RESUMEN
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.
Asunto(s)
Dieta Alta en Grasa , Ginsenósidos/farmacología , Trastornos del Metabolismo de la Glucosa/prevención & control , Obesidad/complicaciones , Proteínas Quinasas Activadas por AMP/efectos de los fármacos , Proteínas Quinasas Activadas por AMP/metabolismo , Animales , Trastornos del Metabolismo de la Glucosa/etiología , Trastornos del Metabolismo de la Glucosa/metabolismo , Resistencia a la Insulina , Masculino , Ratones , Obesidad/metabolismo , Transducción de Señal , Factores de TiempoRESUMEN
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.
Asunto(s)
Animales , Masculino , Ratones , Dieta Alta en Grasa , Ginsenósidos/farmacología , Trastornos del Metabolismo de la Glucosa/prevención & control , Obesidad/complicaciones , Proteínas Quinasas Activadas por AMP/efectos de los fármacos , Proteínas Quinasas Activadas por AMP/metabolismo , Trastornos del Metabolismo de la Glucosa/etiología , Trastornos del Metabolismo de la Glucosa/metabolismo , Resistencia a la Insulina , Obesidad/metabolismo , Transducción de Señal , Factores de TiempoRESUMEN
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.
Asunto(s)
Fenómenos Fisiológicos Nutricionales de los Adolescentes , Medicina Basada en la Evidencia , Trastornos del Metabolismo de la Glucosa/etiología , Resistencia a la Insulina , Estado Nutricional , Deficiencia de Vitamina D/fisiopatología , Adolescente , Conducta del Adolescente , Desarrollo del Adolescente , Trastornos del Metabolismo de la Glucosa/prevención & control , Humanos , Prevalencia , Conducta Sedentaria , Índice de Severidad de la Enfermedad , Deficiencia de Vitamina D/epidemiología , Deficiencia de Vitamina D/metabolismoRESUMEN
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.
Asunto(s)
Conducta Alimentaria/fisiología , Intestinos/microbiología , Microbiota/fisiología , Proteína 4 Similar a la Angiopoyetina , Angiopoyetinas/metabolismo , Animales , Dieta Alta en Grasa/efectos adversos , Trastornos del Metabolismo de la Glucosa/etiología , Humanos , Hipertensión/etiología , Trastornos del Metabolismo de los Lípidos/etiología , Lipopolisacáridos/metabolismo , Obesidad/etiología , Prebióticos , Probióticos , Factores de RiesgoRESUMEN
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.
Asunto(s)
Animales , Humanos , Conducta Alimentaria/fisiología , Intestinos/microbiología , Microbiota/fisiología , Angiopoyetinas/metabolismo , Dieta Alta en Grasa/efectos adversos , Trastornos del Metabolismo de la Glucosa/etiología , Hipertensión/etiología , Trastornos del Metabolismo de los Lípidos/etiología , Lipopolisacáridos/metabolismo , Obesidad/etiología , Prebióticos , Probióticos , Factores de RiesgoRESUMEN
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.
Asunto(s)
Trastornos del Metabolismo de la Glucosa/etiología , Hipertrigliceridemia/complicaciones , Adulto , Glucemia/análisis , Diabetes Mellitus Tipo 2/etiología , Femenino , Estudios de Seguimiento , Intolerancia a la Glucosa/etiología , Humanos , Hipertrigliceridemia/sangre , Insulina/sangre , Masculino , Persona de Mediana Edad , Factores de Riesgo , Factores de TiempoRESUMEN
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.
Asunto(s)
Dieta Alta en Grasa/efectos adversos , Modelos Animales de Enfermedad , Intolerancia a la Glucosa/etiología , Trastornos del Metabolismo de la Glucosa/etiología , Resistencia a la Insulina , Obesidad/etiología , Animales , Ratones , Obesidad/fisiopatologíaRESUMEN
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.
Asunto(s)
Animales , Ratones , Modelos Animales de Enfermedad , Dieta Alta en Grasa/efectos adversos , Intolerancia a la Glucosa/etiología , Trastornos del Metabolismo de la Glucosa/etiología , Resistencia a la Insulina , Obesidad/etiología , Obesidad/fisiopatologíaRESUMEN
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.
