Envolvimento da inflamação subclínica e do estresse oxidativo na resistência à insulina associada a obesidade.
DOI:
https://doi.org/10.34019/1982-8047.2018.v44.16950Palavras-chave:
Pos-graduação em SaúdeResumo
A epidemia global da obesidade é um dos mais importantes problemas de saúde pública. Excessiva adiposidade é um crucial fator de risco no surgimento de várias doenças metabólicas, incluindo hipertensão, diabetes mellitus do tipo 2 e doença do fígado gorduroso não alcoólico. Essas condições patológicas estão estritamente associadas com a resistência à insulina. Baseado nos esforços das últimas décadas, ocorreu marcante desenvolvimento na investigação sobre resistência à insulina induzida pela obesidade, especialmente em termos do mecanismo envolvido neste processo. Dentre esses, a inflamação subclínica ou crônica de baixo grau na obesidade tem sido o mais aceito. Este estado inflamatório é caracterizado por altos níveis circulantes de citocinas inflamatórias, incluindo TNF alfa e IL beta, e aumentado infiltração de macrófagos em tecidos periféricos. No entanto, recentemente, tem ocorrido grande interesse no papel que o estresse oxidativo desempenha na indução da resistência à insulina. Sob ativação, muitas células imunes geram radicais livres e, da mesma maneira, a síntese de espécies reativas de oxigênio promovem um status inflamatório. Estudos têm mostrado níveis elevados de espécies reativas e estresse oxidativo em indivíduos e animais obesos e/ou resistentes a insulina; isso parece estar associado a redução da função e da atividade e biogênese mitocondrial causada pelo aumento de lipídeos circulantes e maior deposição de gordura ectópica. Essa revisão discorre sobre o mecanismo fisiopatológico de como a inflamação subclínica induz resistência à insulina na obesidade. Ainda, descreve o papel que o estresse oxidativo desempenha neste processo, bem como a produção de radicais livres na obesidade.
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