Nutrición del Alma (Spanish Edition)

Es hora de que ese espejo se transforme en tu amigo. Muchos recurrimos a la comida para tapar lo que sentimos.

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Te lo digo por experiencia. Esta es una pregunta muy personal. Entonces, en este instante, te invito a que te hagas la siguiente pregunta: Mi respuesta personal, basada tanto en mi vivencia como en las respuestas de las miles de personas que han llegado a Yes You Can! No, no existe el gordito feliz.

Porque esa etiqueta la he vivido y sentido en carne propia cuando era gordo, y la realidad es que no era feliz.

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Aparecieron hombres y mujeres defendiendo esta postura y diciendo que su gordura no les afectaba su nivel de felicidad. Pero lo que ninguno debe negar es el tema de la salud. Y cuando hay enfermedad, no puede haber verdadera felicidad.

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El tema de la salud no me parece algo debatible, pero los sentimientos de cada quien hay que respetarlos. Por eso quiero ayudarte a sanar tu alma, a alivianar no solo tu cuerpo sino tus emociones, para que encuentres tu verdadera felicidad. No tienes idea de lo bien que te vas a sentir una vez que comprendas, aceptes y alcances tu salud emocional. Atria Books June Length: YesYouCan — Gaby Espino. The role of [ 18 F]Fluorodeoxiglucose positron emission tomography and [ In]diethylenetriaminepentaacetate- d -Phe-pentetreotide scintigraphy in the localization of ectopic adrenocorticotropin-secreting tumors causing Cushing's syndrome.

J Clin Endocrinol Metab, 89 , pp.

Flurodeoxyglucose positron emission tomography in the localization of ectopic ACTH-secreting neuroendocrine tumours. Clin Endocrinol Oxf , 64 , pp. Gammagrafia de receptores de somatostatina. Rev Esp Med Nucl, 22 , pp. Pituitary, 12 , pp. Clin Endocrinol Oxf , 59 , pp. Eur J Endocrinol, , pp. Whole body 18 F dopa PET for detection of gastrointestinal carcinoid tumors.

Radiology, , pp. Functional imaging of malignant paragangliomas and carcinoid tumors. Eur J Nucl Med, 28 , pp. Med Sci Monit, 13 , pp. Subscribe to our Newsletter. Print Send to a friend Export reference Mendeley Statistics. Statement on the current treatment of severe obesity in Si continua navegando, consideramos que acepta su uso.

Rimonabant treatment ip of ad libitum fed rats did not affect gastric ghrelin secretion, in either the sham operated rats or in vagotomized animals Figure 3A. Surgical vagotomy increased gastric ghrelin secretion in the fed animals fed: As expected, food restriction for 36 hours increased gastric ghrelin secretion with respect to the ad libitum animals fed: Surprisingly, rimonabant treatment of the fasted animals reversed the increased levels of gastric ghrelin secretion induced by the food deprivation fast: Vagotomized animals in the fasting condition, exhibited a non-significant decrease in gastric ghrelin secretion compared to the control group Figure 3B.

In keeping with the ex vivo data, rimonabant treatment did not affect circulating ghrelin levels in the ad libitum animals Figure 3C. Increased circulating ghrelin levels were observed in the fasted animals relative to the ad libitum group fed: Similar to gastric ghrelin secretion, pharmacological cannabinoid receptor blockade prevented the food-deprivation induced increase in circulating ghrelin levels fast: Variation in ghrelin secretion from gastric explants in vitro treated with rimonabant.

Vagotomized animals exhibited increased gastric ghrelin secretion fed: Gastric explants from the fasted animals exhibited higher levels of ghrelin secretion than those from the ad libitum fed animals fed: In contrast to the in vivo data, rimonabant directly added to the stomachs of food-deprived animals was not able to revert the increased levels of gastric ghrelin secretion induced by fasting fast: To reconfirm the lack of effect of rimonabant directly added to stomachs of food-deprived animals, two additional doses of rimonabant were tested 2.

These doses were not able to revert the increased levels of gastric ghrelin secretion induced by fasting fast: A decrease in ghrelin mRNA levels was observed in animals subjected to surgical vagotomy fed: Ghrelin protein levels and representative Western blot from the mucosa from ad libitum fed animals C or hours fasted animals D. Fasting for 36 hours did not affect the gastric ghrelin mRNA with respect to the ad libitum animals, although a slight tendency toward an increase in ghrelin mRNA was observed fed: However, rimonabant treatment ip of fasted animals slightly decreased ghrelin mRNA levels fast: Ghrelin mRNA levels were not changed in the vagotomized fasted animals fast: Additionally, rimonabant treatment did not induce any effects in the animals subjected to surgical vagotomy Figure 4B.