Asunto(s)
Adiposidad , Índice de Masa Corporal , Resistencia a la Insulina , Grasa Intraabdominal , Obesidad/complicaciones , Grosor de los Pliegues Cutáneos , Abdomen , Área Bajo la Curva , Niño , Colombia/epidemiología , Femenino , Trastornos del Metabolismo de la Glucosa/epidemiología , Trastornos del Metabolismo de la Glucosa/etiología , Humanos , Modelos Logísticos , Masculino , Pubertad , Curva ROCRESUMEN
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.
Asunto(s)
Trastornos del Metabolismo de la Glucosa/etiología , Pancreatitis/complicaciones , Enfermedad Aguda , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Estudios de Seguimiento , Trastornos del Metabolismo de la Glucosa/diagnóstico , Trastornos del Metabolismo de la Glucosa/epidemiología , Prueba de Tolerancia a la Glucosa , Humanos , Masculino , Persona de Mediana Edad , Prevalencia , Estudios Prospectivos , Factores de Riesgo , Índice de Severidad de la EnfermedadRESUMEN
OBJECTIVE: This study examines the prevalence and correlates of poor glycemic control in Mexican Americans aged 75 years and older with diabetes. METHODS: Data are from the 5(th) wave (2004-05) of the Hispanic Established Population for the Epidemiological Study of the Elderly (H-EPESE). A total of 2,069 Mexican Americans aged 75 and over were interviewed. Six hundred eighty nine subjects (33.5%) reported having been diagnosed with diabetes and 209 (30.3%) subjects agreed to a blood test of their HbA(1)c level. RESULTS: Of the 209 diabetic subjects with an HbA(1)c test, 73 (34.9%) had good glycemic control (HbA(1)c <7%) and 136 (65.1%) had poor glycemic control (HbA(1)c >7%). Bivariate analysis revealed that subjects with poor control had longer disease duration, had lower education, used the glucometer more frequently, and had more diabetes-complications when compared to those in the good glycemic control group. Multivariable logistic regression analysis found the following factors associated with poor glycemic control: <8 years of education, foreign-born, smoking, obesity, longer disease duration, daily glucometer use, and having macro-complications. DISCUSSION: Prevalence of poor glycemic control is very high in this population with very high and rising prevalence of diabetes. Further studies are needed to explore the effect of these and other characteristics on glycemic control among older Mexican Americans and to develop appropriate interventions to improve diabetes outcomes and increase life-expectancy.
Asunto(s)
Diabetes Mellitus/terapia , Trastornos del Metabolismo de la Glucosa/etiología , Trastornos del Metabolismo de la Glucosa/prevención & control , Americanos Mexicanos/estadística & datos numéricos , Factores de Edad , Anciano , Anciano de 80 o más Años , Glucemia/metabolismo , Complicaciones de la Diabetes/epidemiología , Complicaciones de la Diabetes/etiología , Complicaciones de la Diabetes/prevención & control , Diabetes Mellitus/sangre , Diabetes Mellitus/epidemiología , Diabetes Mellitus/etnología , Femenino , Trastornos del Metabolismo de la Glucosa/epidemiología , Humanos , Masculino , Factores de Riesgo , Clase Social , Resultado del TratamientoRESUMEN
Insulin resistance condition is associated to the development of several syndromes, such as obesity, type 2 diabetes mellitus and metabolic syndrome. Although the factors linking insulin resistance to these syndromes are not precisely defined yet, evidence suggests that the elevated plasma free fatty acid (FFA) level plays an important role in the development of skeletal muscle insulin resistance. Accordantly, in vivo and in vitro exposure of skeletal muscle and myocytes to physiological concentrations of saturated fatty acids is associated with insulin resistance condition. Several mechanisms have been postulated to account for fatty acids-induced muscle insulin resistance, including Randle cycle, oxidative stress, inflammation and mitochondrial dysfunction. Here we reviewed experimental evidence supporting the involvement of each of these propositions in the development of skeletal muscle insulin resistance induced by saturated fatty acids and propose an integrative model placing mitochondrial dysfunction as an important and common factor to the other mechanisms.
