RESUMO
Both subjective and objectively measured social status has been associated with multiple health outcomes, including weight status, but the mechanism for this relationship remains unclear. Experimental studies may help identify the causal mechanisms underlying low social standing as a pathway for obesity. Our objective was to investigate the effects of experimentally manipulated social status on ad libitum acute dietary intakes and stress-related outcomes as potential mechanisms relating social status and weight. This was a pilot feasibility, randomized, crossover study in Hispanic young adults (n=9; age 19-25; 67% female; BMI ≥18.5 and ≤30kg/m(2)). At visit 1, participants consumed a standardized breakfast and were randomized to a high social status position (HIGH) or low social status position (LOW) in a rigged game of Monopoly™. The rules for the game differed substantially in terms of degree of 'privilege' depending on randomization to HIGH or LOW. Following Monopoly™, participants were given an ad libitum buffet meal and energy intakes (kcal) were estimated by pre- and post-weighing foods consumed. Stress-related markers were measured at baseline, after the game of Monopoly™, and after lunch. Visit 2 used the same standardized protocol; however, participants were exposed to the opposite social status condition. When compared to HIGH, participants in LOW consumed 130 more calories (p=0.07) and a significantly higher proportion of their daily calorie needs in the ad libitum buffet meal (39% in LOW versus 31% in HIGH; p=0.04). In LOW, participants reported decreased feelings of pride and powerfulness following Monopoly™ (p=0.05) and after their lunch meal (p=0.08). Relative to HIGH, participants in LOW demonstrated higher heart rates following Monopoly™ (p=0.06), but this relationship was not significant once lunch was consumed (p=0.31). Our pilot data suggest a possible causal relationship between experimentally manipulated low social status and increased acute energy intakes in Hispanic young adults, potentially influenced by decreased feelings of pride and powerfulness. Increased energy intake over time, resulting in positive energy balance, could contribute to increased risk for obesity, which could partially explain the observed relationship between low social standing and higher weight. Larger and longitudinal studies in a diverse sample need to be conducted to confirm findings, increase generalizability, and assess whether this relationship persists over time.
Assuntos
Ingestão de Alimentos/fisiologia , Ingestão de Energia/fisiologia , Comportamento Alimentar/fisiologia , Comportamento Alimentar/psicologia , Classe Social , Adulto , Antropometria , Pressão Sanguínea/fisiologia , Estudos Cross-Over , Dieta , Feminino , Preferências Alimentares , Frequência Cardíaca/fisiologia , Humanos , Masculino , Projetos Piloto , Reforço Psicológico , Fatores de Risco , Escala Visual Analógica , Adulto JovemRESUMO
UNLABELLED: Greater body mass is associated with a greater risk of mental health conditions and more frequent mental health treatment use. However, factors that might influence perceived mental health treatment need and mental health treatment use among those of greater weight, including hope thinking, trauma history and perceived mental health treatment stigma, are not well understood. OBJECTIVE: The objective of this study was to determine if hope thinking, trauma history and/or perceived mental health treatment stigma mediate the relationships of body mass index [BMI] with perceived mental health treatment need and mental health treatment use. METHOD: Primary care clinic patients in the Midwest United States (N = 196; BMI range = 18.5 to 47.0, mean = 29.26 ± 6.61, median = 27.90) were recruited to complete a battery of self-report measures that assessed perceived mental health treatment need, mental health treatment use, hope thinking (Trait Hope Scale), trauma history (a single-item traumatic event history screen from the posttraumatic stress disorder module of the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition), and perceived mental health treatment stigma (Stigma Scale for Receiving Psychological Help). RESULTS: Reduced hope thinking and a greater incidence of past trauma accounted for greater perceived mental health treatment need and greater mental health treatment use among those of greater BMI. BMI was not related to perceived unmet mental health treatment need. CONCLUSION: Increased perceived mental health treatment need and mental health treatment use among those of greater BMI may be explained by lower hope thinking and a greater incidence of trauma in this population. Heavier patients may benefit from interventions designed to augment hope and address traumatic histories.
Assuntos
Serviços de Saúde Mental/estatística & dados numéricos , Saúde Mental , Sobrepeso/psicologia , Aceitação pelo Paciente de Cuidados de Saúde/psicologia , Transtornos de Estresse Pós-Traumáticos/psicologia , Índice de Massa Corporal , Manual Diagnóstico e Estatístico de Transtornos Mentais , Comportamentos Relacionados com a Saúde , Necessidades e Demandas de Serviços de Saúde , Humanos , Sobrepeso/terapia , Qualidade de Vida , Percepção SocialRESUMO
BACKGROUND: Public health and clinical interventions for obesity in free-living adults may be diminished by individual compensation for the intervention. Approaches to predict weight outcomes do not account for all mechanisms of compensation, so they are not well suited to predict outcomes in free-living adults. Our objective was to quantify the range of compensation in energy intake or expenditure observed in human randomized controlled trials (RCTs). METHODS: We searched multiple databases (PubMed, CINAHL, SCOPUS, Cochrane, ProQuest, PsycInfo) up to 1 August 2012 for RCTs evaluating the effect of dietary and/or physical activity interventions on body weight/composition. INCLUSION CRITERIA: subjects per treatment arm ≥5; ≥1 week intervention; a reported outcome of body weight/body composition; the intervention was either a prescribed amount of over- or underfeeding and/or supervised or monitored physical activity was prescribed; ≥80% compliance; and an objective method was used to verify compliance with the intervention (for example, observation and electronic monitoring). Data were independently extracted and analyzed by multiple reviewers with consensus reached by discussion. We compared observed weight change with predicted weight change using two models that predict weight change accounting only for metabolic compensation. FINDINGS: Twenty-eight studies met inclusion criteria. Overfeeding studies indicate 96% less weight gain than expected if no compensation occurred. Dietary restriction and exercise studies may result in up to 12-44% and 55-64% less weight loss than expected, respectively, under an assumption of no behavioral compensation. INTERPRETATION: Compensation is substantial even in high-compliance conditions, resulting in far less weight change than would be expected. The simple algorithm we report allows for more realistic predictions of intervention effects in free-living populations by accounting for the significant compensation that occurs.
