RESUMO
Exercise is accepted as a method to improve weight loss maintenance; however, the mechanisms by which this occurs have yet to be elucidated. In this pilot study, 13 women with obesity underwent a structured weight loss program (goal 8%-10% weight loss) and were then randomized to either a 12-wk diet (n = 7) or an aerobic exercise training (n = 6) intervention aimed at maintaining weight loss. At baseline, post-weight loss, and following the weight loss maintenance interventions, measurements of appetite (hunger and satiety) and appetite-regulating hormones (leptin, ghrelin, peptide tyrosine tyrosine, and glucagon-like peptide 1) were obtained after an overnight fast and for 3 h after a standardized test meal. Ad libitum energy intake was measured at a lunch meal. During the weight loss phase, participants lost 9.1% ± 1.1% of baseline body weight. Participants in both groups maintained weight loss during the 12-wk weight loss maintenance intervention. No differences in fasting leptin (P = 0.68) or in ghrelin (P = 0.30), peptide tyrosine tyrosine (P = 0.93), and glucagon-like peptide 1 (P = 0.98) area under the curve were detected between groups. Similarly, ratings of hunger (P = 0.99) and satiety (P = 0.65) area under the curve after the standardized test meal also did not differ between the groups nor did ad libitum energy intake at lunch. In summary, the 12-wk diet and exercise interventions were equally effective at maintaining weight loss in women, and no differences in measures of appetite regulation and food intake were found.
RESUMO
OBJECTIVE: To evaluate the hypothesis that metabolic measures (fasting glucose, insulin, and Homeostatic Model of Assessment for Insulin Resistance [HOMA-IR] levels) are inversely associated with performance on cognitive tasks using data from young (4- to 6-year-old), typically developing, healthy children. STUDY DESIGN: Data were obtained from children participating in the Healthy Start study, a pre-birth cohort in Colorado. HOMA-IR, glucose, and insulin values were centered and scaled using the study sample means and SD. Thus, they are reported in number of SD units from the mean. Fully corrected T scores for inhibitory control (Flanker task), cognitive flexibility (Dimensional Change Card Sort test), and receptive language (Picture Vocabulary test) were obtained via the National Institutes of Health Toolbox cognition battery. RESULTS: Children included in this analysis (n = 137) were 4.6 years old, on average. Per 1-SD unit, fasting glucose (B = -2.0, 95% CI -3.5, -0.5), insulin (B = -1.7, 95% CI -3.0, -0.4), and HOMA-IR values (B = -1.8, 95% CI -3.1, -0.5) were each significantly and inversely associated with inhibitory control (P < .05 for all, respectively). Fasting glucose levels were also inversely associated with cognitive flexibility (B = -2.0, 95% CI -3.7, -0.2, P = .03). CONCLUSIONS: Our data suggest that metabolic health may impact fluid cognitive function in healthy, young children.
Assuntos
Biomarcadores/sangue , Glicemia/análise , Cognição , Insulina/metabolismo , Criança , Pré-Escolar , Transtornos Cognitivos/sangue , Estudos de Coortes , Colorado/epidemiologia , Jejum , Feminino , Homeostase , Humanos , Insulina/sangue , Resistência à Insulina , Idioma , Masculino , Mães , Testes Neuropsicológicos , Análise de RegressãoRESUMO
While current treatments for schizophrenia often provide much relief for positive symptoms such as hallucinations, other symptoms, particularly cognitive deficits, persist and contribute to substantial suffering and reduced quality of life for patients. In searching for novel therapeutic avenues to treat cognitive deficits in schizophrenia, recent work is exploring nicotinic receptor neurobiology. Supported by a large body of evidence, with contributions from studies of smoking behaviors, genetics, receptor distribution and function, animal models and nicotinic effects on illness symptoms, the alpha7 nicotinic receptor has emerged as a potential therapeutic target. Despite promise in early clinical trials, however, no drug targeting nicotinic systems has succeeded in larger phase 3 trials. Following a brief review of nicotinic receptor biology and the evidence that has led to pursuit of alpha7 nicotinic agonism as a therapeutic strategy, this review will provide an update on the status of recent trials, discuss potential issues that may have contributed to negative outcomes, and point to new directions and promising advances in developing alpha7 nicotinic receptor-based treatment for cognitive symptoms in schizophrenia. IMPLICATIONS: By examining alpha7 nicotinic receptor biology and recent efforts to target the receptor in clinical trials, it is hoped that investigators will be motivated to explore novel, promising directions focusing on the receptor as a strategy to treat cognitive symptoms in schizophrenia.