Obesidade induzida por consumo de dieta: modelo em roedores para o estudo dos distúrbios relacionados com a obesidade / Diet-induced obesity: rodent model for the study of obesity-related disorders

A obesidade vem aumentando significativamente em todo o mundo, e os fatores ambientais, como o consumo excessivo de alimentos e o sedentarismo, são os principais fatores relacionados com a gênese dessa doença. Em animais de laboratório, a gênese da obesidade está relacionada, em sua maioria, com mutações genéticas, porém esse modelo é muito distante do encontrado nos humanos. A adoção de dietas hipercalóricas ou hiperlipídicas vem sendo utilizada como modelo de indução da obesidade em animais, devido à sua semelhança com a gênese e às respostas metabólicas decorrentes da obesidade em humanos. Assim, o objetivo dessa revisão de literatura é apresentar os diferentes tipos de dietas utilizadas para a indução da obesidade em roedores, as modificações metabólicas induzidas e identificar alguns cuidados que devem ser tomados para que esse modelo seja eficaz para o estudo das complicações relacionadas com a obesidade. Realizou-se busca na base de dados PubMed utilizando as expressões: 1-"hipercaloric diet" AND "rodent", 2- "hiperlipidic diet" AND "rodent", sendo selecionadas aquelas consideradas mais relevantes a partir dos critérios: data de publicação (1995-2011), a utilização de animais wild type, a descrição detalhada sobre a dieta utilizada e a análise de parâmetros bioquímicos e vasculares de interesse. Foram inseridas referências para introduzir assuntos como o aumento da prevalência da obesidade e questões relacionadas com a gênese da obesidade em humanos. Podemos considerar eficiente o modelo de obesidade induzida por dieta em roedores quando o objetivo é o estudo da fisiopatologia das complicações metabólicas e vasculares associadas à obesidade.

Obesity has been significantly increasing worldwide, and environmental factors such as excessive food intake and sedentary lifestyle are the main factors related to the genesis of this disease. In laboratory animals, the genesis of obesity is related mostly to genetic mutations, but this model is far from that found in humans. The use of hypercaloric or hyperlipidemic diets has been used as a model of obesity induction in animals, because of its similarity to the genesis and metabolic responses caused by obesity in humans. The objective of this review is to show the different types of diets used to induce obesity in rodents, the induced metabolic alterations, and to identify some points that should be taken into account so that the model can be effective for the study of obesity-related complications. A search was performed in the PubMed database using the following keywords: 1- "hypercaloric diet" AND "rodent", 2- "hyperlipidic diet" AND "rodent", selecting those considered the most relevant according to the following criteria: date of publication (1995-2011); the use of wild-type animals; detailed description of the diet used and analysis of biochemical and vascular parameters of interest. References were included to introduce subjects such as the increased prevalence of obesity and questions related to the genesis of obesity in humans. The model of diet-induced obesity in rodents can be considered effective when the objective is the study of the physiopathology of metabolic and vascular complications associated with obesity.

Síndrome de ovarios poliquísticos, una mirada desde la ginecología infantojuvenil y el riesgo vascular / Polycystic ovary syndrome, a look from the infantile-juvenile Gynecology and the vascular risk

INTRODUCCIÓN: El síndrome de ovario poliquístico (SOP) constituye un dilema diagnóstico, con manifestaciones clínicometabólicas de alto riesgo. OBJETIVO: caracterizar variables de riesgo vascular en adolescentes con SOP, desde Enero 2007- Agosto 2010 asistidas en una consulta de Ginecología Infantojuvenil del Policlínico Felipe Rodríguez Ramos, San Antonio de los Baños. MÉTODOS: Se realizó un estudio casos/control desde enero 2007- agosto 2010 en el Policlínico Felipe Rodríguez Ramos, San Antonio de los Baños, con 2 grupos de 60 adolescentes muestreados aleatoriamente: A (con SOP), B (negativo), se definió: edad de la menarquia, cifras de tensión arterial según circunferencia abdominal (CA), relación índice masa corporal (IMC) Ýndice FSH/LH (realizado entre 3ro. y 5to. día del ciclo si menstruaba), niveles de glicemia, utilidad del ultrasonido transvaginal sobre el abdominal. RESULTADOS: La media global fue de 13,2 años para la menarquia, existió en el Grupo A tendencia a la izquierda según modelo Gaussiano. Tenían aumentada su CA, 42 de las pacientes con SOP, un 54,7 por ciento de ellas hipertensas, hubo correlación entre variables de -0,78. En el grupo A un 81,6 por ciento tuvo aumentado el IMC, igualmente las de menor índice de hormona folículo estimulante / hormona luteinizante (FSH/LH) (55 por ciento), con coeficiente de Spearman cercano a -1. Solo 37 pacientes del total presentaron cifras de glicemia alteradas, predominando la prediabetes (22,5 por ciento) significativo en A con alto riesgo relativo. La sensibilidad del ultrasonido transvaginal fue superior en ambos grupos, mayor en el A (0,55). CONCLUSIONES: Prehipertensas con distribución central de la grasa y mal control endocrino-metabólico, temprano debutan las adolescentes con SOP, potencializando el riesgo más allá de un buen diagnóstico ultrasonográfico

