Comparison of Statins Dose Intensity on HbA1c Control in Outpatients with Type 2 Diabetes: A Prospective Cohort Study

The effect of statins dose intensity (SDI) on glycemic control in patients with existing diabetes is unclear. Also, there are many contradictory findings were reported in the literature; thus, it is limiting the possibility to draw conclusions. This project was designed to compare the effect of SDI on glycated hemoglobin (HbA1c%) control in outpatients with Type 2 diabetes in the endocrine clinic at Hospital Pulau Pinang, Malaysia, between July 2015 and August 2016. A prospective cohort study was conducted, where records of 345 patients with Type 2 diabetes (Moderate-SDI group 289 patients and high-SDI cohort 56 patients) were reviewed to identify demographics and laboratory tests. The target of glycemic control (HbA1c < 7% for patient < 65 years, and < 8% for patient ≥ 65 years) was estimated, and the results were presented as descriptive statistics. From 289 moderate-SDI cohorts with a mean age of 57.3 ± 12.4 years, only 86 (29.8%) cases were shown to have controlled glycemia, while there were 203 (70.2%) cases with uncontrolled glycemia with confidence interval (CI) of 95% (6.2–10.8). On the other hand, the high-SDI group of 56 patients with Type 2 diabetes with a mean age 57.7±12.4 years is distributed among 11 (19.6%) patients with controlled diabetes, and 45 (80.4%) of them had uncontrolled glycemia, CI: 95% (7.1–11.9). The study has demonstrated that the relative risk (RR) of uncontrolled glycemia in patients with Type 2 diabetes that used high-SDI is 1.15, and the excessive relative risk (ERR) is 15%. The absolute risk (AR) is 10.2%, and the number needed to harm (NNH) is 10. Outpatients with Type 2 diabetes who use high-SDI of statin have a higher risk of uncontrolled glycemia than outpatients who had been treated with a moderate-SDI.

Apolipoprotein E Gene Polymorphism and Its Association with Cardiovascular Heart Disease Risk Factors in Type 2 Diabetes Mellitus

Apolipoprotein E (APOE) gene polymorphism has influence on serum lipids which relates to cardiovascular risk. The purpose of this study was to determine the frequency distribution of APOE alleles among Malaysian Type 2 Diabetes Mellitus (DM) patients with and without coronary artery disease (CAD) and their association with serum lipid profiles. A total of 115 patients were recruited in which 78 patients had Type 2 DM without CAD and 37 patients had Type 2 DM with CAD. The APOE polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The APOE ɛ3 allele was the most common one in both groups. There was no significant association between the APOE genotypes and the CAD status in Type 2 DM using Pearson χ2 test. Further analysis indicated there were no significant differences in all lipid parameters between E2, E3 and E4 subgroups in both groups. The study showed that the E4 allele carriers of Type 2 DM with CAD patients had higher LDL-C level and lower HDL-C level compared to the other allele carriers. However, analyses showed these levels were not statistically different. The study also showed that the Type 2 DM with CAD group with E2 allele had higher triglyceride (TG). In conclusion, further study with larger sample size is needed to confirm role of E4 as a marker of CAD among Type 2 DM patients in Malaysian population.

Synthesis and Characterization of Chromium (III) Complexes with L-Glutamic Acid, Glycine and LCysteine

Some Chromium (III) complexes were synthesized with three amino acids: L Glutamic Acid, Glycine, and L-cysteine as the ligands, in order to provide a new supplement containing Cr(III) for patients with type 2 diabetes mellitus. The complexes have been prepared by refluxing a mixture of Chromium(III) chloride in aqueous solution with L-glutamic acid, Glycine, and L-cysteine after pH adjustment by sodium hydroxide. These complexes were characterized by Infrared and Uv-Vis spectrophotometer and Elemental analyzer. The product yields of four products were 87.50 and 56.76% for Cr-Glu complexes, 46.70% for Cr-Gly complex and 40.08% for Cr-Cys complex respectively. The predicted structure of the complexes are [Cr(glu)2(H2O)2].xH2O, Cr(gly)3..xH2O and Cr(cys)3.xH2O., respectively.

Visfatin and Apelin Are New Interrelated Adipokines Playing Role in the Pathogenesis of Type 2 Diabetes Mellitus Associated Coronary Artery Disease in Postmenopausal Women

Visfatin and apelin are two new adipokines that recently gained a special interest in diabetes research. This study was conducted to study the interplay between these two adipokines and their correlation with other inflammatory and biochemical parameters in type 2 diabetic (T2D) postmenopausal women with CAD. Visfatin and apelin were measured by enzyme-linked immunoassay (ELISA). Visfatin was found to be significantly higher in the following groups: T2D patients without CAD, non-obese and obese T2D patients with CAD when compared to control group. Apelin was found to be significantly lower in non-obese and obese T2D patients with CAD when compared to control group. Visfatin and apelin were found to be significantly associated with each other and with other biochemical parameters. The current study provides evidence for the interplay between visfatin and apelin through the inflammatory milieu characteristic of T2D and their possible role in the pathogenesis of CAD complication of T2D. 