Assuntos
Ingestão de Energia/fisiologia , Metabolismo Energético/fisiologia , Obesidade/prevenção & controle , Saúde Pública , Redução de Peso/fisiologia , Adulto , Algoritmos , Humanos , Valor Preditivo dos Testes , Ensaios Clínicos Controlados Aleatórios como AssuntoRESUMO
BACKGROUND: Cellular glucose uptake can be enhanced by upregulating Ras signaling in either insulin-dependent or -independent manner. In presence of insulin and intact insulin signaling, Ras has a negligible role in glucose uptake. Conversely, when insulin signaling is impaired in obesity or diabetes, the insulin-independent Ras pathway may be valuable for enhancing glucose disposal. We previously reported that Ad36, a human adenovirus, enhances cellular glucose uptake by upregulating the Ras/Glut4 pathway. Here, we investigated if Ad36-upregulated Ras via the insulin-independent pathway, to enhance glucose uptake. Furthermore, uncontrolled upregulation of Ras is linked with oncogenic cell transformation, if the tumor-suppressor gene p53 is also downregulated. Hence, we determined if upregulation of Ras by Ad36 would induce oncogenic cell transformation. Finally, we determined the relevance of Ad36 to insulin resistance in humans. METHODS: Insulin receptor (IR) was knocked down with small interfering RNA in 3T3-L1 adipocytes, to determine if Ad36 increases the Ras/Glut4 pathway and glucose uptake without IR-signaling. Next, the effects of Ad36 on cell transformation and p53 abundance were determined. Finally, overweight or obese women were screened for seropositivity to Ad36, as an indicator of natural Ad36 infection. Associations of Ad36 infection with adiposity and C-reactive proteins (CRPs)-two key markers of insulin resistance, and with glucose disposal, were determined. RESULTS: Unaffected by IR knock-down, Ad36 significantly increased the Ras pathway, Glut4 translocation and glucose uptake in 3T3-L1 adipocytes. Despite Ras upregulation, Ad36 did not transform 3T3-L1 cells. This may be because Ad36 significantly increased p53 protein in 3T3-L1 cells or mice adipose tissue. Ad36 seropositivity was associated with greater adiposity and CRP levels, yet a significantly higher systemic glucose disposal rate. CONCLUSIONS: Overall, the study offers Ras/Glut4 pathway as an alternate to enhance glucose disposal when insulin signaling is impaired, and, importantly, provides Ad36 as a tool to understand the modulation of that pathway.
Assuntos
Infecções por Adenovirus Humanos/diagnóstico , Adenovírus Humanos/isolamento & purificação , Transportador de Glucose Tipo 4/metabolismo , Glucose/metabolismo , Receptor de Insulina/metabolismo , Proteínas ras/metabolismo , Células 3T3-L1 , Animais , Western Blotting , Técnicas de Cultura de Células , Feminino , Genes p53/genética , Transportador de Glucose Tipo 4/genética , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Reação em Cadeia da Polimerase em Tempo Real , Transdução de Sinais , Regulação para Cima , Proteínas ras/genéticaRESUMO
Drugs that improve chronic hyperglycemia independently of insulin signaling or reduction of adiposity or dietary fat intake may be highly desirable. Ad36, a human adenovirus, promotes glucose uptake in vitro independently of adiposity or proximal insulin signaling. We tested the ability of Ad36 to improve glycemic control in vivo and determined if the natural Ad36 infection in humans is associated with better glycemic control. C57BL/6J mice fed a chow diet or made diabetic with a high-fat (HF) diet were mock infected or infected with Ad36 or adenovirus Ad2 as a control for infection. Postinfection (pi), systemic glycemic control, hepatic lipid content, and cell signaling in tissues pertinent to glucose metabolism were determined. Next, sera of 1,507 adults and children were screened for Ad36 antibodies as an indicator of past natural infection. In chow-fed mice, Ad36 significantly improved glycemic control for 12 wk pi. In HF-fed mice, Ad36 improved glycemic control and hepatic steatosis up to 20 wk pi. In adipose tissue (AT), skeletal muscle (SM), and liver, Ad36 upregulated distal insulin signaling without recruiting the proximal insulin signaling. Cell signaling suggested that Ad36 increases AT and SM glucose uptake and reduces hepatic glucose release. In humans, Ad36 infection predicted better glycemic control and lower hepatic lipid content independently of age, sex, or adiposity. We conclude that Ad36 offers a novel tool to understand the pathways to improve hyperglycemia and hepatic steatosis independently of proximal insulin signaling, and despite a HF diet. This metabolic engineering by Ad36 appears relevant to humans for developing more practical and effective antidiabetic approaches.