From Influenza Virus to Novel Corona Virus (SARS-CoV-2)-The Contribution of Obesity.

From the beginning of 2020, the governments and the health systems around the world are tackling infections and fatalities caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) resulting in the coronavirus disease 2019 (COVID-19). This virus pandemic has turned more complicated as individuals with co-morbidities like diabetes, cardiovascular conditions and obesity are at a high risk of acquiring infection and suffering from a more severe course of disease. Prolonged viral infection and obesity are independently known to lower the immune response and a combination can thus result in a "cytokine storm" and a substantial weakening of the immune system. With the rise in obesity cases globally, the chances that obese individuals will acquire infection and need hospitalization are heightened. In this review, we discuss why obesity, a low-grade chronic inflammation, contributes toward the increased severity in COVID-19 patients. We suggest that increased inflammation, activation of renin-angiotensin-aldosterone system, elevated adipokines and higher ectopic fat may be the factors contributing to the disease severity, in particular deteriorating the cardiovascular and lung function, in obese individuals. We look at the many lessons learnt from the 2009 H1N1 influenza A pandemic and relate it to the very little but fast incoming information that is available from the SARS-CoV-2 infected individuals with overweight and obesity.

N,N-Dimethlyacetamide Prevents the High-Fat Diet-Induced Increase in Body Weight.

Increased body weight caused by visceral fat accumulation is on the rise and is reaching epidemic proportions worldwide. Hence, means and ways to tackle the problem of increased adiposity is of utmost importance. In this work, we report the effect of a water-soluble small molecule N,N-Dimethlyacetamide (DMA) on weight gain and adiposity in vitro and in vivo. To monitor the in vitro effect of DMA on adipogenesis, 3T3-L1 preadipocytes and pluripotent C2C12 cells were differentiated to adipocytes in the presence of DMA (5 mM and 10 mM). Oil red O staining and reverse transcriptase polymerase chain reaction (RT-PCR) were performed to evaluate the differentiation to adipocytes. To study the in vivo effect of DMA on body weight, experiments were done with C57BL/6J male mice (6 weeks old). The mice were randomly assigned to receive either high-fat diet (HFD; 45% fat) or a normal diet (7% fat) and were either intraperitoneally injected with DMA or phosphate-buffered saline (PBS) once a week for 20 weeks. Glucose tolerance test was performed on living mice. Post-experiment, the epididymal and subcutaneous adipose tissue were excised from the sacrificed animal, and histology, RT-PCR and plasma triglyceride assay were performed. DMA had no inhibitory effect on adipocyte differentiation when applied only once. However, sustained treatment with DMA inhibited the adipocyte differentiation in both 3T3-L1 and C2C12 cells, and significantly lowered the expression of adipocyte markers, in particular, fatty acid-binding protein 4 (fabp4). Under HFD, C57BL/6J mice treated with DMA had lower body weight compared with PBS treatment. Moreover, the HFD-induced higher body weight was controlled when the mice were switched from PBS to DMA treatment. Further, the HFD-mediated adipocyte hypertrophy from epididymal and subcutaneous adipose tissue was significantly reduced with DMA treatment. Interestingly, the glucose clearance and triglyceride levels in the plasma were improved in mice when DMA treatment was initiated early. Taken together, our results show that DMA exhibits a clear potential to prevent weight gain and restricts adiposity in response to high-fat feeding.

Regulatory role of G protein-coupled estrogen receptor for vascular function and obesity.

We found that the selective stimulation of the intracellular, transmembrane G protein-coupled estrogen receptor (GPER), also known as GPR30, acutely lowers blood pressure after infusion in normotensive rats and dilates both rodent and human arterial blood vessels. Stimulation of GPER blocks vasoconstrictor-induced changes in intracellular calcium concentrations and vascular tone, as well as serum-stimulated cell proliferation of human vascular smooth muscle cells. Deletion of the GPER gene in mice abrogates vascular effects of GPER activation and is associated with visceral obesity. These findings suggest novel roles for GPER in protecting from cardiovascular disease and obesity.

Evaluation of the safety and immunogenicity of pneumococcal seven-valent conjugate vaccine (Prevenar) administered in previously unvaccinated Spanish children aged 24 to 36 months.

This study evaluates the safety and immunogenicity of pneumococcal seven-valent conjugate vaccine (Prevenar) in 115 children, aged 2-3 years (24-36 months), who have not been previously vaccinated with Prevenar. SAFETY: As for local reactions, 40% of children reported erythema, 32.2% induration and 39.1% tenderness at the injection site. Regarding systemic reactions, fever > or 38 C was recorded in 7% of patients. Other commonly reported events were decreased appetite (24.3%), restlessness (20%), and fussiness (18.3%). IMMUNOGENICITY: After vaccination, more than 98% of the subjects achieved antibody levels of > or = 0.15 microg/mL for all seven serotypes and more than 95% achieved antibody levels > or = 0.50 microg/mL for all serotypes. CONCLUSIONS: Pneumococcal seven-valent conjugate vaccine (Prevenar) was safe, well tolerated and highly immunogenic when administered in previously unvaccinated children aged 14-36 months.