The molecular integration of nutrient- and pathogen-sensing pathways has become of great interest in understanding the mechanisms of insulin resistance in obesity. The double-stranded RNA-dependent protein kinase (PKR) is one candidate molecule that may provide cross talk between inflammatory and metabolic signaling. The present study was performed to determine, first, the role of PKR in modulating insulin action and glucose metabolism in physiological situations, and second, the role of PKR in insulin resistance in obese mice. We used Pkr(-/-) and Pkr(+/+) mice to investigate the role of PKR in modulating insulin sensitivity, glucose metabolism, and insulin signaling in liver, muscle, and adipose tissue in response to a high-fat diet. Our data show that in lean Pkr(-/-) mice, there is an improvement in insulin sensitivity, and in glucose tolerance, and a reduction in fasting blood glucose, probably related to a decrease in protein phosphatase 2A activity and a parallel increase in insulin-induced thymoma viral oncogene-1 (Akt) phosphorylation. PKR is activated in tissues of obese mice and can induce insulin resistance by directly binding to and inducing insulin receptor substrate (IRS)-1 serine307 phosphorylation or indirectly through modulation of c-Jun N-terminal kinase and inhibitor of κB kinase β. Pkr(-/-) mice were protected from high-fat diet-induced insulin resistance and glucose intolerance and showed improved insulin signaling associated with a reduction in c-Jun N-terminal kinase and inhibitor of κB kinase β phosphorylation in insulin-sensitive tissues. PKR may have a role in insulin sensitivity under normal physiological conditions, probably by modulating protein phosphatase 2A activity and serine-threonine kinase phosphorylation, and certainly, this kinase may represent a central mechanism for the integration of pathogen response and innate immunity with insulin action and metabolic pathways that are critical in obesity.
The authors of the above manuscript would like to apologize and retract it because in some paragraphs there are verbatim and unquoted sentences from others texts, although most of them, but not all, have been referenced. A corrected version of this review will be available in the next volume of Arq Bras Endocrinol Metab. This retraction confirm the integrity of papers published in Arq Bras Endocrinol Metab.
Obesity is a pandemic which has been rapidly developing for three decades. When a population is submitted to the same nutritional stress, some individuals are less susceptible to dietinduced weight gain and hyperglycemia. This observation suggests that other mechanisms are involved which are not directly related to the human genome. The human gut contains an immense number of microorganisms, collectively known as the microbiota. Evidence that gut microbiota composition can differ between obese and lean humans has led to the speculation that gut microbiota can participate in the pathophysiology of obesity. Different mechanisms have been proposed to explain the link between gut flora and obesity. The first mechanism consists in the role of the gut microbiota to increase energy extraction from indigestible dietary polysaccharides. The second, consists in the role of gut flora to modulate plasma lipopolysaccharide levels which triggers chronic low-grade inflammation leading to obesity and diabetes. A third mechanism proposes that gut microbiota may induce regulation of host genes that modulate how energy is expended and stored. However, further studies are needed to clarify a number of issues related to the relationship between the gut microbiota and obesity. Arq Bras Endocrinol Metab. 2009;53(2):139-144. KeywordsObesity; gut flora; energy extraction; lipopolysaccharide resumo A obesidade é uma pandemia que afeta milhões de pessoas em todo o mundo. Quando uma população é submetida ao mesmo estresse nutricional, alguns indivíduos são menos suscetíveis ao ganho de peso induzido pela dieta e à hiperglicemia. Essa observação sugere que outros mecanismos não diretamente relacionados ao genoma humano estejam envolvidos. O intestino humano é colonizado por milhões de bactérias, que coletivamente constituem a flora comensal normal. A evidência de que a composição da flora intestinal pode ser diferente em humanos magros e obesos levou à especulação de que a flora intestinal pode participar na fisiopatologia da obesidade. Diferentes mecanismos foram propostos para tentar explicar a correlação entre flora intestinal e obesidade. O primeiro mecanismo consiste no papel da flora intestinal na extração de energia de polissacarídeos não digeríveis. O segundo mecanismo envolve a modulação dos níveis de lipopolissacarídeo pela flora intestinal, o que desencadeia uma inflamação crônica subclínica que acarreta obesidade e diabetes. Um terceiro mecanismo propõe que a flora intestinal pode induzir a regulação de genes do hospedeiro que modulam como a energia é gasta e armazenada. Entretanto, estudos adicionais são necessários para estabelecer o papel da flora intestinal no desenvolvimento da obesidade. Arq Bras Endocrinol Metab. 2009;53(2):139-144. DescritoresObesidade; flora intestinal; extração de energia; lipopolissacarídeo
Objetivo: avaliar a prevalência de traumatismo dentário e fatores associados em adolescentes de 15 a 19 anos da cidade do Recife/PE. Metodologia: a amostra foi composta por 148 adolescentes de ambos os sexos. Os dados foram coletados por meio de exames clínicos e entrevistas realizadas nos intervalos das aulas. Os testes Qui-quadrado de Pearson e Exato de Fisher foram utilizados para verificar a associação entre as variáveis. O nível de significância utilizado foi de 5%. A prevalência encontrada foi de aproximadamente 15%. Resultados: os dentes mais afetados foram os incisivos centrais superiores. A maioria dos adolescentes apresentou um único dente atingido por trauma. As principais causas de trauma dental foram: brincando com outras pessoas (45,5%) e quedas (18,2%). Não houve associação entre a presença de traumatismo dental e overjet acentuado e/ou cobertura labial inadequada. Não foi observada diferença estatística entre prevalência de traumatismo e o sexo dos adolescentes. O tipo de escola não foi associado à presença de traumatismo. Conclusão: a prevalência de traumatismo dental em adolescentes de 15 a 19 anos de idade da cidade do Recife foi relativamente alta, porém não foi observada associação entre overjet e cobertura labial. Traumatismo dentário, Adolescentes, Prevalência. Objective: To evaluate the prevalence of traumatic tooth injuries and associated factors in Adolescents aged 15 to 19 years in the city of Recife, PE, Brazil. Method: The sample consisted of 148 adolescents of both genders. Data were collected by clinical examinations and interviews conducted between classes. Pearson's chi-square and Fisher's exact tests were used to assess the association among the variables. The significance level was set at 5%. The prevalence was approximately 15%. Results: The most affected teeth were the maxillary central incisors. Most adolescents had a single hit tooth trauma. The main causes of dental trauma were playing with someone (45.5%) and falls (18.2%). There was no association between dental trauma and severe overjet and/or inadequate lip coverage. There was no statistically significant difference (p>0.05) between the prevalence of trauma and gender of the adolescents. The type of school was not associated with the presence of traumatic tooth injuries. Conclusion: The prevalence of dental trauma in adolescents aged 15 to 19 years in Recife was relatively high, but no association was found between overjet and lip coverage.
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