Rimonabant treatment of fasted animals increased the ghrelin contents of the stomachs rimonabant: Additionally, as shown in the representative western blot in Figure 4 , the fasted animals exhibited lower stomach ghrelin contents compared to the fed animals fast: Rimonabant treatment ip of the ad libitum fed rats did not affect gastric CB1 mRNA levels in either the sham operated rats or the vagotomized animals Figure 4E. In contrast to ghrelin, CB1 mRNA levels decreased Figure 4F significantly after peripheral rimonabant treatment of fasted animals fast: Additionally, and in accordance with previous studies, the intracellular pathway was inhibited by rapamycin treatment control: All the values are represented as percentages over control.

Blockage of the mTOR pathway with chronic rapamycin treatment blocked the effects of rimonabant on gastric ghrelin secretion Figure 6A , ghrelin mRNA expression in gastric mucosae Figure 6B or circulating ghrelin levels Figure 6C. However, the groups that received rapamycin treatment exhibited higher levels of gastric ghrelin secretion Control: Similarly, plasma ghrelin levels were increased in the animals that received rapamycin treatment control: To confirm the inhibitory effects of the blockade of the peripheral CB1 receptors on gastric ghrelin secretion from the stomach and plasma ghrelin levels, several measures were performed on samples from fasting animals treated with an alternative CB1 antagonist AM AM treatment ip of fasted animals inhibited the elevated levels of gastric ghrelin secretion induced by food deprivation fast: Corroborating ex vivo data, pharmacological cannabinoid receptor blockade with AM prevented food-deprivation-induced increases in circulating ghrelin levels fast: As rimonabant treatment, gastric phospho-S6K1 responded to AM treatment in a manner similar to that pmTOR, although the phospho-S6K1 response did not reach statistical significance control: All values are represented as the percentages over control.

The main findings of the present work are as follows: Previous studies have suggested that the endocannabinoid system is involved in appetite and feeding [22] , and multiple experimental protocols have demonstrated the food intake-reducing effects of rimonabant, which is an antagonist of the CB1 receptor. Accordingly, in the present work, peripherally injected rimonabant was found to prevent the increase in food intake elicited by central ghrelin administration Figure 1A and B.

Moreover, a more surprising finding was that rimonabant perse was able to induce a reduction in basal food intake amounts but only in the animals that were fasted overnight Figure 1B. However, the anorexigenic effects of rimonabant disappeared if the animals had previously been subjected to surgical vagotomy Figure 1C ; this finding highlight the requeriment of an intact vagus connection for the effects of the cannabinoid system on appetite.

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This finding has previously been suggested by the work of Gomez et al. However, another study from Madsen et al. The main difference between the work of Madsen et al. In the previous study, rimonabant was administered via oral gavage, whereas in our work and the work of Gomez rimonabant was administered intraperitoneally. It has been repeatedly shown that animals in fasting states exhibit increased levels of ghrelin that induce orexigenic effects mainly via the activation of the vagus nerve [24] , [25] , and the present study supports the possibility that peripheral rimonabant acts locally at the gastric level to reduce ghrelin secretion and consequently, downregulate food intake.

The immunohistochemical studies performed in the present work showed that the neuroendocrine cells producers of ghrelin are distributed near the CB1-positive cells in the stomach and have patterns of distribution that are similar to those of the CB1-positive cells Figure 2. CB1 expression in rats has been described in pre and postganglionic cholinergic neural elements that innervate the smooth muscle and mucosal and submucosal blood vessels [26].

However, these studies did not demonstrate the localization of these receptors to the neuroendocrine cells of the stomach. After finding an anorexigenic effect of rimonabant on basal and ghrelin-stimulated food intake and immunopositivity for CB1 and ghrelin in the neuroendocrine cells of the stomach, we next determined whether the interaction between these systems was mediated locally in the stomach. To do this, we used an organ culture model of gastric tissue that was previously developed and validated by our group [19] , [20] , [25] , [27].

With this model, peripherally administered rimonabant was shown to reverse the gastric increase in ghrelin secretion induced by fasting Figure 3B. However, in fed animals, which exhibit basal levels of ghrelin secretion, the administration of rimonabant failed to produce any effect Figure 3A.

