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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.

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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.

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This study aimed to review and synthesize the available scientific evidence on the relationship between serum 25(OH)D concentrations and glucose metabolism among adolescents. A total of 19 studies were included. Many studies did not find a relation between 25(OH)D concentrations and insulin sensitivity, but most studies have shown that vitamin D status influences glucose dysregulation in youth due to particularities of this life stage. Considering the prevalence of vitamin D deficiency and insufficiency were high among adolescents, the importance for vitamin D status correction in this young group, in which chronic diseases are not expected but getting every day more common, is mandatory.

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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.

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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.

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BACKGROUND: Because the role of 2-h postload glucose and insulin levels as confounders in the relationship between hypertriglyceridemia and development of metabolic glucose disorders (MGD) has not been elucidated, the aim of this study was to determine whether triglyceride levels ≥ 1.7 mmol/L are a risk factor of developing MGD in otherwise healthy men and women. METHODS: A total of 341 healthy men and non-pregnant women, 30 to 50 years of age, were enrolled in a 15-year follow-up study and allocated into the exposed (triglycerides ≥ 1.7 mmol/L) and non-exposed (triglycerides <1.7 mmol/L) groups. Follow-up visits were scheduled every 3 years to complete 5 visits (mean 3.8 visits). At final follow-up, about 15 years later (mean 13.6 years), contact was re-established in 236 individuals to complete 3540 person-years of follow-up. At baseline, all subjects in both groups were required to be free of impaired fasting glucose (IFG), impaired glucose tolerance (IGT), IFG+IGT, and type 2 diabetes. RESULTS: The Poisson regression models, adjusted by age, sex, family history of diabetes, waist circumference, body mass index, total body fat, blood pressure, fasting and postload glucose, fasting and postload insulin, and HOMA-IR index, showed a significant association between triglycerides ≥ 1.7 mmol/L and IFG (relative risk - RR - 1.40; 95% CI 1.2-2.2), IGT (RR 1.60; 95% CI 1.3-2.2), IFG+IGT (RR 1.80; 95% CI 1.5-2.7), and type 2 diabetes (RR 3.0; 95% CI 2.5-3.8). CONCLUSIONS: Serum triglyceride levels ≥ 1.7 mmol/L are an independent risk factor of developing IFG, IGT, IFG+IGT, and type 2 diabetes in young and middle-aged, men and women.

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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.

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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.

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OBJECTIVE: To compare BMI with abdominal skinfold thickness (ASF), waist circumference and waist-to-height ratio in the prediction of insulin resistance (IR) in prepubertal Colombian children. DESIGN: We calculated age- and sex-specific Z-scores for BMI, ASF, waist circumference, waist-to-height ratio and three other skinfold-thickness sites. Logistic regression with stepwise selection (P = 0·80 for entry and P = 0·05 for retention) was performed to identify predictors of IR and extreme IR, which were determined by age- and sex-specific Z-scores to identify the ≥ 90th and ≥ 95th percentile of homeostasis model assessment (HOMAIR), respectively. We used receiver operating characteristic curves to compare the area under the curve between models. SETTING: Bucaramanga, Colombia. SUBJECTS: Children (n 1261) aged 6-10 years in Tanner stage 1 from a population-based study. RESULTS: A total of 127 children (seventy girls and fifty-seven boys) were classified with IR, including sixty-three children (thirty-three girls and thirty boys) classified with extreme IR. Only ASF and BMI Z-scores were retained as predictors of IR by stepwise selection. Adding ASF Z-score to BMI Z-score improved the area under the curve from 0·794 (95 % CI 0·752, 0·837) to 0·811 (95 % CI 0·770, 0·851; P for contrast = 0·01). In predicting extreme IR, the addition of ASF Z-score to BMI Z-score improved the area under the curve from 0·837 (95 % CI 0·790, 0·884) to 0·864 (95 % CI 0·823, 0·905; P for contrast = 0·01). CONCLUSIONS: ASF Z-score predicted IR independent of BMI Z-score in our population of prepubertal children. ASF and BMI Z-scores together improved IR risk stratification compared with BMI Z-score alone, opening new perspectives in the prediction of cardiometabolic risk in prepubertal children.

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OBJECTIVE: To estimate the prevalence of altered metabolism of carbohydrates in patients with mild acute pancreatitis. METHODS: We included 85 patients diagnosed with pancreatitis. We used to evaluate prognosis Balthazar and Ranson criteria. All patients were interviewed and examined. Was performed routine laboratory and Oral glucose tolerance test (OGTT) We excluded patients with previous diagnosis of diabetes mellitus, alcoholic pancreatitis, severe hypertriglyceridemia and recurrent/ severe pancreatitis. RESULTS: 30 women and 27 men. After performing the OGTT were classified into three groups. Group 1 (n: 19): normal OGTT; Group 2 (n: 33): GAA, IHC, or both, and Group 3 (n = 5): with diabetes mellitus. Patients in group 3 had a higher average age (p = 0.02), and higher diastolic blood pressure (DBP) (p = 0.048). We observe a significant difference in fasting glucose values (p = 0.0001) and 120 minutes post-OGTT in all groups (p = 0.0001). HOMA was found higher (p = 0.031) in group 2. CONCLUSIONS: This study showing a link between mild acute pancreatitis and dysfunction of glucose metabolism, which found older patients, DBP and those with metabolic syndrome, had a higher prevalence of 65.66% of Pre diabetes and diabetes.

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