RESUMO
BACKGROUND: In patients with major depressive disorder (MDD), poor antidepressant treatment response might be associated with an excessive body mass index (BMI). However, the impact of underweight on treatment response is unclear. Moreover, it has not been studied whether a continuous or categorical BMI measure should be used to predict of treatment response. METHODS: Post-hoc analysis of data collected in a clinical trial including adults with MDD (n=202) reporting outcomes of antidepressant medication, i.e. paroxetine, mirtazapine or paroxetine+mirtazapine. Measures included baseline BMI (underweight=BMI <18.5, normal weight:=BMI:18.5-23.9, overweight=BMI≥24) and symptom severity (17-item-Hamilton Depression scale; HAMD-17) assessed at weeks 0, 2, 3, 4, 6 and 8. Univariate analyses were used to explore the effect of baseline BMI on HAMD-17 reduction, response (defined as ≥50% HAMD-17 reduction) and remission (defined as HAMD-17 ≤7) at endpoint. Pearson correlation were used to explore the relationship between body weight, BMI as continuous measure and HAMD-17 reduction. Logistic regression was used to determine the predictors for remission. Multiple linear regression was used to establish the correlation of BMI with change of HAMD-17. RESULTS: 111 (55.0%) patients were normal weight, 20 (9.9%) were underweight, 71 (35.1%) were overweight. Underweight patients showed the best improvement to antidepressant treatment. Non-remitters had greater body weight and BMI than remitters (P<0.05). The reduction of HAMD-17 was correlated with baseline body weight (r=-0.16, P=0.032) and BMI (r=-0.19, P=0.012). Logistic regression found patients with BMI<24 to be 2 times (OR=1.958, 95%CI: 1.015, 3.774) remitters (P=0.045) than overweight patients. The multiple linear regression showed that the change of HAMD-17 total score decreased with increasing BMI (ß=-0.32, P = 0.016). CONCLUSION: We confirmed that BMI can predict treatment outcomes in MDD. For the first time we found that underweight patients benefit most from antidepressant treatment. The findings may be useful to physicians in their decision regarding the choice of antidepressants according to BMI.
Assuntos
Transtorno Depressivo Maior , Adulto , Antidepressivos/uso terapêutico , Índice de Massa Corporal , Transtorno Depressivo Maior/tratamento farmacológico , Transtorno Depressivo Maior/epidemiologia , Humanos , Paroxetina/uso terapêutico , Resultado do TratamentoRESUMO
This study aimed to verify the effects of berberine (BBR) on the fat metabolism proteins involved in the sirtuin 3 (SIRT3)/adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) pathway in the liver tissues of rats with high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD). Forty-eight rats were randomly divided into the normal control (NC) group, HFD group or BBR group, with 16 rats in each group. After 8 and 16 weeks of treatment, serum and liver samples were collected. Subsequently, body parameters, biochemical parameters and liver pathology were examined. The expression levels of proteins involved in the SIRT3/AMPK/ACC pathway in the liver were detected by Western blotting. After 8 and 16 weeks of a HFD, the successful establishment of rat models with different degrees of NAFLD was confirmed by hematoxylin and eosin (H&E) and Oil Red O staining. NAFLD rat models exhibited obesity and hyperlipidemia, and the protein expression levels of SIRT3, p-AMPK, p-ACC, and CPT-1A in the liver were significantly decreased compared to those in the NC group. The concurrent administration of BBR with the HFD effectively improved serum and liver lipid profiles and ameliorated liver injury. Furthermore, the protein expression levels of SIRT3, p-AMPK, p-ACC, and CPT-1A in the liver were significantly increased in the BBR group as compared with those in the HFD group. In conclusion, our data suggest that the mechanism by which BBR ameliorates HFD-induced hepatic steatosis may be related to the activation of the SIRT3/AMPK/ACC pathway in the liver.
Assuntos
Berberina/administração & dosagem , Dieta Hiperlipídica/efeitos adversos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Obesidade/induzido quimicamente , Transdução de Sinais/efeitos dos fármacos , Acetil-CoA Carboxilase/metabolismo , Adenilato Quinase/metabolismo , Animais , Berberina/farmacologia , Carnitina O-Palmitoiltransferase/metabolismo , Modelos Animais de Doenças , Metabolismo dos Lipídeos/efeitos dos fármacos , Masculino , Hepatopatia Gordurosa não Alcoólica/induzido quimicamente , Hepatopatia Gordurosa não Alcoólica/metabolismo , Obesidade/complicações , Obesidade/metabolismo , Fosforilação/efeitos dos fármacos , Distribuição Aleatória , Ratos , Sirtuínas/metabolismoRESUMO
This study evaluated the life quality of Chinese parents of preschool children with autism spectrum disorder (ASD) and their association with child social impairment and childcare burden. The participants included 406 families of children with ASD and 513 families with typically developing (TD) children. The findings indicated that parents in the ASD group had a lower quality of life than parents in the TD group, whereas only mother of children with ASD experienced a greater childcare burden than mother with TD children. Lower parental quality of life were associated with higher social impairment of children. To further clarify the correlativity of child social impairment, parental quality of life and childcare burden, the mediation analyses were conducted. The results showed that childcare burden mediated the influence of child social impairment on maternal quality of life, while it has no mediating effect on fathers. It implies that social impairment of children affects parental quality of life in different ways.