Role of Oxidative DNA Damage in Pathogenesis of Diabetic Neuropathy

Oxidative stress is considered to be the cause for onset and the progression of type 2 diabetes mellitus (T2DM) and complications including neuropathy. It is a deleterious process that can be an important mediator of damage to cell structures: protein, lipids and DNA. Data suggest that in patients with diabetes and diabetic neuropathy DNA repair is impaired, which prevents effective removal of lesions. Objective: The aim of our study was to evaluate the association of the hOGG1 (326 Ser/Cys) and XRCC1 (194 Arg/Trp, 399 Arg/Gln) gene polymorphisms whose protein is involved in the BER pathway with DNA repair efficiency in patients with diabetes type 2 and diabetic neuropathy compared to the healthy subjects. Genotypes were determined by PCR-RFLP analysis in 385 subjects, including 117 with type 2 diabetes, 56 with diabetic neuropathy and 212 with normal glucose metabolism. The polymorphisms studied include codon 326 of hOGG1 and 194, 399 of XRCC1 in the base excision repair (BER) genes. Comet assay was carried out using peripheral blood lymphocytes from the patients and controls. This test enabled the evaluation of DNA damage in cells exposed to hydrogen peroxide alone and in the combination with the endonuclease III (Nth). The results of the analysis of polymorphism were statistically examination by calculating the odds ratio (OR) and their 95% confidence intervals (95% CI) using the ¤ç2-tests. Our data indicate that patients with diabetes mellitus type 2 (including those with neuropathy) had higher frequencies of the XRCC1 399Arg/Gln polymorphism in homozygote (GG) (OR: 1.85 [95% CI: 1.07-3.22], P=0.3) and also increased frequency of 399Gln (G) allele (OR: 1.38 [95% CI: 1.03-1.83], P=0.3). No relation to other polymorphisms with increased risk of diabetes or diabetic neuropathy. In T2DM patients complicated by neuropathy, there was less efficient repair of oxidative DNA damage induced by hydrogen peroxide in both the presence and absence of the Nth enzyme. The results of our study suggest that the XRCC1 399 Arg/Gln polymorphism is a significant risk factor of T2DM in Polish population. Obtained data suggest a decreased efficiency of DNA repair in cells from patients with diabetes and neuropathy may be associated with oxidative stress. Additionally, patients with neuropathy are characterized by even greater sensitivity to oxidative damage than patients with diabetes, which suggests participation of free radicals in the pathogenesis of neuropathy.

Analysis of Metallothionein Gene MT1A (rs11076161) and MT2A (rs10636) Polymorphisms as a Molecular Marker in Type 2 Diabetes Mellitus among Malay Population

Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder that characterized by the presence of high glucose in blood that cause from insulin resistance and insufficiency due to deterioration β-cell Langerhans functions. T2DM is commonly caused by the combination of inherited genetic variations as well as our own lifestyle. Metallothionein (MT) is a known cysteine-rich protein responsible in helping zinc homeostasis which is important in insulin signaling and secretion as well as protection our body from reactive oxygen species (ROS). MT scavenged ROS and free radicals in our body happen to be one of the reasons of T2DM and its complications. The objective of this study was to investigate the association of MT1A and MT2A polymorphisms between T2DM and control subjects among Malay populations. This study involved 150 T2DM and 120 Healthy individuals of Malay ethnic with mixed genders. The genomic DNA was extracted from buccal cells and amplified for MT1A and MT2A loci; the 347bp and 238bp banding patterns were respectively produced by mean of the Polymerase Chain Reaction (PCR). The PCR products were digested with Mlucl and Tsp451 restriction enzymes respectively and producing fragments lengths of (158/189/347bp) and (103/135/238bp) respectively. The ANOVA test was conducted and it shown that there was a significant difference between diabetic and control subjects for age, BMI, WHR, SBP, FPG, HBA1C, LDL, TG, TC and family history with (P0.05). The genotype frequency for AA, AG and GG of MT1A polymorphisms was 72.7%, 22.7% and 4.7% in cases and 15%, 55% and 30% in control respectively. As for MT2A, genotype frequency of GG, GC and CC was 42.7%, 27.3% and 30% in case and 5%, 40% and 55% for control respectively. Both polymorphisms show significant difference between two investigated groups with (P=0.000). The Post hoc test was conducted and shows a significant difference between the genotypes within each polymorphism (P=0. 000). The MT1A and MT2A polymorphisms were believed to be the reliable molecular markers to distinguish the T2DM subjects from healthy individuals in Malay populations.