ABSTRACT
Obesity and its consequent type 2 diabetes are significant threats to global health. Emerging evidence indicates that ginsenosides from ginseng (Panax ginseng) have anti-diabetic activity. We hypothesized that ginsenosides Rg1 could suppress dietary-induced obesity and improve obesity-related glucose metabolic disorders. Our results showed that ginsenoside Rg1 attenuated dietary-induced body weight gain and fat accumulation in white adipocyte tissue of mice fed a high-fat diet. Furthermore, we found that ginsenosides Rg1 not only decreased fasting glucose concentration and the 2-h postprandial glucose concentration, but also improved insulin resistance and glucose intolerance in those mice. Ginsenoside Rg1 also activated the AMPK pathway in vitro and in vivo and increased plasma membrane translocation of GLUT4 in C2C12 skeletal muscle cells. In conclusion, our observations suggested that ginsenoside Rg1 inhibited dietary-induced obesity and improved obesity-related insulin resistance and glucose intolerance by activation of the AMPK pathway.
Subject(s)
Animals , Male , Mice , Diet, High-Fat , Ginsenosides/pharmacology , Glucose Metabolism Disorders/prevention & control , Obesity/complications , AMP-Activated Protein Kinases/drug effects , AMP-Activated Protein Kinases/metabolism , Glucose Metabolism Disorders/etiology , Glucose Metabolism Disorders/metabolism , Insulin Resistance , Obesity/metabolism , Signal Transduction , Time FactorsABSTRACT
A microbiota intestinal, adquirida no período pós-natal, é composta por grande diversidade de bactérias que desempenham diferentes funções no hospedeiro humano, entre elas a absorção de nutrientes, proteção contra patógenos e modulação do sistema imune. O conteúdo bacteriano intestinal ainda não é totalmente conhecido, mas sabe-se que é influenciado por fatores internos e principalmente externos que modulam sua composição e função. Estudos indicam que a microbiota intestinal difere em indivíduos magros e obesos e ainda naqueles que mantêm hábitos alimentares diferentes. Há evidências de que as relações entre dieta, inflamação, resistência à insulina e risco cardiometabólico são em parte mediadas pela composição de bactérias intestinais. Conhecimentos sobre a microbiota poderão reverter em diferentes estratégias para manipular as populações bacterianas e promover saúde. Esta revisão aborda a relevância do conhecimento sobre o papel de fatores ou padrões alimentares na composição da microbiota, assim como mecanismos fisiopatológicos de doenças metabólicas crônicas e as potencialidades de prebióticos e probióticos sobre o perfil de risco cardiometabólico.
The gut microbiota obtained after birth is composed of a large range of bacteria that play different roles in the human host, such as nutrient uptake, protection against pathogens and immune modulation. The intestinal bacterial content is not completely known, but it is influenced by internal, and mainly by external factors, which modulate its composition and function. Studies indicate that the gut microbiota differs in lean and obese individuals, and in individuals with different food habits. There is evidence that the relationship between diet, inflammation, insulin resistance, and cardiometabolic risk are, in part, mediated by the composition of intestinal bacteria. Knowledge about the gut microbiota may result in different strategies to manipulate bacterial populations and promote health. This review discusses the relevance of understanding the role of dietary factors or patterns in the composition of the microbiota, as well as pathophysiological mechanisms of chronic metabolic diseases, and the potential of prebiotics and probiotics on the cardiometabolic risk profile.
Subject(s)
Animals , Humans , Feeding Behavior/physiology , Intestines/microbiology , Microbiota/physiology , Angiopoietins/metabolism , Diet, High-Fat/adverse effects , Glucose Metabolism Disorders/etiology , Hypertension/etiology , Lipid Metabolism Disorders/etiology , Lipopolysaccharides/metabolism , Obesity/etiology , Prebiotics , Probiotics , Risk FactorsABSTRACT
OBJETIVO: Validar um modelo de obesidade induzida por dieta hiperlipídica, de baixo custo, fácil reprodutibilidade, que mimetizasse características observadas no humano e viabilizasse posteriores proposições terapêuticas. MATERIAIS E MÉTODOS: Dezesseis camundongos Swiss receberam dieta padrão (DP) ou dieta hiperlipídica (DH), durante 10 semanas. RESULTADOS: Embora o grupo DP tenha apresentado maior consumo de água (p < 0,01) e ração (p < 0,001), o grupo DH apresentou maior ganho de peso corpóreo (p < 0,5) e aumento de coxins adiposos (p < 0,001), favorecendo maior índice de adiposidade (p < 0,001), glicemia (p < 0,01) e área sob a curva nos testes de tolerância à insulina (p < 0,001) e à glicose (p < 0,01). CONCLUSÃO: Validou-se um modelo de obesidade induzida por dieta hiperlipídica associada à resistência à ação da insulina e à intolerância à glicose, em um período de 10 semanas.
