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PURPOSE OF REVIEW: In the USA, 8-10 million people are morbidly obese, which is associated with a high frequency of comorbidities. The most effective treatment is surgery. Of around 180 000 bariatric operations performed in 2005, 80% were Roux-en-Y gastric bypass, consisting of a small gastric pouch to minimize food intake and a Roux-en-Y of distal small bowel bypassing the upper gastrointestinal tract. The precise mechanisms whereby Roux-en-Y gastric bypass achieves sustained weight loss remain unknown. To gain insight into the catabolic events of sustained weight loss we developed a diet-induced obese Roux-en-Y gastric bypass rat model. We review our rat model data from the novel viewpoint of the catabolic state, comparing it with the limited human data available and the catabolic events occurring in cancer anorexia/cachexia syndrome. RECENT FINDINGS: Current data suggest the involvement of mechanisms other than restrictive and malabsorptive factors of the Roux-en-Y gastric bypass, classically thought of as the mechanisms responsible for weight loss. Based on available data, gastrointestinal hormones and cytokines play a key role in reducing food intake and regulating energy homeostasis. Because of the cross talk between peripheral modulators and the hypothalamus, a critical role for their interaction in the outcome of Roux-en-Y gastric bypass is emerging. SUMMARY: In our Roux-en-Y gastric bypass rat model many of the changes in gastrointestinal hormones, adipokines and cytokines as well as in hypothalamic neuropeptides and neurotransmitters resemble the changes observed in the anorexia/cachexia rat model, suggesting that Roux-en-Y gastric bypass triggers a catabolic state responsible for loss of appetite and prolonged body weight reduction. [ABSTRACT FROM AUTHOR]

PURPOSE OF REVIEW: The clinical course of most chronic diseases is associated with declined energy intake and nutrient-resistant progressive myopathy, characterized by accelerated proteolysis and impaired function. This anorexia/cachexia syndrome leads to deterioration of quality of life, and increased morbidity and mortality. The clinical efficacy of currently available therapeutic strategies is limited and more effective treatments are needed. RECENT FINDINGS: Chronic systemic inflammation, triggered and sustained by cytokines, and increased oxidative stress contribute to the pathogenesis of the anorexia/cachexia syndrome. Carnitine and nicotine have recently been tested as immunomodulating and antioxidant agents. In particular, carnitine supplementation has been shown to reduce chronic inflammation and oxidative stress in hemodialysis patients and, in cancer patients, yielding to reduced fatigue and improved outcome. Nicotine is able to induce the anti-inflammatory activity of the vagus nerve. In animal models of sepsis and cancer, the nicotine-induced supplementation resulted in better protection of nutritional status and improved survival. SUMMARY: In the continuous effort to develop more efficacious strategies against the anorexia/cachexia syndrome, carnitine and nicotine may represent a further therapeutic tool. More clinical studies are needed, however, before their use can be routinely suggested. [ABSTRACT FROM AUTHOR]

Obesity is increasing in severity and prevalence in the United States and represents a major public health issue. No effective pharmacologic treatment leading to sustained weight loss currently exists. The growing interest in the regulation of food intake stems from the current drug treatments for obesity, almost all of which interfere with the monoamine system. Our knowledge of potential interactions between the orexigenic and anorexigenic pathways is limited and fragmented, making the development of targeted drug therapy for obesity difficult. The present review of the interaction of neuropeptides and monoamines emphasizes the complexity of the central mechanisms that regulate feeding behavior. Two main systems are implicated in food intake regulation: neuropeptide Y (NPY) and pro-opiomelanocortin. alpha-Melanocyte-stimulating hormone is a tridecapeptide cleaved from pro-opiomelanocortin that acts to inhibit food intake. The predominant NPY orexigenic receptors are NPY-Y1 and NPY-Y5, and the two anorexigenic melanocortin receptors involved in hypothalamic food intake control are MC3-R and MC4-R. Both neuropeptides interact with monoamines in the hypothalamus to control physiologic states such as hunger, satiation, and satiety. Serotonin suppresses food intake and body weight, acting mainly through the serotonin 1B receptor. Dopamine regulates hunger and satiety by acting in specific hypothalamic areas, through the D1 and D2 receptors. Noradrenaline activation of alpha1- and beta2-adrenoceptors decreases food intake, and stimulation of the alpha2-adrenoceptor increases food intake. A better understanding of the detailed mechanisms underlying the pathogenesis of hyperphagia and hypophagia is needed to develop new therapeutic approaches to obesity. [ABSTRACT FROM AUTHOR]

