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Background This work aimed to evaluate the influence of single nucleotide polymorphisms (SNPs) in the SLC47A1 (922-158G>A; rs2289669) and SLC47A2 (−130G>A; rs12943590) genes on the relative change in HbA1c in type 2 diabetes mellitus (T2DM) patients of South India who are taking metformin as monotherapy. It also aims to study the effects of these SNPs on the dose requirement of metformin for glycemic control and the adverse effects of metformin. Methods Diabetes patients on metformin monotherapy were recruited based on the eligibility criteria (n=105). DNA was extracted and genotyping was performed with a real-time PCR system using TaqMan® SNP genotyping assay method. The HbA1c levels were measured using Bio-Rad D-10™ Hemoglobin Analyzer. Results After adjusting for multiple comparisons (Bonferroni correction) the difference found in the glycemic response between the “GG” genotype and “AG/AA” genotype groups of the SLC47A2 gene was not significant (p=0.027; which was greater than the critical value of 0.025). Patients with “GG” genotype showed a 5.5% decrease in HbA1c from baseline compared to those with the “AG/AA” genotype (0.1% increase). The SNP in the SLC47A1 gene also did not influence the glycemic response to metformin (p=0.079). The median dose requirements based on the genotypes of the rs12943590 variant (p=0.357) or rs2289669 variant (p=0.580) were not significantly different. Similarly, there was no significant difference in the occurrence of adverse effects across the genotypes in both the SLC47A1 (p=0.615) and SLC47A2 (p=0.309) genes. Conclusions The clinical response to metformin was not associated with the SNPs in the SLC47A1 and SLC47A2 genes coding for the multidrug and toxin extrusion protein (MATE) transporters. Furthermore, the studied SNPs had no influence on the dose requirement or adverse effects of metformin.

Introduction: Type 2 Diabetes Mellitus (DM) is on the verge of becoming a pandemic in India. Type 2 DM patient have two to four times increased risk of carotid artery disease. Adipokines have been regarded recently as direct link between diabetes and atherosclerosis. Visceral Adipose Tissue Derived Serine Protease Inhibitor (VASPIN); one of the most recently discovered adipokine, inhibits the proteases responsible for insulin resistance, carotid plaque development and rupture. In literature, few studies have addressed the role of VASPIN in pathogenesis of Acute Coronary Syndrome (ACS) in patients with type 2 DM. Aim:To find association between serum VASPIN with lipid profile, creatine kinase-total, creatine kinase-MB, troponin-I, age, height, weight, blood pressure, smoking, family history of ACS and to prove the hypothesis of low serum VASPIN level as predictor of ACS in patients with type 2 DM. Materials and Methods:Forty-one type 2 DM patients (controls) and 41 type 2 DM patients with ACS (cases) were enrolled in the study. Anthropometric measurements were performed and fasting serum biochemical parameters and VASPIN were measured. The results of cases and controls were compared by student t-test or Mann-Whitney test. All the parameters were correlated with serum VASPIN by Pearson's or Spearman's correlation.Results: Fasting serum VASPIN concentration was significantly (p< 0.0001) lower in the cases (0.43±0.22 pg/ml) than in the controls (0.83±0.29 pg/ml). Correlation analysis undertaken on all type 2 DM showed that serum VASPIN concentration was negatively correlated with age, waist circumference, hip circumference, systolic and diastolic blood pressure, duration of diabetes, serum Creative Kinase-Total, CK-MB and urea (p< 0.05). Utilizing Receiver Operating Characteristic (ROC) curve, the serum VASPIN level of less than 0.594pg/ml showed greatest risk of ACS among type 2 DM patients (p< 0.0001). Conclusion:Type 2 DM patients with low serum vaspin concentration were at risk of ACS independent of other cardiovascular risk factors.Aswathy Jaya Sathyaseelan et al., Vaspin in Diabetes with Acute Coronary Syndrome www.jcdr.net

Background:Genetic polymorphisms of the angiotensin-renin pathway have been thought to influence the development of diabetic nephropathy. However, there are conflicting results regarding this association in previous studies on populations with varying ethnicity.Aims:Primary aim was to compare the frequency of distribution of angiotensin-converting enzyme (ACE) gene (insertion/deletion [I/D]) polymorphism in Tamilian Indian type 2 diabetic individuals with and without microalbuminuria. Secondary objective was to compare the frequency of distribution of the 3 genotypes in diabetic patients with urinary albumin/creatinine ratio (ACR) < 30 mg/dL, urinary ACR = 30 to 300 mg/dL, and urinary ACR > 300 mg/dL.Methods:A total of 179 consecutive diabetic individuals between 40 and 70 years, from Puducherry and Tamilnadu of Dravidian descent participated in the study conducted from 2012 to 2014. Inclusion criteria were as follows: age ≥ 40 years and duration of type 2 diabetes mellitus for ≥5 years. Patients were divided into 2 groups based on ACR values. Group 1 consisted of 50 individuals with urinary ACR < 30 mg/g of creatinine, and group 2 consisted of 129 individuals with urinary ACR > 30 mg/g. Angiotensin I–converting enzyme (ACE) gene polymorphism was determined by allele-specific polymerase chain reaction method using a primer pair flanking the polymorphic region of its intron 16. Furthermore, group 2 patients were subdivided into those with urinary ACR = 30 to 300 mg/g of creatinine and those with urinary ACR > 300 mg/g of creatinine, and distribution of ACE gene polymorphism was compared in the three groups.Statistics:Statistical analysis was done using SPSS version 17.0. Independent Student t test was used to compare mean values between the 2 groups. Odds ratio was calculated for testing association between ACE gene (I/D) polymorphism and presence of microalbuminuria. P < .05 was considered significant. Comparison of ACE genotypes among 3 groups of patients (ACR < 30 mg/g, ACR = 30-300 mg/g, and ACR > 300 mg/g) was done using 1-way analysis of variance with Bonferroni multiple comparison test as post hoc analysis.Conclusions:Heterozygous I/D genotype was more frequent in the study population (45.8%) than the other genotypes. There was no difference in the genotype distribution in patients with varying levels of albuminuria.

We report a case of a 41-year-old lady, who developed severe hypotension and sinus bradycardia, following oral consumption of 20 g of phenytoin and 500 mg of glibenclamide. She required high dose of inotropes and a temporary transvenous pacer for her hemodynamic instability. This life-threatening cardiotoxicity of phenytoin could have been due to its interaction with sulphonylurea. It is imperative to be aware of drug interactions, due to which, life-threatening cardiovascular manifestations following phenytoin toxicity can occur.