Effect of Dipeptidyl Peptidase Inhibitors-4 and Sulfonylurea on Serum Adiponectin Levels in Patients with Newly Diagnosed Type 2 Diabetes Mellitus.

Diabetes mellitus implies a group of common metabolic disorders that share a phenotype of hyperglycemia. Peripheral insulin resistance and impaired insulin secretion forms two legs of this common, globally important non communicable disorder. Adiponectin is a hormone released by adipocytes which aids in enhancing insulin sensitivity, decreasing inflammatory mediators. Baseline adiponectin can predict diabetes and change in its value with change in metabolic parameters highlights the gravity of this molecule in more refined diagnosis and treatment of diabetes. AIMS: The objective was to ascertain change in adiponectin value in diabetics who were given either DPP-4 inhibitors or SU group drugs. Another objective was to find out correlation of serum adiponectin levels with various parameters involved in sugar and fat metabolism such as FBS, PPBS, HbA1c, LDL, HDL, VLDL, TG. MATERIAL: Total of 50 participants were taken, out of which 40 were diabetics and 10 were controls. They were selected using inclusion and exclusion criteria. Diabetics were divided into two arms with 20 participants each (a. dpp group b.su group). Clinical history, examination, sample collection was done. Serum adiponectin assay was performed using RayBio ELISA kit. OBSERVATION: Serum adiponectin levels in dpp group was higher at end of third month as compared to 0 month (45.9 +/- 5.9 vs. 39.8 +/- 4.1 mcg/dl; p<0.05). Likewise, adiponectin levels in su group was higher at end of third month as compared to 0 month (43.9 +/- 3.6 vs. 39.8 +/- 3.5 mcg/dl; p<0.05). CONCLUSION: Improvement in glycemic parameters (HbA1c, FBS, PPBS) is associated with rise in serum levels of adiponectin. General population possess higher levels of adiponectin as compared to diabetics. Adiponectin can serve as a marker for early diagnosis to diabetes. It can also aid in targeted therapy for metabolic disorders.

Genetic variants related to insulin metabolism are associated with gestational diabetes mellitus.

The current study sought to investigate the associations of common genetic risk variants with gestational diabetes mellitus (GDM) risk in the north Indian population and to evaluate their utility in identifying GDM cases. A case-control study, including 300 pregnant women, was included, and clinical and pathological information was collected. The amplification-refractory mutation system (ARMS) was used for genotyping four single nucleotide polymorphisms (SNPs), namely FTO (rs9939609), PPARG2 (rs1801282), SLC30A8 (rs13266634), and TCF7L2 (rs12255372). The odds ratio and confidence interval were determined for each SNP in different genetic models. Further, attributable risk, population penetrance, and relative risk were also calculated. The risk allele A of FTO (rs9939609) poses a two times higher risk of GDM (p = 0.02, OR = 2.5). The CG and GG genotypes of PPARG2 (rs1801282) have half a lower risk of GDM. In SLC30A8 (rs13266634), the recessive model analysis showed a two times higher risk of having GDM, while the recessive model (TT vs. GG + GT) analysis in TCF7L2 (rs12255372) indicates a lower risk of GDM. Finally, the relative risk, population penetrance, and attributable risk for risk allele in all four variants was higher in GDM mothers. All four polymorphisms were found to be significantly associated with BMI, HbA1c, and insulin. Our study first time confirmed a significant association with GDM for four variants, FTO, PPARG2, SLC30A8, and TCF7L2, in the North Indian population.

BCG vaccination policy, natural boosting and pediatric brain and CNS tumor incidences.

Bacille Calmette-Guérin (BCG) vaccination supposedly imparts and augments "trained immunity" that cross-protects against multiple unrelated pathogens and enhances general immune surveillance. Gradual reductions in tuberculosis burden over the last 3-5 decades have resulted in the withdrawal of BCG vaccination mandates from developed industrialized countries while reducing to a single neonatal shot in the rest. Concurrently, a steady increase in early childhood Brain and CNS (BCNS) tumors has occurred. Though immunological causes of pediatric BCNS cancer are suspected, the identification of a causal protective variable with intervention potential has remained elusive. An examination of the countries with contrasting vaccination policies indicates significantly lower BCNS cancer incidence in 0-4-year-olds (per hundredthousand) of countries following neonatal BCG inoculations (n=146) vs. non-BCG countries (n=33) [Mean: 1.26 vs. 2.64; Median: 0.985 vs. 2.8; IQR: 0.31-2.0 vs. 2.4-3.2; P=<0.0001 (two-tailed)]. Remarkably, natural Mycobacterium spp. reexposure likelihood is negatively correlated with BCNS cancer incidence in 0-4-year-olds of all affected countries [r(154): -0.6085, P=<0.0001]. Seemingly, neonatal BCG vaccination and natural "boosting" are associated with a 15-20-fold lower BCNS cancer incidence. In this opinion article, we attempt to synthesize existing evidence implying the immunological basis of early childhood BCNS cancer incidence and briefly indicate possible causes that could have precluded objective analysis of the existing data in the past. We draw the attention of the stakeholders to consider the comprehensive evaluation of immune training as a potential protective variable through well-designed controlled clinical trials or registry-based studies as feasible for its potential applications in reducing childhood BCNS cancer incidence.