The present data support the results obtained from the food intake studies in which the administration of rimonabant to fed animals did not produce an anorexigenic effects Figure 1A , but did produce strong effects in overnight fasted animals Figure 1B. In the light of this finding, we can affirm that the modulation of gastric ghrelin secretion by CB1 is required for the anorexigenic effect of antagonists of this receptor. Moreover, in accordance with the lack of effect of rimonabant on food intake in vagotomized animals Figure 1C , the gastric studies of the present work indicate that the inhibition of ghrelin by rimonabant was abolished after vagotomy Figure 3B , which, in turn, indicates that the vagus connection needs to be intact to ensure efficient interactions between ghrelin and CB1.

Consequently, in the in vitro experiment in which, gastric tissues received one rimonabant treatment in isolation from the complete organism i. To corroborate these results and to assess whether the secretion of ghrelin by the stomach is reflected in circulating ghrelin levels, the plasma ghrelin levels of the experimental groups were measured. These data corroborate the findings of other authors who have described the regulation of ghrelin plasma levels by peripheral treatment with different agonists or antagonist of the CB1 receptor [28] , [29].

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The studies of the secretion, protein contents and mRNA levels of ghrelin in gastric tissue allowed us to establish a gastric mechanism for the regulation of ghrelin by cannabinoids. The above mentioned mechanism was clearly demonstrated by the decrease in ghrelin secretion from the stomach Figure 3B that was induced by rimonabant ip treatment; this reduction in ghrelin secretion was accompanied by increased amounts of protein storage in the ghrelin-positive cells Figure 4D , as measured by Western blot, which was accompanied by no effect on ghrelin mRNA levels Figure 4B.

Moreover, an increase in gastric ghrelin secretion by the fasted animals compared to the ad libitum fed group was observed Figure 3A and B ; this finding was reflected by the reduced ghrelin content inside the cells as shown by Western blots Figure 4E and F. Together, the data presented in the present work reinforce the physiological mechanism of the regulation of gastric ghrelin secretion that has previously been reported in other conditions by our group [20]. The CB1 mRNA expression levels in the gastric mucosae were assayed with real-time PCR in the experimental models, and, to us, the most interesting findings was the significant decrease in CB1 mRNA levels in the stomachs of fasted animals after peripheral rimonabant treatment and the lack of an effect in the fed animals Figure 4E and F.

These data reinforce the finding that the effects of rimonabant on ghrelin and the regulation of food intake are observed only in fasted animals. The rimonabant induced downregulation of CB1 might be associated with the decreases in ghrelin secretion by the stomach [11]. In contrast, surgical vagotomy induced decreases in CB1 receptors in both fed and fasted animals, which might explain the lack of effect of rimonabant on food intake in the animals subjected to surgical vagotomy Figure 1C.

The second part of this study focused on the search for the intracellular mechanism responsible for the interaction between ghrelin and the endocannabinoid system in the stomach. The possible role of the mTOR pathway in mediating the gastric interaction between ghrelin and endocannabinoid system was explored. In accordance with our results, it has previously been described that mTOR phosphorylation in the gastric mucosa is downregulated by fasting, and we demonstrated that this effect was reverted after rimonabant administration Figure 5A.

It has previously been reported that the inhibition of gastric mTOR signaling leads to increased expressions of ghrelin mRNA, GOAT mRNA, tissue preproghrelin content and circulating ghrelin and that there is an inverse relationship between gastric mTOR signaling and ghrelin expression and secretion during changes in energy status [30].

To do this, the effects of the administration of rimonabant to fasting animals that had received chronic rapamycin treatment on gastric and plasma ghrelin levels were tested. Moreover, the injection of rimonabant into the fasted animals whose mTOR pathways had been blocked by rapamycin treatment did not affect gastric ghrelin secretion Figure 6A , ghrelin mRNA Figure 6B or circulating ghrelin levels Figure 6C , thus demonstrating that the mTOR pathway is responsible for the interaction between the endocannabinoid system and ghrelin at the gastric level.

However, the involvement of additional gastric-level signaling routes in this system should not be excluded and the futures studies should focused on identifying additional intracellular pathways involved in this system of gastric regulation.

Consequently, the gastric tissue responds by inhibiting the increased ghrelin secretion that is normally observed in fasting states, which results in decreased food intake due to decreased vagally mediated orexigenic signaling to the brain. In conclusion, the present work demonstrates the existence of a gastric mechanism for the interaction between the endogenous cannabinoid system CB1 and ghrelin that is mediated throught the intracellular mTOR pathway and, results in a physiological effect on the regulation of food intake that requires the vagus nerve.



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