Reducción de la ingesta de alimento balanceado por consumo de agua endulzada con sacarosa en ratas Wistar / Reduction of balanced food intake by consumption of water sweetened with sucrose in Wistar rats

El azúcar de mesa, que se obtiene de la caña de azúcar, es el edulcorante más utilizado en la elaboración de los alimentos. El azúcar es importante en la obtención de energía, es necesario para la síntesis de ácidos grasos, de ácidos nucleicos, evita el estrés oxidativo y el desarrollo de anemia. Puede ocasionar caries, diabetes, obesidad, arteriosclerosis y otras patologías. En el presente trabajo se valoró el efecto que tiene la ingesta crónica de agua endulzada con sacarosa al 30% sobre el consumo de alimento balanceado, el perfil lipídico, la concentración de glucosa sérica, y sobre algunos marcadores del estado nutricional como el peso y las proteínas séricas totales, en machos de ratas Wistar. El agua endulzada con sacarosa al 30% se administró a un grupo de 9 ratas Wistar durante 3 meses y se tomó como grupo control a un grupo de 9 ratas que bebieron agua natural. El consumo de alimentos por ambos grupos, así como los marcadores de química sanguínea se analizaron al final del tratamiento. Los niveles de glucosa, lípidos y proteínas séricas totales se midieron mediante espectroscopía. Los resultados mostraron que el consumo de agua endulzada con sacarosa al 30% redujo en más de un 90% el consumo de alimento balanceado; sin embargo, no afectó el perfil lipídico ni el nivel de glucosa en sangre, así como tampoco el nivel de proteínas séricas totales. El consumo de agua endulzada con sacarosa podría provocar desnutrición a largo plazo ya que ocasiona una reducción en la ingesta de alimento rico en nutrientes.

Sugar, obtained from sugarcane, is the most commonly used sweetener in food processing. Sugar is an important food for energy generation and it is necessary for the synthesis of fatty acids and nucleic acids. It prevents oxidative stress and anemia development. However, its consumption can cause dental caries, diabetes, obesity, arteriosclerosis and other pathologies. In the present work, the effect of chronic intake of water sweetened with 30% sucrose on balanced food consumption, lipid profile, serum glucose concentration, as well as some markers of nutritional status such as weight and total serum proteins was assessed in male Wistar rats. The water sweetened with 30% sucrose was administered to a group of 9 Wistar rats for 3 months, having 9 rats as a control group that drank natural water. Food consumption between both groups as well as blood chemistry markers were analyzed at the end of the treatment. Glucose, lipid levels as well as total serum proteins were measured by spectroscopy. The results showed that the consumption of water sweetened with 30% sucrose reduced the consumption of balanced food by more than 90%, however, it did not affect the lipid profile, the level of glucose in the blood or the level of total serum proteins concentration. Consumption of sucrose-sweetened water could lead to long-term malnutrition by reducing the intake of nutrient-rich food.

O açúcar comum, obtido a partir da cana de açúcar, é o adoçante mais utilizado na elaboração dos alimentos. O açúcar é importante para a geração de energia; necessário para a síntese de ácidos graxos e de ácidos nucleicos. Previne o estresse oxidativo e o desenvolvimento de anemia. No entanto, seu consumo pode causar cárie dentária, diabetes, obesidade, arteriosclerose e outras patologias. No presente trabalho, foi avaliado o efeito da ingestão crônica de água adoçada com sacarose a 30% sobre o consumo de alimentos ricos em nutrientes, perfil lipídico, concentração sérica de glicose e alguns marcadores do estado nutricional, como o peso. e as proteínas séricas totais em ratos Wistar machos. A água adoçada com sacarose a 30% foi administrada a um grupo de 9 ratos Wistar por 3 meses, tendo como grupo controle um grupo de 9 ratos que beberam água natural. O consumo de alimentos entre os dois grupos e os marcadores de química sanguínea foram analisados no final do tratamento. Os níveis de glicose, lipídios e proteínas séricas totais foram medidos por espectroscopia. Os resultados mostraram que o consumo de água adoçada com sacarose a 30% reduziu em mais de 90% o consumo de alimentos ricos em nutrientes, no entanto, não afetou o perfil lipídico, o nível de glicose em sangue nem o nível de proteínas séricas totais. O consumo de água adoçada com sacarose poderia levar à desnutrição no longo prazo, visto que produz uma redução na ingestão de alimentos ricos em nutrientes.

