Análisis del efecto del consumo crónico de alcohol en el desarrollo de resistencia a la insulina ligada a una posible alteración en los niveles de adiponectina en sangre

El lipopolisacárido es el principal componente de la pared celular de todas las bacterias Gram negativas, las cuales forman parte de la flora intestinal. Se ha establecido que en los humanos, el consumo excesivo de alcohol está asociado con una aparición transitoria de lipopolisacarido en la circulación sanguínea de personas sanas. Los monocitos y los macrófagos presentes de manera abundante en el bazo, son las principales células que unen al lipopolisacárido a través del receptor TLR4, esto desencadena una gran producción de citocinas inflamatorias como el TNF-α, IL-1 e IL-6. Estudios recientes han demostrado que el TNF-α reduce la expresión de la adiponectina. La adiponectina es una hormona producida principalmente por el tejido adiposo, necesaria para evitar la resistencia a la insulina. El objetivo de este trabajo, fue estudiar el efecto del consumo crónico de alcohol, en el desarrollo de resistencia a la insulina ligada a una posible alteración en los niveles de adiponectina en sangre

Effect of the moderate and high intensity chronic exercise on plasma tumor necrosis factor alpha and Langerhans islets histology in healthy rats

Tumor necrosis factor alpha (TNF-α), a pro-inflammatory cytokine, negatively affects β-cell physiology and morphology, as occurs during type 1 diabetes mellitus and metabolic syndrome. Physical exercise is a good tool to reduce the pro-inflammatory state. PURPOSE: The present study investigated the effects of moderate and high-intensity chronic exercise on plasma TNF-α levels in a basal state; it further analyzed whether these cytokine changes are associated with changes in the pancreatic Langerhans islets morphology under healthy state. METHODS: Two month-old healthy male Wistar rats were divided into three groups: control (C) (n = 7), moderate intensity training (MIT) (n = 7), and high intensity training (HIT) (n = 5). The training protocol consisted of 24 exercise sessions, which involved running in a treadmill. The training intensity was 60% of the maximal oxygen consumption (VO2max) for MIT and 80% VO2max for HIT. Forty-eight hours after the last training session, plasma samples were obtained from the three groups to determine TNF-α and insulin levels with ELISA method. The duodenal pancreas was dissected to analyze the Langerhans islets. The correlation analysis among the nuclei/total islet area was carried out. RESULTS: The HIT group showed lower TNF-α plasma levels compared with the C group. Systemic insulin levels were not significantly modified in basal state by the chronic exercise intensity. In addition all the experimental groups showed a positive nuclei/islet area correlation. CONCLUSIONS: Under healthy conditions, the high intensity training reduces the plasma TNF-α level, but this effect is not associated with functionality or morphology changes of the pancreatic Langerhans islets. This study emphasizes the importance of one threshold in the exercise training to reduce the plasmatic TNF-α levels in a healthy state model

Análisis del consumo crónico de etanol en el desarrollo de un fenotipo similar al de la diabetes tipo 1

En el citoplasma de las células de los eucariotes existen tres enzimas citoplasmáticas que para llevar a cabo su acción requieren de la coenzima NAD+. Estas enzimas son: la alcohol deshidrogenasa, la gliceraldehido 3-fosfato deshidrogenasa y la lactato deshidrogenasa. Esta propuesta de investigación se plantea partiendo de la teoría de que en una ingesta excesiva de alcohol, la enzima alcohol deshidrogenasa necesaria para biotransformar el etanol a acetaldehído, secuestraría todo el NAD+ citoplasmático, frenando la vía metabólica de la glucolisis y con ello disminuyendo la generación de adenosin trifosfato (ATP) y la liberación de insulina en las células beta pancreáticas. El presente trabajo abordó el estudio del consumo crónico de etanol en ratas Wistar en un posible desarrollo transitorio de un cuadro clínico similar al que se presenta en la diabetes mellitus tipo 1