INTRODUCTION: The polycystic ovary syndrome (POS) is a diagnosis dilemma with clinical-metabolic manifestations of high risk. OBJECTIVE: To characterize the vascular risk variables in adolescents with POS from January, 2007 to August, 2020 treated in an infantile-juvenile Gynecology consultation of Felipe Rodríguez Ramos Polyclinic of San Antonio de los Baños municipality. METHODS: A case-control study was conducted from January, 2007 to August, 2010 in the above mentioned polyclinic with two groups of 6- adolescent each random sampled: A (with POS), B (negative), defining: age at menarche, figures of blood pressure according to abdominal circumference (AC), body mass index (BMI), FSH/LH (carried out the third and the fifth day of menstrual cycle if there was menstruation), glycemia levels, usefulness of transvaginal ultrasound (US) over the abdominal one. RESULTS: The global mean was of 13.2 years for menarche, in Group A there was a trend to left according to Gauss's model. In forty two patients with POS AC was increased, a 54.7 percent of them were hypertensive and a correlation of -0,78 between variables. In A group a 81.6 percent had increased her BMI, as well as those with a minor rate of FSH/LH (55 percent), with a Spearmen coefficient near of a -1. Only 37 patients of total had figures of altered glycemia, with significant predominance of pre-diabetes (22.5 percent) in A with a relative high risk. Sensitivity of transvaginal US was high in both groups, higher in the A group (0.55). CONCLUSIONS: In the pre-hypertensive group with a central distribution of fat and a poor endocrine-metabolic control there is an early onset in the adolescents with POS, strengthening the risk beyond a good ultrasonography diagnosis

Phospholipase D is involved in oxidative stress-induced migration of vascular smooth muscle cells via tyrosine phosphorylation and protein kinase C

Oxidative stress has been implicated in mediation of vascular disorders. In the presence of vanadate, H2O2 induced tyrosine phosphorylation of PLD1, protein kinase C-a (PKC-a), and other unidentified proteins in rat vascular smooth muscle cells (VSMCs). Interestingly, PLD1 was found to be constitutively associated with PKC-a in VSMCs. Stimulation of the cells by H2O2 and vanadate showed a concentration-dependent tyrosine phosphorylation of the proteins in PLD1 immunoprecipitates and activation of PLD. Pretreatment of the cells with the protein tyrosine kinase inhibitor, genistein resulted in a dose-dependent inhibition of H2O2-induced PLD activation. PKC inhibitor and down-regulation of PKC abolished H2O2-stimulated PLD activation. The cells stimulated by oxidative stress (H2O2) caused increased cell migration. This effect was prevented by the pretreatment of cells with tyrosine kinase inhibitors, PKC inhibitors, and 1-butanol, but not 3-butanol. Taken together, these results suggest that PLD might be involved in oxidative stress-induced migration of VSMCs, possibly via tyrosine phosphorylation and PKC activation.

Efectos oculares del suplemento de sacarosa en la dieta y su correlación con la cantidad de agregados plaquetarios circulantes en la rata

Varios modelos experimentales reproducen las manifestaciones oculares de la diabetes mellitus, así es el caso del modelo no diabético de suplemento de sacarosa en la rata, el cual es un modelo no diabético que reproduce la nagiopatía diabética, con secreción de insulina normal. Durante seis meses de experimentación, encontramos cambios oculares importantes como cataratas bilaterales, despoblación de las células ganglionares de la retina, así como hipoagregabilidad plaquetaria in vitro. Todo esto, en ausencia de niveles altos de glucosa en la sangre, indica una alta disponibilidad metabólica de la glucosa, lo que determina las lesiones en el cristalino y retina encontradas en este estudio. Este modelo experimental tambien confirma el desarrollo de la hipoagregabilidad plaquetaria in vitro, la cual puede ser atribuída a la estimulación de las plaquetas in vivo.