ABSTRACT
BACKGROUND/OBJECTIVES: Proinflammatory cytokines are increased in obese adipose tissue, including inflammasome key masters. Conversely, IL-18 protects against obesity and metabolic dysfunction. We focused on the IL-18 effect in controlling adipose tissue remodeling and metabolism. MATERIALS/SUBJECTS AND METHODS: We used C57BL/6 wild-type (WT) and interleukine-18 deficient (IL-18-/-) male mice fed a chow diet and samples from bariatric surgery patients. RESULTS: IL-18-/- mice showed increased adiposity and proinflammatory cytokine levels in adipose tissue, leading to glucose intolerance. IL-18 was widely secreted by stromal vascular fraction but not adipocytes from mice's fatty tissue. Chimeric model experiments indicated that IL-18 controls adipose tissue expansion through its presence in tissues other than bone marrow. However, IL-18 maintains glucose homeostasis when present in bone marrow cells. In humans with obesity, IL-18 expression in omental tissue was not correlated with BMI or body fat mass but negatively correlated with IRS1, GLUT-4, adiponectin, and PPARy expression. Also, the IL-18RAP receptor was negatively correlated with IL-18 expression. CONCLUSIONS: IL-18 signaling may control adipose tissue expansion and glucose metabolism, as its absence leads to spontaneous obesity and glucose intolerance in mice. We suggest that resistance to IL-18 signaling may be linked with worse glucose metabolism in humans with obesity.
Subject(s)
Adipose Tissue , Interleukin-18 , Mice, Inbred C57BL , Obesity , Animals , Interleukin-18/metabolism , Mice , Male , Adipose Tissue/metabolism , Humans , Obesity/metabolism , Glucose Intolerance/metabolism , Disease Models, Animal , Mice, KnockoutABSTRACT
Abstract Periodontal diseases (PD) are inflammatory conditions that affect the teeth supporting tissues. Increased body fat tissues may contribute to activation of the systemic inflammatory response, leading to comorbidities. Some studies have shown that individuals with obesity present higher incidence of PD than eutrophics. Objective: To investigate the impact of obesity on periodontal tissues and oral microbiota in mice. Methodology: Two obesity mice models were performed, one using 12 weeks of the dietary protocol with a high-fat (HF) diet in C57BL/6 mice and the other using leptin receptor-deficient mice (db/db-/-), which became spontaneously obese. After euthanasia, a DNA-DNA hybridization technique was employed to evaluate the microbiota composition and topical application of chlorhexidine (CHX), an antiseptic, was used to investigate the impact of the oral microbiota on the alveolar bone regarding obesity. Results: Increased adipose tissue may induce alveolar bone loss, neutrophil recruitment, and changes in the oral biofilm, similar to that observed in an experimental model of PD. Topical application of CHX impaired bone changes. Conclusion: Obesity may induce changes in the oral microbiota and neutrophil recruitment, which are associated with alveolar bone loss.
ABSTRACT
OBJETIVO: investigar a influência do risco nutricional, detectado ao início da internação, no desfecho terapêutico de pacientes.MÉTODOS: estudo de coorte prospectiva com 495 pacientes admitidos no pronto-atendimento de um hospital universitário, submetidos à triagem de risco nutricional com base no Nutritional Risk Screening, 2002. Ao final da internação, buscaram-se os prontuários para avaliação do desfecho, complicações e presença da terapia nutricional.RESULTADOS: do total de pacientes, 53,9% eram do sexo feminino, 71,3% tinham idade inferior a 60 anos e 11,7% evoluíram com cuidados paliativos/óbito. Segundo o índice de massa corporal, 15,5% dos pacientes foram classificados como desnutridos. O risco nutricional foi encontrado em 54,5% e associou-se fortemente ao desfecho terapêutico cuidados paliativos/óbito (HR: 5,92; IC 95%: 2,68-13,08), assim como seus componentes, estresse metabólico da doença (HR: 3,33; IC 95°%: 1,61-6,86) e estado nutricional prejudicado (moderado = HR: 3,24; IC 95°%: 1,31-8,00; grave = HR: 6,45; IC 95%: 2,36-17,63), após o ajuste por potenciais fatores de confusão.CONCLUSÃO: a prevalência de risco nutricional detectada foi alta e sua presença estava relacionada a pior desfecho terapêutico.
Objective: To investigate the influence of nutritional risk, detected upon being admitted to a hospital, on therapeutic outcomes in patients. Methods: This prospective cohort study was conducted with 495 patients admitted to the emergency clinic of a public hospital, where they were screened for nutritional risk based on the Nutritional Risk Screening 2002. At the end of hospitalization, the outcome, complications, and the presence of nutritional therapy were evaluated based on the medical records. Results: Of the total patients, 53.9% were female, 71.3% were less than 60 years of age, and 11.7% had the therapeutic outcome of palliative care / death. According to Body Mass Index (BMI), 15.5% of the patients were classified as malnourished. Nutritional risk was found in 54.5%, which correlated strongly with the therapeutic outcome of palliative care/death (HR: 5.92, 95% CI: 2.68 to 13.08) as well as their components of increased nutritional requirements (HR: 3.33, 95% CI: 1.61 to 6.86) and impaired nutritional status (HR = moderate: 3.24, 95% CI: 1.31 to 8.00, severe = HR: 6.45, 95% CI: 2.36 to 17.63) after adjustment for potential confounding factors. Conclusion: The prevalence of nutritional risk detected in the sample was high, and its presence was related to a poor therapeutic outcome.