Presencia de dislipidemias en áreas de alta marginación

Las dislipidemias se clasifican de acuerdo con las concentraciones en sangre de triglicéridos (TG), colesterol total, colesterol asociado a lipoproteínas de baja densidad (C-LDL) y de alta densidad (C-HDL). Las dislipidemias pueden ocasionar enfermedades cardiovasculares como la aterosclerosis y el infarto de miocardio. El propósito de este estudio fue describir las principales dislipidemias en zonas de alta marginación. Se analizó mediante espectrofotometría la concentración en sangre de triglicéridos, colesterol total, colesterol asociado a lipoproteínas de alta densidad (C-HDL) y de colesterol asociado a lipoproteínas de baja densidad (C-LDL) en 93 sujetos que habitan zonas de alta marginación en el Estado de Colima con un rango de edad de 12 a 100 años. Las dislipidemias más frecuentes en zonas marginales fueron la hipoalfalipoproteinemia (39.36%), la hipertrigliceridemia (16.13%) y la dislipidemia mixta (10.75%). De acuerdo a los resultados es necesario promover estrategias que ayuden a elevar el colesterol asociado a lipoproteínas de alta densidad en personas que habitan zonas de alta marginación

Effects of Moderate- and High-Intensity Chronic Exercise on the Adiponectin Levels in Slow-Twitch and Fast-Twitch Muscles in Rats

Background and objectives: Adipose tissue and skeletal muscle secrete adiponectin, a hormone abundantly secreted by adipocytes, that through the adiponectin receptor, regulate glucose and lipid metabolism. Adiponectin appears to protect skeletal muscles from inflammatory damage induced by oxidative stress. It has been suggested that decreased adiponectin levels could be associated with pathologic conditions, including obesity and diabetes. Furthermore, some studies suggest that exercise could have a beneficial effect by increasing adiponectin levels, but this observation remains controversial. It is also unknown if physical exercise modifies adiponectin expression in skeletal muscles. The aim of this study was to investigate the effect of chronic exercise on serum adiponectin and adiponectin expression in slow-twitch (soleus) and fast-twitch (plantaris) muscles in healthy rats. Materials and methods: Two-month-old male Wistar rats were randomly divided into three groups with n = 6 in each group: control (C), moderate-intensity training (MIT), and high-intensity training (HIT). The rats were conditioned to run on a treadmill for the 8-week period. Forty-eight hours after the last session, blood samples were collected for adiponectin measurements and total RNA was isolated from plantaris and soleus muscles to measure by RT-qPCR adiponectin receptor 1 and adiponectin mRNA expression level. Results: MIT and HIT groups had reduced adiponectin protein levels in serum and the plantaris muscle, but not changes in adiponectin protein were observed in the soleus muscle. No significant differences in Adiponectin receptor 1 (AdipoR1) gene expression were observed following intense or moderate exercise in either muscle group studied. Conclusions: Our study shows that decreasing levels of circulating adiponectin is a result of physical exercise and should not be generalized as a predictive marker of disease

Dystrophin Dp71 in PC12 cell adhesion.

Previously, we reported that PC12 cells with decreased Dp71 expression (antisense-Dp71 cells) display deficient nerve-growth-factor-induced neurite outgrowth. In this study, we show that disturbed neurite outgrowth of antisense-Dp71 cells is accompanied by decreased adhesion activity on laminin, collagen and fibronectin. In wild-type cells, the immunostaining of Dp71 and beta1-integrin overlaps in the basal area contacting the substrate, but staining of both proteins decrease in the antisense-Dp71 cells. Morphology of antisense-Dp71 cells at the electron microscopic level is characterized by the lack of filopodia, cellular projections involved in adhesion. Our findings suggest that Dp71 is required for the efficient PC12 cell attachment to beta1-integrin-dependent substrata and that decreased adhesion activity of the antisense-Dp71 cells could determine their deficiency to extend neurites