RESUMO
Vitamin D deficiency has been related with metabolic alterations in polycystic ovary syndrome (PCOS). As well, hyperactivation of adrenal axis can be programmed early in life and could be related later with PCOS development. Our aim was to establish the relationship between vitamin D and adrenal parameters with metabolic alterations and inflammation markers in PCOS. In 73 patients and 33 controls, 25-hydroxyvitamin D (25-OH-D), total and bioavailable testosterone (TT and bioT), androstenedione (A4), SHBG, cortisol, insulin, and C-reactive protein (hs-CRP) were determined; HOMA and lipid accumulation product (LAP) index were calculated. All parameters were higher in patients than in controls, except for SHBG and 25-OH-D which were lower. Binary regression analysis showed that differences in TT, bioT, A4, insulin and HOMA were independent of body mass index and waist circumference but SHBG, hs-CRP, LAP and 25-OH-D were related to body weight and fat distribution. Binary logistic regression analysis showed that cortisol and 25-OH-D could be associated to PCOS development. Correlations found between LAP and insulin, HOMA and hs-CRP confirm it is a good indicator of metabolic complications. Vitamin D and cortisol association to PCOS development justifies future research to understand the role of vitamin D in PCOS and analyze patient's perinatal history and its possible relationship with hyperactivation of adrenal axis in adult life.
Assuntos
Glândulas Suprarrenais/metabolismo , Biomarcadores/metabolismo , Inflamação/metabolismo , Síndrome do Ovário Policístico/metabolismo , Vitamina D/metabolismo , Adolescente , Corticosteroides/metabolismo , Adulto , Índice de Massa Corporal , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Obesidade/metabolismo , Deficiência de Vitamina D/metabolismo , Circunferência da Cintura/fisiologia , Adulto JovemAssuntos
Conexinas/genética , Perda Auditiva/genética , Mutação , Deleção de Sequência , Austrália/epidemiologia , Sequência de Bases/genética , Bélgica/epidemiologia , Brasil/epidemiologia , Conexina 26 , Conexina 30 , Análise Mutacional de DNA , Efeito Fundador , França/epidemiologia , Frequência do Gene , Haplótipos , Perda Auditiva/epidemiologia , Humanos , Israel/epidemiologia , Itália/epidemiologia , Espanha/epidemiologia , Reino Unido/epidemiologia , Estados Unidos/epidemiologiaRESUMO
Tuberculosis in seals is caused by Mycobacterium pinnipedii, a member of the Mycobacterium tuberculosis complex. In this study, we evaluated the extent of genetic variability among Mycobacterium bovis and M. pinnipedii by microarray-based comparative genomics. We identified two deletions that are exclusive to M. pinnipedii: PiD1 that removes the orthologues of the M. tuberculosis genes Rv3530c and Rv3531c, and PiD2 that encompasses genes Rv1977 and Rv1978. Interestingly, a deletion overlapping the previously described RD2 region was identified in some isolates of Mycobacterium microti and further characterised.