Asunto(s)
Resistencia a la Insulina , Mitocondrias Musculares/metabolismo , Músculo Esquelético/metabolismo , Animales , Dieta Alta en Grasa/efectos adversos , Ácidos Grasos no Esterificados/sangre , Ácidos Grasos no Esterificados/metabolismo , Trastornos del Metabolismo de la Glucosa/etiología , Trastornos del Metabolismo de la Glucosa/metabolismo , Humanos , Inflamación/etiología , Inflamación/metabolismo , Músculo Esquelético/patología , Estrés OxidativoRESUMEN
Hyperandrogenemia predisposes an organism toward developing impaired insulin sensitivity. The aim of our study was to evaluate endocrine and metabolic effects during early allostasis induced by a fructose-rich diet (FRD) in normal (control; CT) and neonatal-androgenized (testosterone propionate; TP) female adult rats. CT and TP rats were fed either a normal diet (ND) or an FRD for 3 weeks immediately before the day of study, which was at age 100 days. Energy intake, body weight (BW), parametrial (PM) fat characteristics, and endocrine/metabolic biomarkers were then evaluated. Daily energy intake was similar in CT and TP rats regardless of the differences in diet. When compared with CT-ND rats, the TP-ND rats were heavier, had larger PM fat, and were characterized by basal hypoadiponectinemia and enhanced plasma levels of non-esterified fatty acid (NEFA), plasminogen activator inhibitor-1 (PAI-1), and leptin. FRD-fed CT rats, when compared with CT-ND rats, had high plasma levels of NEFA, triglyceride (TG), PAI-1, leptin, and adiponectin. The TP-FRD rats, when compared with TP-ND rats, displayed enhanced leptinemia and triglyceridemia, and were hyperinsulinemic, with glucose intolerance. The PM fat taken from TP rats displayed increase in the size of adipocytes, decrease in adiponectin (protein/gene), and a greater abundance of the leptin gene. PM adipocyte response to insulin was impaired in CT-FRD, TP-ND, and TP-FRD rats. A very short duration of isocaloric FRD intake in TP rats induced severe metabolic dysfunction at the reproductive age. Our study supports the hypothesis that the early-androgenized female rat phenotype is highly susceptible to developing endocrine/metabolic dysfunction. In turn, these abnormalities enhance the risk of metabolic syndrome, obesity, type 2 diabetes, and cardiovascular disease.
Asunto(s)
Tejido Adiposo/metabolismo , Andrógenos/metabolismo , Fructosa/farmacología , Trastornos del Metabolismo de la Glucosa/etiología , Hiperandrogenismo/complicaciones , Obesidad/etiología , Adipocitos/patología , Adipoquinas/metabolismo , Adiponectina/metabolismo , Adiposidad , Animales , Peso Corporal , Sacarosa en la Dieta/administración & dosificación , Sacarosa en la Dieta/farmacología , Modelos Animales de Enfermedad , Ingestión de Energía , Ácidos Grasos no Esterificados/sangre , Femenino , Genitales Femeninos , Trastornos del Metabolismo de la Glucosa/sangre , Trastornos del Metabolismo de la Glucosa/metabolismo , Hiperandrogenismo/sangre , Insulina/metabolismo , Leptina/sangre , Leptina/genética , Obesidad/sangre , Inhibidor 1 de Activador Plasminogénico/sangre , Ratas , Ratas Sprague-Dawley , Factores de Riesgo , Propionato de Testosterona/metabolismo , Triglicéridos/sangreRESUMEN
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.
