Vaccination in the context of the COVID-19 pandemic.

In this review, we described the history of vaccination, the different types of vaccines, and how vaccination coverage has been affected by the current COVID-19 pandemic. The effectiveness of the vaccines under metabolic host conditions is analyzed, especially when people have lost their immunocompetence, such as in patients with chronic kidney disease who are in dialysis treatment. Vaccines are produced in a variety of industrial methods, modifying costs. The novel field of vaccinomics includes the set of immune responses, the satisfactory levels of neutralizing antibodies, the production of metabolites, and the induction of protein expression. Finally, an analysis is made of the confusing messages regarding vaccination that are disseminated on social networks, and general recommendations are given.

En esta revisión se describen el historial de vacunación, los diferentes tipos de vacunas y cómo la cobertura de vacunación se ha visto afectada por la pandemia actual de COVID-19. Se analiza la efectividad de las vacunas en condiciones metabólicas del huésped, especialmente cuando las personas han perdido su inmunocompetencia, como los pacientes con enfermedad renal crónica que están en tratamiento de diálisis. Las vacunas se producen con una variedad de métodos industriales, modificando los costos. El nuevo campo de la vacunómica incluye el conjunto de respuestas inmunitarias, los niveles satisfactorios de anticuerpos neutralizantes, la producción de metabolitos y la inducción de la expresión de proteínas. Finalmente, se analizan los confusos mensajes sobre vacunación que se difunden en las redes sociales y se dan recomendaciones generales.

Growth hormone ameliorates high glucose-induced steatosis on in vitro cultured human HepG2 hepatocytes by inhibiting de novo lipogenesis via ChREBP and FAS suppression.

OBJECTIVE: Growth hormone (GH) deficiency has been associated with increased steatosis but the molecular mechanism has not been fully elucidated. We investigated the effect of GH on lipid accumulation of HepG2 cells cultured on an in vitro steatosis model and examined the potential involvement of insulin-like growth factor 1 (IGF-1) as well as lipogenic and lipolytic molecules. METHODS: Control and steatosis conditions were induced by culturing HepG2 cells with 5.5 or 25 mmol/l glucose for 24 h, respectively. Afterward, cells were exposed to 0, 5, 10 or 20 ng/ml GH for another 24 h. Lipid content was quantified as well as mRNA and protein levels of IGF-1, carbohydrate responsive element-binding protein (ChREBP), sterol regulatory element-binding protein 1c (SREBP1c), fatty acid synthase (FAS), carnitine palmitoyltransferase 1A (CPT1A), and peroxisome proliferator-activated receptor alpha (PPAR-alpha) by qPCR and western blot, respectively. Data were analyzed by one-way ANOVA and the Games-Howell post-hoc test. RESULTS: In the steatosis model, HepG2 hepatocytes showed a significant 2-fold increase in lipid amount as compared to control cells. IGF-1 mRNA and protein levels were significantly increased in control cells exposed to 10 ng/ml GH, whereas high glucose abolished this effect. High glucose also significantly increased both mRNA and protein of ChREBP and FAS without having effect on SREBP1c, CPT1A and PPAR-alpha. However, GH inhibited ChREBP and FAS production, even in HepG2 hepatocytes cultured under steatosis conditions. CONCLUSIONS: Growth hormone ameliorates high glucose-induced steatosis in HepG2 cells by suppressing de novo lipogenesis via ChREBP and FAS down-regulation.