs), and multiple logistic regression (MLR) models were applied, using demographic, anthropometric, and biochemical characteristics, on a sample of 9528 individuals from Mashhad City in Iran. Methods: This study has randomly selected 6654 (70%) cases for training and reserved the remaining 2874 (30%) cases for testing. The three methods were compared with the help of ROC curve. Results: The prevalence rate of type 2 diabetes was 14% in our population. The ANN model had 78.7% accuracy, 63.1% sensitivity, and 81.2% specificity. Also, the values of these three parameters were 76.8%, 64.5%, and 78.9%, for SVM and 77.7%, 60.1%, and 80.5% for MLR. The area under the ROC curve was 0.71 for ANN, 0.73 for SVM, and 0.70 for MLR. Conclusion: Our findings showed that ANN performs better than the two models (SVM and MLR) and can be used effectively to identify the associated risk factors of type 2 diabetes.

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Background: Type 2 diabetes mellitus (T2DM) is related to the gut microbiota with numerous molecular mechanisms. Modulating the gut microbiota by probiotics could be effective in management of T2DM. The aim of the present trial was to evaluate the effect of Lactobacillus casei on glycemic control and serum sirtuin1 (SIRT1) and fetuin-A in patients with T2DM. Methods: Forty patients with T2DM (n = 20 for each group) were divided into intervention (probiotic) and placebo groups. The intervention group received a daily capsule containing 10⁸ cfu of L. casei for eight weeks. The patients in placebo group took capsules containing maltodextrin for the same time duration. Anthropometric measurements, dietary intake questionnaires, and blood samples were collected, and the patients were assessed by an endocrinologist at the beginning and at the end of the trial. Results: Fasting blood sugar, insulin concentration, and insulin resistance significantly decreased in probiotic group compared with placebo group (-28.32 [-50.23 to -6.41], 0.013; -3.12 [-5.90 to -0.35], 0.028; -32.31 [-55.09 to -9.54], 0.007, respectively). Moreover, HbA1c reduced after intervention, but the reduction was not significant (-0.45 [-0.96 to 0.05], 0.077). In comparison with placebo, the L. casei supplementation significantly increased SIRT1 and decreased fetuin-A levels at the end of the trial (0.52 [0.026 to 1.02], 0.040; -17.56 [-32.54 to -2.58], 0.023, respectively).  Conclusion: L. casei supplementation affected SIRT1 and fetuin-A levels in a way that improved glycemic response in subjects with T2DM. Affecting the SIRT1 and fetuin-A levels introduces a new known mechanism of probiotic action in diabetes management.

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Background: Hypercoagulability and hypofibrinolysis are among the symptoms exhibited by diabetic patients. Our study aimed to address the polymorphic nature of Alu DNA fragment in the human tissue plasminogen activator gene within diabetes mellitus (DM) Jordanian patients. Methods: Genomic DNA was isolated from 76 DM patients and 60 non-diabetic Jordanian individuals, and the Alu fragment was amplified using PCR. Results: The results showed that 80% of the non-diabetic Jordanian subjects were homozygotes for the deletion of the Alu fragment (Alu^-/-), 16.7% were homozygotes for its insertion (Alu^+/+), and 3.3% were heterozygotes (Alu^+/-). Besides, 36.8% of the diabetic patients exhibited the Alu^-/- or Alu^+/- genotype, and 26.3% were Alu^+/+. The Alu^-/- genotype occurred less frequently in the diabetic individuals. Conclusion: The high frequency of the Alu^-/- genotype constitutes a protective deletion with respect to DM within the normal subjects. 

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Background: Mixed lineage kinase domain-like pseudokinase (MLKL), one of the main downstream components of the necroptosis or programmed necrosis has recently been demonstrated in advanced atherosclerotic lesions. However, its precise role in the atherosclerosis pathogenesis still requires more elucidation. Our study was set to delineate both the changes in peripheral MLKL gene expression and its influence on disease severity in atherosclerotic patients with and without type 2 diabetes mellitus. Methods: The study involved 50 patients (20 non-diabetics and 30 diabetics) undergoing coronary artery bypass graft and 20 apparently healthy controls. Taqman RT-PCR was used to quantify MLKL mRNA expression levels, while ELISA was employed to estimate serum insulin and high sensitivity C-reactive protein (hsCRP) levels. Results: Compared with the control group, MLKL gene was up regulated significantly in cardiovascular diseases (CVD; p ≤ 0.001). Higher MLKL expression was demonstrated in diabetic CVD group than non-diabetic group (p < 0.05). Correlation studies reported positive associations between MLKL and markers of dyslipidemia, inflammation, and insulin resistance. Multiple regression analysis revealed that FBG levels, hsCRP levels, and total white blood cells count were significant predictors for MLKL levels. Receiver operating characteristic curve showed a significant diagnostic value of MLKL for CVD. Moreover, regression analysis demonstrated that MLKL and hsCRP were independent predicting factors for the severity of CVD. Conclusion: MLKL is linked to hallmarks of atherosclerosis and could explain increased cardiovascular risk in diabetic patients. Thus, it can be a potential drug target for treatment of atherosclerotic patients.