Anorexia and reduced food intake are important issues in the management of patients with cancer because they contribute to the development of malnutrition, increase morbidity and mortality, and impinge on quality of life. Accumulating evidence indicates that cancer anorexia is multifactorial in its pathogenesis, and most of the hypothalamic neuronal signalling pathways modulating energy intake are likely to be involved. Several factors are considered to be putative mediators of cancer anorexia, including hormones (eg, leptin), neuropeptides (eg, neuropeptide Y), cytokines (eg, interleukin 1 and 6, and tumour necrosis factor), and neurotransmitters (eg, serotonin and dopamine). These pathways are not isolated and distinct pathogenic mechanisms but are closely inter-related. However, convincing evidence suggests that cytokines have a vital role, triggering the complex neurochemical cascade which leads to the onset of cancer anorexia. Increased expression of cytokines during tumour growth prevents the hypothalamus from responding appropriately to peripheral signals, by persistently activating anorexigenic systems and inhibiting prophagic pathways. Hypothalamic monoaminergic neurotransmission may contribute to these effects. Thus, the optimum therapeutic approach to anorectic cancer patients should include changes in dietary habits, achieved via nutritional counselling, and drug therapy, aimed at interfering with cytokine expression or hypothalamic monoaminergic neurotransmission. [ABSTRACT FROM AUTHOR]

Objectives: Obese Zucker rats display neurochemical modifications in the brain characteristic of dehydration, but are nevertheless hyperphagic. This suggests that the obese animals can be resistant to dehydration-induced anorexia. The aim of this study was to test the hypothesis by comparing the effects of dehydration on food intake and feeding pattern between obese and lean Zucker rats., Methods: Intracellular dehydration in obese (fa/fa) and lean (Fa/Fa) Zucker rats was induced by replacing drinking water with hyperosmotic sodium chloride solutions (1.8% and 2.7%, consecutively, 4 d each). Daily food intake, meal size, and meal number were measured using an automated computerized rat eater meter before, during, and after the dehydration., Results: After 8 d of hyperosmotic challenge, body weight decreased by 15% and 10% in lean and obese rats, respectively. Obese rats displayed higher food intake and meal size than lean rats before, during, and after the dehydration. Drinking 1.8% and 2.7% sodium chloride solutes decreased gradually food intake and meal size in both lean and obese rats; however, obese rats had a higher percentage of food intake than lean rats during the osmotic challenge. Higher ratios of food to water intake characterized obese rats and the percentage of such ratios in obese versus lean rats were increased during the 2.7% sodium chloride load. Meal number was not affected by dehydration in obese rats, but it was decreased in lean rats during the 2.7% sodium chloride load and remained low during refeeding after the dehydration, when the meal size was increased., Conclusion: Dehydration-induced anorexia is present in both obese and lean Zucker rats; however, obese rats are more resistant to dehydration by preserving their meal size and food intake. These results support a role for feeding-associated dehydration in the pathogenesis of hyperphagia and obesity., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