Moderate and high intensity chronic exercise reduces plasma tumor necrosis factor alpha and increases the Langerhans islet area in healthy rats.

OBJECTIVE: This study aimed to examine the effects of moderate (MIT) and high-intensity training (HIT) chronic exercise on plasma tumor necrosis factor alpha (TNF-α) level and its impact on Langerhans islet morphology in healthy rats. METHODS: Two-month old normal male Wistar rats were divided into three groups: control (C, n=6), MIT (n=6), and HIT (n=4). The training protocol consisted in 24 sessions of running on a treadmill at 60-80% maximal oxygen consumption (VO2max) for MIT, and >80% VO2max for HIT. TNF-α and insulin were measured with ELISA tests. Duodenal pancreas was dissected to analyze the Langerhans islets by immunohistochemistry, a correlation analysis was performed with the nuclei/total islet area. Results: HIT and MIT rats showed lower TNF-α plasma levels than controls. Plasma insulin level decreased significantly in HIT compared with C and MIT. In addition, the islet area and nuclei density per islet were higher in the exercise groups compared with C. However, none of the groups showed PD1 immunoreactivity. CONCLUSIONS: Under healthy conditions, the chronic exercise reduced plasmatic TNF-α level, and in the same sense, increased the size of the Langerhans islets, depending to the exercise intensity.

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.

Effects of moderate- and high-intensity chronic exercise on brain-derived neurotrophic factor expression in fast and slow muscles.

INTRODUCTION: Brain-derived neurotrophic factor (BDNF) protein expression is sensitive to cellular activity. In the sedentary state, BDNF expression is affected by the muscle phenotype. METHODS: Eighteen Wistar rats were divided into the following 3 groups: sedentary (S); moderate-intensity training (MIT); and high-intensity training (HIT). The training protocol lasted 8 weeks. Forty-eight hours after training, total RNA and protein levels in the soleus and plantaris muscles were obtained. RESULTS: In the plantaris, the BDNF protein level was lower in the HIT than in the S group (P < 0.05). A similar effect was found in the soleus (without significant difference). In the soleus, higher Bdnf mRNA levels were found in the HIT group (P < 0.001 vs. S and MIT groups). In the plantaris muscle, similar Bdnf mRNA levels were found in all groups. CONCLUSIONS: These results indicate that high-intensity chronic exercise reduces BDNF protein level in fast muscles and increases Bdnf mRNA levels in slow muscles.

Análisis del efecto de la sal en el desarrollo de obesidad / Analysis of the effect of salt intake on the development of obesity

Introducción: el transporte de la glucosa y de muchos aminoácidos en el intestino es realizado por el cotransportador SGLT1 únicamente si esta unido al ion sodio. La sal aporta un ion sodio por cada molécula que se consume y en los humanos su ingesta comúnmente es de diez veces más de la cantidad necesaria y generalmente se acompaña de dietas ricas en carbohidratos. Este trabajo se planteo pensando en que una estrategia simple para reducir de peso sería el disminuir la cantidad de sal en los alimentos. Objetivo: estudiar el efecto que tiene la sal en la dinámica de la absorción de glucosa y el efecto de una dieta rica en carbohidratos y sal en el desarrollo de obesidad en ratas Wistar. Métodos: para corroborar la hipótesis se evaluó el efecto de la sal en la dinámica de la absorción de la glucosa en el intestino realizando curvas de tolerancia a la glucosa con sal y sin sal. También se analizó si una dieta rica en carbohidratos y sal favorece el desarrollo de obesidad en ratas Wistar. Resultados: los experimentos mostraron que la ingesta de sal no influye en la dinámica de la absorción intestinal de la glucosa, ni en el desarrollo de obesidad en la rata Wistar. Conclusión: el sodio que de manera natural recircula desde el citoplasma de los enterocitos hacia la luz del intestino mantiene saturado al cotransportador de la glucosa SGLT1 y garantiza en todo momento el transporte de la glucosa que se ingiere en la dieta.

