Relación entre el funcionamiento familiar y el cumplimiento del cuidador en la atención a personas con autismo / Relationship between family functioning and compliance of the caregiver in the care of people with autism

Objetivo: determinar la relación entre el funcionamiento familiar y el cumplimiento del cuidador en la atención a personas con autismo. Material y métodos: estudio analítico, descriptivo y de corte transversal. La muestra fue de 31 cuidadores de personas con autismo. Para la recolección de los datos se usó como instrumentos, cuestionarios para determinar el funcionamiento familiar y el cumplimiento de la atención, previamente a la recolección de datos se sometió el instrumento utilizado a una prueba de confiabilidad a través de la prueba piloto. Para el procesamiento de datos se utilizó el programa SPSS y para el análisis estadístico la prueba de correlación de Pearson. Resultados: el desempeño familiar funcional en el hogar de la persona con autismo obtuvo un 51,6 por ciento en el total de cuidadores, donde la dimensión ©afectividad¯ alcanzó un mayor nivel (8,4 puntos). El 58,1 por ciento presentó un cumplimiento eficiente en la atención a las personas con autismo y la dimensión cognitiva alcanzo un mayor nivel con 14,2 ptos., la correlación es r =0,445. Conclusiones: la relación entre el funcionamiento familiar y el cumplimiento del cuidador en la atención a las personas con autismo presentan una correlación positiva y significativa, el cual indica que a puntajes altos de funcionamiento familiar le corresponde puntajes altos de cumplimiento en la atención y viceversa en puntajes bajos.

Objetive: To determine the relationship between family functioning and compliance of the caregiver in caring for people with autism. Material and Methods: Analytical, descriptive and cross-sectional studio. The sample consisted of 31 caregivers of people with autism. For data collection questionnaire was used as tools to determine family functioning and compliance of care prior to the data collection instrument used to test reliability through the pilot was subjected. For data processing we used SPSS and statistical analysis was Pearson correlation test. Results: Showed that functional family functioning in the home of the person with autism scored one (51.6 percent) of all careers. Being affectivity dimension who reached a higher level (8.4 points). The (58.1 percent) presented efficient fulfillment in caring for people with autism and cognitive dimension reached a higher level (14.2ptos). Conclusions. The relationship between family functioning and compliance with the caregiver in caring for people with autism have a positive and statistically significant correlation, indicating that higher scores on family functioning corresponds compliance high scores on attention and vice versa in low scores.

TLE3 is a dual-function transcriptional coregulator of adipogenesis.

PPARγ and Wnt signaling are central positive and negative regulators of adipogenesis, respectively. Here we identify the groucho family member TLE3 as a transcriptional integrator of the PPARγ and Wnt pathways. TLE3 is a direct target of PPARγ that participates in a feed-forward loop during adipocyte differentiation. TLE3 enhances PPARγ activity and functions synergistically with PPARγ on its target promoters to stimulate adipogenesis. At the same time, induction of TLE3 during differentiation provides a mechanism for termination of Wnt signaling. TLE3 antagonizes TCF4 activation by ß-catenin in preadipocytes, thereby inhibiting Wnt target gene expression and reversing ß-catenin-dependent repression of adipocyte gene expression. Transgenic expression of TLE3 in adipose tissue in vivo mimics the effects of PPARγ agonist and ameliorates high-fat-diet-induced insulin resistance. Our data suggest that TLE3 acts as a dual-function switch, driving the formation of both active and repressive transcriptional complexes that facilitate the adipogenic program.

Dissection of the insulin-sensitizing effect of liver X receptor ligands.