A complex role of the immune system has been highlighted in the development and progression of hepatocellular carcinoma (HCC). Natural Killer cells (NK) and natural killer T cells (NKT) cells are among the innate immune lymphocytes that predominate in the liver and can prevent tumor growth and metastasis. The aim of the study was to measure the percentages of NK and NKT cells among a sample of Egyptian patients with HCC and to find the association between their frequencies and disease progression. The study included 2 groups; the HCC patient group (n=40) and the healthy control group (n=20). Blood samples were drawn from all subjects for complete blood picture, liver enzymes and alpha fetoprotein serum level measurement. Flow cytometric analysis was performed for CD3 and CD16/56 for determining the percentages of NK and NKT cells. The frequencies of NK cells and NKT cells were significantly decreased in HCC patients (6.58± 1.76 and 5.26 ± 1.13 respectively) as compared to healthy controls (9.01±1.62 and 6.88 ± 1.88 respectively) (P < 0.001 and 0.0008 respectively) and in HCC patients with metastasis (6.01± 1.11 and 5.07± 1.10 respectively) than HCC patients without metastasis (7.75± 1.98 and 5.89± 0.88 respectively) (P= 0.004 and 0.03 respectively). We concluded that the reduced percentages of NK cells and NKT cells in HCC patients especially in those with metastasis point to their important roles in the occurrence and progression of HCC., (Copyright© by the Egyptian Association of Immunologists.)

Background: We tested the hypothesis that nebulized budesonide would improve lung mechanics and oxygenation in patients with early acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) during protective mechanical ventilation strategy without adversely affecting systemic hemodynamics., Methods: Patients with ALI/ARDS were included and assigned into two groups; budesonide group (30 cases) in whom 1 mg-2 ml budesonide suspension was nebulized through the endotracheal tube and control group (30 cases) in whom 2 ml saline (placebo) were nebulized instead of budesonide. This regimen was repeated every 12 h for three successive days alongside with constant ventilator settings in both groups. Hemodynamics, airway pressures, and PaO 2 /FiO 2 were measured throughout the study period (72 h) with either nebulized budesonide or saline. Furthermore, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) were analyzed serologically as markers of inflammation at pre- and post-nebulization sessions., Results: We found a significant difference between the two groups regarding PaO 2 /FiO 2 ( P = 0.023), peak ( P = 0.021), and plateau ( P = 0.032) airway pressures. Furthermore, TNF-α, IL-1β, and IL-6 were significantly reduced after budesonide nebulizations. No significant difference was found between the two groups regarding hemodynamic variables., Conclusion: Nebulized budesonide improved oxygenation, peak, and plateau airway pressures and significantly reduced inflammatory markers (TNF-α, IL-1β and IL-6) without affecting hemodynamics., Trial Registry: Australian New Zealand Clinical Trial Registry (ANZCTR) at the number: ACTRN12615000373572., Competing Interests: There are no conflicts of interest.

There are no indications to prescribed special diets for postoperative patients. Low-sodium and low-fat or low-cholesterol diets are examples of restricted diets, especially in patients with heart disease and atherosclerosis. These restricted diets are unpalatable. Postoperative nausea, paralytic ileus, and vomiting caused by residual anesthetic effects and opioids used for pain control further contribute to the problem. Long-term adherence to these diets is necessary to derive benefits. Prescribing regular and palatable diets in the immediate postoperative period to meet protein and energy goals is important for wound healing and is commensurate with best clinical practices. In the following, we review the pertinent literature and offer clinical evidence that routine special diet orders for postoperative patients are not necessary., (Published by Elsevier Inc.)

We provide a practical approach to the complex management problem of chyle leaks that occur after surgical procedures or trauma, or when they occur spontaneously in association with malignancies. The volume of chyle loss causes significant problems due to loss of fluid, electrolytes, proteins, and lymphocytes, causing deleterious effects on wound healing and immunity. Enteral feeding is not always possible as long chain fatty acids are absorbed through the intestinal lacteals, the original source of chyle. Regular diets increase the leak and delay healing. Nutritional support involves coordinated care between healthcare providers to provide a combination of various modalities, including nil by mouth, parenteral nutrition, enteral feeding with formula modifications, and oral diet., (Published by Elsevier Inc.)