OBJECTIVE: Validate a model of high-fat diet-induced obesity, of low cost, easy reproducibility, that could express characteristics observed in human, and would enable subsequent therapy proposals. MATERIALS AND METHODS: Sixteen Swiss mice received a standard diet (DP) or high-fat diet (DH) for 10 weeks. RESULTS: Although the DP group had greater water (p < 0.01) and feed (p < 0.001) consumption, the DH group had greater body weight (p < 0.5) and adipose tissue gain (p < 0.001), favoring higher adiposity index (p < 0.001), glucose (p < 0.01), and area under the curve in the insulin (p < 0.001) and glucose (p < 0.01) tolerance tests. CONCLUSION: A high-fat diet-induced obesity model has been validated, which was also associated with insulin resistance and glucose intolerance after a period of 10 weeks.
Subject(s)
Animals , Mice , Disease Models, Animal , Diet, High-Fat/adverse effects , Glucose Intolerance/etiology , Glucose Metabolism Disorders/etiology , Insulin Resistance , Obesity/etiology , Obesity/physiopathologyABSTRACT
La obesidad es uno de los componentes del síndrome metabólico. Este último diagnóstico pudiese implicar en algunos casos mayor riesgo de desarrollo de complicaciones cardio-metabólicas en la edad adulta, más frecuentes en los niños y adolescentes obesos con antecedentes familiares, los cuales mejoran con el manejo adecuado del peso. esta situación constituye un motivo de preocupación para el pediatra, por la mayor probabilidad de persistencia en la edad adulta y porque constituye un factor de riesgo en la aparición de enfermedades crónicas no transmisibles del adulto (ECNT): hipertensión, perfil lipídico anormal, diabetes tipo 2, síndrome metabólico y enfermedad cardiovascular ateroesclerótica. El síndrome metabólico (SM) consiste en la asociación de un conjunto de indicadores antropométricos, bioquímicos y fisiológicos que implican mayor riesgo para el desarrollo de enfermedad cardio-metabólica. Aún existen controversias en cuanto a los criterios diagnósticos y a los valores límite para su clasificación (puntos de corte), la prevalencia es mayor en niños, niñas y adolescentes obesos que en aquellos con peso normal. Esta discrepancia en los criterios ha ocasionado confusión, dificultad al comparar estudios y poblaciones, y para establecer las implicaciones clínicas del síndrome. En el presente artículo se revisan los aspectos epidemiológicos, factores de riesgo, algunos componentes del síndrome (obesidad, dislipidemia, presión arterial alta y resistencia a la insulina) y los criterios actuales para el diagnóstico en niños y adolescentes.
Obesity is one of the components of metabolic syndrome. This diagnosis in some cases may involve greater risk of developing cardiometabolic complications in the adult age, more common in obese children and adolescents with family history, which improve with proper handling of weight. This situation is a matter of concern to the pediatrician for the likelyhood to persist into adulthood and because it constitutes a risk factor of the onset of chronic non-communicable diseases in adults, such as hypertension, abnormal lipid profile, diabetes type 2, metabolic syndrome and atherosclerotic cardiovascular disease. The metabolic syndrome (MS) is the association of a set of anthropometric, biochemical and physiological signs that involve higher risk for developing cardio-metabolic disease. Although there are some controversies regarding the diagnostic criteria and cut-off points, the prevalence is higher in obese children and adolescents than in those with normal weight. This discrepancy in the criteria has caused confusion, difficulty in comparing studies and populations, and also to establish the clinical implications of the syndrome. In this article will review the epidemiological aspects, risk factors, some components of the syndrome (obesity, dyslipidemia, high blood pressure and insulin resistance) and the current criteria for diagnosis in children and adolescents.