Introduction: Intestinal transport of glucose and many amino acids is performed by the SGLT1 cotransporter only when the latter is bound to the sodium ion. Salt contributes a sodium ion per molecule ingested. Human salt intake is often tenfold the required amount, and is generally accompanied by a carbohydrate-rich diet. The present study is based on the assumption that reducing the amount of salt in foods is a simple weight-loss strategy. Objective: Study the effect of salt on glucose absorption dynamics and the effect of a diet rich in carbohydrates and salt on the development of obesity in Wistar rats. Methods: To corroborate the hypothesis, an evaluation was conducted of the effect of salt on intestinal glucose absorption, based on glucose tolerance curves with and without salt. An analysis was also made of whether a diet rich in carbohydrates and salt leads to the development of obesity in Wistar rats. Results: Experiments showed that salt intake does not influence intestinal glucose absorption or the development of obesity in Wistar rats. Conclusion: Sodium naturally recirculating from the cytoplasm of enterocytes to the intestinal lumen keeps the SGLT1 glucose cotransporter saturated and at all times ensures the transport of the glucose ingested in the diet.

Análisis del efecto de la sal en el desarrollo de obesidad: ¿existe la obesidad salada? / Analysis of the effect of salt intake on the development of obesity: is there such a thing as "salty obesity"?

Objetivos: el transporte de la glucosa y de muchos aminoácidos en el intestino se realiza por el cotransportador SGLT1 únicamente si está unido al ion sodio. La sal aporta un ion sodio por cada molécula que se consume y en los humanos su ingesta comúnmente es de diez veces más de la cantidad necesaria y, por lo general, se acompaña de dietas ricas en carbohidratos. El presente proyecto evaluó, si el consumo abundante de sal en la dieta conlleva al desarrollo de obesidad. Este trabajo se planteó pensando en que una estrategia simple para reducir de peso sería el disminuir la cantidad de sal en los alimentos. Métodos: para corroborar la hipótesis se evaluó el efecto de la sal en la dinámica de la absorción de la glucosa en el intestino realizando curvas de tolerancia a la glucosa con sal y sin sal. También se analizó si una dieta rica en carbohidratos y sal favorece el desarrollo de obesidad en ratas wistar. Resultados: los experimentos mostraron que la ingesta de sal no influye en la dinámica de la absorción intestinal de la glucosa, ni en el desarrollo de obesidad en la rata wistar. Conclusión: el sodio que, de manera natural, recircula desde el citoplasma de los enterocitos hacia la luz del intestino mantiene saturado al cotransportador de la glucosa SGLT1 y garantiza, en todo momento, el transporte de la glucosa que se ingiere en la dieta.

Objectives: intestinal transport of glucose and many amino acids is performed by the SGLT1 cotransporter only when the latter is bound to the sodium ion. Salt contributes a sodium ion per molecule ingested. Human salt intake is often tenfold the required amount, and is generally accompanied by a carbohydrate-rich diet. The present paper evaluates whether an abundant salt intake leads to the development of obesity. It is based on the assumption that reducing the amount of salt in foods is a simple weight-loss strategy. Methods: to corroborate the hypothesis, an evaluation was conducted of the effect of salt on intestinal glucose absorption, based on tolerance curves for glucose with and without salt. An analysis was also made of whether a diet rich in carbohydrates and salt leads to the development of obesity in Wistar rats. Results: experiments showed that salt intake does not influence intestinal glucose absorption or the development of obesity in Wistar rats. Conclusion: sodium naturally recirculating from the cytoplasm of enterocytes to the intestinal lumen keeps the SGLT1 glucose cotransporter saturated and at all times ensures the transport of the glucose ingested in the diet.

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.