The liver X receptors (LXRalpha and beta) are nuclear receptors that coordinate carbohydrate and lipid metabolism. Treatment of insulin-resistant mice with synthetic LXR ligands enhances glucose tolerance, inducing changes in gene expression expected to decrease hepatic gluconeogenesis (via indirect suppression of gluconeogenic enzymes) and increase peripheral glucose disposal (via direct up-regulation of glut4 in fat). To evaluate the relative contribution of each of these effects on whole-body insulin sensitivity, we performed hyperinsulinemic-euglycemic clamps in high-fat-fed insulin-resistant rats treated with an LXR agonist or a peroxisome proliferator-activated receptor gamma ligand. Both groups showed significant improvement in insulin action. Interestingly, rats treated with LXR ligand had lower body weight and smaller fat cells than controls. Insulin-stimulated suppression of the rate of glucose appearance (Ra) was pronounced in LXR-treated rats, but treatment failed to enhance peripheral glucose uptake (R'g), despite increased expression of glut4 in epididymal fat. To ascertain whether LXR ligands suppress hepatic gluconeogenesis directly, mice lacking LXRalpha (the primary isotype in liver) were treated with LXR ligand, and gluconeogenic gene expression was assessed. LXR activation decreased expression of gluconeogenic genes in wild-type and LXRbeta null mice, but failed to do so in animals lacking LXRalpha. Our observations indicate that despite inducing suggestive gene expression changes in adipose tissue in this model of diet-induced insulin resistance, the antidiabetic effect of LXR ligands is primarily due to effects in the liver that appear to require LXRalpha. These findings have important implications for clinical development of LXR agonists as insulin sensitizers.

N-Acylthiadiazolines, a new class of liver X receptor agonists with selectivity for LXRbeta.

We have identified a novel liver X receptor (LXR) agonist (2) that activates the LXRbeta subtype with selectivity over LXRalpha. LXRbeta selectivity was confirmed using macrophages derived from LXR mutant mice. Despite its selectivity and modest potency, the compound can induce APO-AI-dependent cholesterol efflux from macrophages with full efficacy. Our results indicate that it is possible to achieve significant LXRbeta selectivity in a small molecule while maintaining functional LXR activity.

T0901317 is a potent PXR ligand: implications for the biology ascribed to LXR.

The liver X receptors (LXRalpha and beta) are nuclear receptors that coordinate carbohydrate and lipid metabolism. Insight into the physiologic roles of the LXRs has been greatly facilitated by the discovery of potent synthetic agonists. Here we show that one of these compounds, T0901317, is also a high-affinity ligand for the xenobiotic receptor pregnane X receptor (PXR). T0901317 binds and activates PXR with the same nanomolar potency with which it stimulates LXR activity. T0901317 induces expression not only of LXR target genes, but also of PXR target genes in cells and animals, including the scavenger receptor CD36, a property not shared by more specific LXR ligands, such as GW3965. Activation of PXR targets may explain why T0901317 induces dramatic liver steatosis, while GW3965 has a milder effect. These results suggest that many of the biological activities heretofore associated with LXR activation may be mediated by PXR, not LXR. Since T0901317 has been widely used in animals to study LXR function, the in vivo effects of this compound ascribed to LXR activation should be re-examined.

The nuclear receptor LXR is a glucose sensor.

The liver has a central role in glucose homeostasis, as it has the distinctive ability to produce and consume glucose. On feeding, glucose influx triggers gene expression changes in hepatocytes to suppress endogenous glucose production and convert excess glucose into glycogen or fatty acids to be stored in adipose tissue. This process is controlled by insulin, although debate exists as to whether insulin acts directly or indirectly on the liver. In addition to stimulating pancreatic insulin release, glucose also regulates the activity of ChREBP, a transcription factor that modulates lipogenesis. Here we describe another mechanism whereby glucose determines its own fate: we show that glucose binds and stimulates the transcriptional activity of the liver X receptor (LXR), a nuclear receptor that coordinates hepatic lipid metabolism. d-Glucose and d-glucose-6-phosphate are direct agonists of both LXR-alpha and LXR-beta. Glucose activates LXR at physiological concentrations expected in the liver and induces expression of LXR target genes with efficacy similar to that of oxysterols, the known LXR ligands. Cholesterol homeostasis genes that require LXR for expression are upregulated in liver and intestine of fasted mice re-fed with a glucose diet, indicating that glucose is an endogenous LXR ligand. Our results identify LXR as a transcriptional switch that integrates hepatic glucose metabolism and fatty acid synthesis.