Asunto(s)
Humanos , Masculino , Femenino , Niño , Adolescente , Circulación Sanguínea/fisiología , /patología , Dislipidemias/etiología , Obesidad/patología , Síndrome Metabólico/epidemiología , Síndrome Metabólico/fisiopatología , Trastornos del Metabolismo de la Glucosa/complicaciones , Trastornos del Metabolismo de la Glucosa/etiología , Aterosclerosis , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/patología , Hipertensión/etiología , Metabolismo de los Lípidos/inmunologíaRESUMEN
BACKGROUND: Although several lines of evidence suggest that hypomagnesaemia is a risk factor for developing type 2 diabetes, there are no studies regarding the association between hypomagnesaemia and the risk for developing impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Our objective was to examine the association between serum magnesium levels and the risk for developing IFG, IGT and type 2 diabetes. MATERIALS AND METHODS: A total of 1122 individuals (20-65 years of age) were enrolled between 1996 and 1997, and 817 individuals re-examined about 10 years later. New-onset IFG (5.6-7.0 mmol L(-1) fasting glucose), IGT (7.8-11.1 mmol L(-1) glucose 2-h postload), and type 2 diabetes were determined from the number of subjects who had these conditions at the second examination without evidence that they were present at the first one. The relative risk of new-onset metabolic glucose disorders and diabetes (dependent variables) was computed using Poisson regression model adjusted for age, sex, family history of diabetes, waist circumference and homeostasis model assessment for insulin resistance index. Serum magnesium levels of < 0.74 mmol L(-1) (independent variable) defined the exposed group. RESULTS: At baseline, 420 (51.4%) individuals had hypomagnesaemia. New-onset IFG and IGT was identified in 276 (33.8%) individuals. The relative risk for IFG, IGT and IFG + IGT was 1.11 (95% confidence interval, 0.5-5.1), 1.38 (95% confidence interval, 1.1-6.3) and 1.49 (95% confidence interval, 1.1-4.9), respectively. New-onset diabetes was identified in 78 (9.5%) individuals (relative risk 2.54; 95% confidence interval, 1.1-4.1). CONCLUSIONS: Hypomagnesaemia is independently associated with the development of IGT, IFG + IGT and type 2 diabetes, but not with the development of IFG.
Asunto(s)
Trastornos del Metabolismo de la Glucosa/etiología , Deficiencia de Magnesio/complicaciones , Magnesio/análisis , Adulto , Anciano , Glucemia/análisis , Colorimetría , Diabetes Mellitus Tipo 2/etiología , Femenino , Estudios de Seguimiento , Intolerancia a la Glucosa , Humanos , Masculino , Persona de Mediana Edad , RiesgoRESUMEN
In this paper we review the associations between maternal and child undernutrition with human capital and risk of adult diseases in low-income and middle-income countries. We analysed data from five long-standing prospective cohort studies from Brazil, Guatemala, India, the Philippines, and South Africa and noted that indices of maternal and child undernutrition (maternal height, birthweight, intrauterine growth restriction, and weight, height, and body-mass index at 2 years according to the new WHO growth standards) were related to adult outcomes (height, schooling, income or assets, offspring birthweight, body-mass index, glucose concentrations, blood pressure). We undertook systematic reviews of studies from low-income and middle-income countries for these outcomes and for indicators related to blood lipids, cardiovascular disease, lung and immune function, cancers, osteoporosis, and mental illness. Undernutrition was strongly associated, both in the review of published work and in new analyses, with shorter adult height, less schooling, reduced economic productivity, and--for women--lower offspring birthweight. Associations with adult disease indicators were not so clear-cut. Increased size at birth and in childhood were positively associated with adult body-mass index and to a lesser extent with blood pressure values, but not with blood glucose concentrations. In our new analyses and in published work, lower birthweight and undernutrition in childhood were risk factors for high glucose concentrations, blood pressure, and harmful lipid profiles once adult body-mass index and height were adjusted for, suggesting that rapid postnatal weight gain--especially after infancy--is linked to these conditions. The review of published works indicates that there is insufficient information about long-term changes in immune function, blood lipids, or osteoporosis indicators. Birthweight is positively associated with lung function and with the incidence of some cancers, and undernutrition could be associated with mental illness. We noted that height-for-age at 2 years was the best predictor of human capital and that undernutrition is associated with lower human capital. We conclude that damage suffered in early life leads to permanent impairment, and might also affect future generations. Its prevention will probably bring about important health, educational, and economic benefits. Chronic diseases are especially common in undernourished children who experience rapid weight gain after infancy.
