Background: Obesity has become global epidemic in the last three decades, whereas Coronary Heart Disease (CHD) still remains the most important cause of mortality in the world. The study was aimed at determining the pattern of lipid profile for the obese and CHD population in Pakistan. As obesity is a strong predisposing risk factor for CHD, we aimed to analyze the lipid parameters in both conditions and compare them with the healthy controls of the same ethnicity. Methods: Blood samples were collected from one thousand individuals (500 with CHD, 250 with obesity, 250 healthy controls). The lipid profile (total Cholesterol, triglycerides, HDL-C, LDL-C and VLDL) was measured using commercially available kits. The pattern of dyslipidemia was then studied by comparing the results in both groups with controls as well as population cutoffs. The quantitative variables were checked for normality and log transformation was done for variables where appropriate. Analysis of variance and logistic regression were done to check the association of lipid parameters with obesity and CHD. Results: The obese and CHD groups showed a dyslipidemic profile than the healthy controls. CHD group had a higher proportion of CHD in any of the first degree blood relatives (36.0% vs. 1.8%), a similar trend was observed in the obese group, where 63.9% cases had positive family history. Among cases, 50.7% had combined lipid abnormalities, i.e., the values of TC, LDL-C, TG and HDL-C, all were deranged. Whereas 49.52% had TC more than normal cut off (> 200 mg/dl), 51.6% had LDL-C > 100 mg/dl. Similarly, 80.4% of patients had TG levels more than upper normal range (> 150 mg/dl) and 64% had HDL values in moderate CHD risk group (< 50 mg/dl). The results show that Pakistani cases are hyperlipidemic for lipid traits except for HDL which is lowered. Patients with comorbidities also had lipid profiles deviated from the normal range. Conclusion: The study provides information regarding the aberration of lipid profile in the metabolic disorders that can increase the predisposition to complications.

Quorum sensing (QS) is a cell density dependent regulatory process that uses signaling molecules to manage the expression of virulence genes and biofilm formation. The study of QS inhibitors has emerged as one of the most fascinating areas of research to discover novel antimicrobial agents. Compounds that block QS have become candidates as unusual antimicrobial agents, as they are leading players in the regulation of virulence of drug-resistant pathogens. Metal and metal oxide nanoparticles offer novel alternatives to combat antibiotic resistance in Gram-negative bacteria aiming their capacity as QS inhibitors. This review provides an insight into the quorum quenching potential of metal and metal oxide nanoparticles by targeting QS regulated virulence of Gram-negative bacteria.

The aim of the current study was to analyze the effect of six type II diabetes GWAS loci rs3923113 (GRB14), rs16861329 (ST6GAL1), rs1802295 (VPS26A), rs7178572 (HMG20A), rs2028299 (AP3S2) and rs4812829 (HNF4A), and an FTO polymorphism (rs9939609) on obesity. The probable mechanism of action of these SNPs was analyzed by studying their association with various biochemical and anthropometric parameters. A total of 475 subjects (obese=250, controls=225) were genotyped by TaqMan assay and their lipid profile was determined. Allele/genotype frequencies and an unweighted/weighted gene score were calculated. The effect of the gene score on anthropometric and biochemical parameters was analyzed. The minor allele frequencies of all variants were comparable to that reported in the original studies and were associated with obesity in these Pakistani subjects. Subjects with 9 risk alleles differ from those with <3 and overall there is no significant effect (P-value for trend 0.26). None of the SNPs were associated with any of the serum lipid traits. We are the first to report the association of these T2D SNPs with obesity. In the Pakistani population the reported effect of six SNPs for obesity is similar to that reported for T2D and having a combination of risk alleles on obesity can be considerable. The mechanism of this effect is unclear, but appears not to be mediated by changing serum lipid chemistry.

Obesity is a complex disorder and has been increasing globally at alarming rates including Pakistan. However, there is scarce research on understanding obesity genetics in Pakistan. Leptin is a hormone secreted by adipocytes in response to satiety and correlates with body weight. Any mutations in the LEP gene have an adverse effect on energy regulation pathway and lead to severe, early onset obesity. To date, only eight mutations have been described in the LEP gene of which p. N103K is one. We aimed to analyze the prevalence of this mutation in Pakistani subjects. A total of 475 subjects were genotyped by PCR–RFLP analysis and their serum profiling was done. Results showed that this mutation was present only in one male child with early onset obesity (10 year). He had very low serum leptin levels suggestive of functional impact of the mutation. The prevalence of such mutations is, however, low due to the drastic effects on the energy regulation. In conclusion, LEP gene mutations contribute significantly to the monogenic forms of obesity and are important due to the availability of treatment options. Such mutations may exert their effect by directly affecting energy regulation pathway and are more prominent in the early stages of life only.

The human GI tract harbors a diverse and dynamic microbial community comprising bacteria, archaea, viruses and eukaryotic microbes, which varies in composition from individual to individual. A healthy microbiota metabolizes various indigestible dietary components of the host, maintains host immune homeostasis and nutrient intake, but, an imbalanced microbiota has been reported to be associated with many diseases, including obesity. Rodent studies have produced evidence in support of the causal role of the gut microbiota in the development of obesity, however, such causal relationship is lacking in humans. The objective of this review is to critically analyze the vast information available on the composition, function and alterations of the gut microbiota in obesity and explore the future prospects of this research area.