Asunto(s)
Desnutrición/complicaciones , Adolescente , Adulto , Composición Corporal , Densidad Ósea , Enfermedades Cardiovasculares/etiología , Niño , Estudios de Cohortes , Femenino , Retardo del Crecimiento Fetal , Trastornos del Metabolismo de la Glucosa/etiología , Humanos , Madres , Factores de Riesgo , Factores SocioeconómicosRESUMEN
OBJECTIVE: To determine the prevalence of abnormalities of glucose metabolism in pediatric outpatients with cystic fibrosis (CF). STUDY DESIGN: Children and adolescents (n = 73, mean age 15.0 +/- 3.7 years) with CF not previously diagnosed with diabetes underwent 3-hour oral glucose tolerance testing. All subjects with CF were clinically stable and were not being treated for active infection. A reference group of young lean adults was used for comparison. Subjects were classified as having normal glucose tolerance (NGT) or abnormal glucose metabolism (AGM), including impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or diabetes, by standard criteria. The insulinogenic index was calculated as a measure of beta-cell function, and insulin resistance was estimated with the homeostatic model assessment. RESULTS: The reference group was significantly older than the patients with CF, but in the control subjects, the AGM and NGT were comparable in body mass index z-scores (-0.8 +/- 1.3, -0.6 +/- 1.1, -0.21 +/- 0.9 kg/m2). Thirty-eight percent of subjects with CF had AGM: 43% IGT, 29% IFG, 14% IGT/IFG, and 14% diabetes. In spite of distinct differences in glycemic response, the subjects with NGT and AGM had marked abnormalities of insulin secretion relative to the control subjects (Insulinogenic index 5.8 +/- 1.0, 5.3 +/- 0.8, and 53.5 +/- 10.0 uU/mL/mmol/L, respectively; P < .0001). Insulin sensitivity did not differ among the 3 groups, although there was a trend toward greater insulin resistance in the subjects with AGM (homeostatic model assessment: CF-NGT 1.5 +/- 0.2, CF-AGM 1.9 +/- 0.3, REF 1.3 +/- 0.1, P = NS). CONCLUSION: Abnormalities in glucose metabolism are frequent in young patients with CF without a prior diagnosis of diabetes and are associated with marked defects in insulin secretion. Given the poor beta-cell function in patients with CF, even small reductions in insulin sensitivity may be an important determinant of AGM.
Asunto(s)
Glucemia/metabolismo , Fibrosis Quística/metabolismo , Trastornos del Metabolismo de la Glucosa/epidemiología , Insulina/metabolismo , Adolescente , Adulto , Niño , Fibrosis Quística/complicaciones , Femenino , Trastornos del Metabolismo de la Glucosa/etiología , Prueba de Tolerancia a la Glucosa , Humanos , Secreción de Insulina , Masculino , PrevalenciaRESUMEN
Tens of dietary trials have been conducted to investigate the metabolic effects of sugar (sucrose) and its impact on human health. All of those studies took into account only the quantity of ingested sugar. By contrast, not a single study attempted to assess whether the form in which sugar is consumed plays a role in producing its metabolic effects. The failure of cohorts of researchers to specify how they administered sugar in their dietary trials may well explain why the results of those studies are extremely contradictory. These discrepant findings, understandably, resulted in conflicting opinions about sugar and in divergent guidelines about its recommended consumption. The evolutionary line of reasoning expounded in this article leads to conclude that the form in which sugar is ingested, not its quantity, constitutes the most important factor in producing the metabolic effects of sugar and its impact on human health. As a consequence, for example, the consumption of 100 g of sugar per day can be either detrimental or innocuous, depending on the form in which sugar is ingested. Specifically, the evolutionary hypothesis advanced in this paper implies that sugar can predispose to type 2 diabetes and can cause unhealthy changes in blood lipids if it is consumed in solid forms or in dense solutions containing more than 250 g/L, whereas sugar is harmless if it is consumed in more dilute concentrations. This evolutionary hypothesis, in view of its intuitively far-reaching clinical implications, should be tested by at least one dietary trial.