Food intake and meal pattern in response to hyperosmotic-induced dehydration in obese and lean Zucker rats.

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.

[Not Available]. / LeRoy el invisible.

En agosto de 1976, un joven llamado LeRoy cayó desde una cornisa fracturándose el fémur. Se sospechó una hemorragia interna importante. Durante una laparotomía se comprobó que todos los órganos internos estaban intactos y los cirujanos ortopédicos arreglaron la fractura. Treintadías después, LeRoy murió. Había comido poco; diariamente, tan solo había recibido tres litros de la glucosa, el equivalente a 510 calorías, por vía intravenosa. La glucosa fue insuficiente para satisfacer sus necesidades nutricionales, perdiendo más del 20% de su peso corporaldurante su estancia en el hospital. La causa de la muerte se debió a "desnutrición médicamente inducida". Mientras tanto, un artículo científico documentó que la prevalencia de desnutrición en los hospitales de Boston era del 44% y que la desnutrición en sí era un predictor de altas tasas de complicaciones y muerte.Como resultado, los médicos sensibilizados formaron una sociedad que creó programas de formación y alentó la formación de equipos de nutrición en los hospitales. La industria comercializó fórmulas de nutrición y catéteres. Las complicaciones en enfermos hospitalizados cayeron en picado, mientras que las tasas de supervivencia aumentaron. California aprobó una legislación para regular el soporte nutricional. Aunque la industria de la atención sanitaria reconoce la importancia de la nutrición en los cuidados al paciente, el Congreso no proporcionó apoyo fiscal para los equipos de nutrición. Como resultado, los hospitales disolvieron sus equipos de nutrición de reciente creación. La educación y las habilidades en nutrición disminuyeron, y las complicaciones hospitalarias y las tasas de mortalidad aumentaron de nuevo.

LeRoy el invisible / LeRoy the invisible

En agosto de 1976, un joven llamado LeRoy cayó desde una cornisa fracturándose el fémur. Se sospechó una hemorragia interna importante. Durante una laparotomía se comprobó que todos los órganos internos estaban intactos y los cirujanos ortopédicos arreglaron la fractura. Treinta días después, LeRoy murió. Había comido poco; diariamente, tan solo había recibido tres litros de la glucosa, el equivalente a 510 calorías, por vía intravenosa. La glucosa fue insuficiente para satisfacer sus necesidades nutricionales, perdiendo más del 20% de su peso corporal durante su estancia en el hospital. La causa de la muerte se debió a "desnutrición médicamente inducida". Mientras tanto, un artículo científico documentó que la prevalencia de desnutrición en los hospitales de Boston era del 44% y que la desnutrición en sí era un predictor de altas tasas de complicaciones y muerte. Como resultado, los médicos sensibilizados formaron una sociedad que creó programas de formación y alentó la formación de equipos de nutrición en los hospitales. La industria comercializó fórmulas de nutrición y catéteres. Las complicaciones en enfermos hospitalizados cayeron en picado, mientras que las tasas de supervivencia aumentaron. California aprobó una legislación para regular el soporte nutricional. Aunque la industria de la atención sanitaria reconoce la importancia de la nutrición en los cuidados al paciente, el Congreso no proporcionó apoyo fiscal para los equipos de nutrición. Como resultado, los hospitales disolvieron sus equipos de nutrición de reciente creación. La educación y las habilidades en nutrición disminuyeron, y las complicaciones hospitalarias y las tasas de mortalidad aumentaron de nuevo (AU)

In August 1976, a young man named LeRoy fell from a ledge, fracturing his femur. Major internal bleeding was suspected. During a laparotomy, the trauma team ensured that all internal organs were intact and the orthopedic team set his fracture. Thirty days later, LeRoy died. He had eaten little; each day he only received three liters of glucose, the equivalent of 510 calories, intravenously. The glucose was insufficient to meet his nutritional needs, and he lost over 20% of his body weight during his hospital stay. The cause of death was due to "physicianinduced" malnutrition. Meanwhile, a paper around the same time documented that the prevalence of malnutrition in Boston hospitals was 44% and that malnutrition itself was a predictor of higher complication and death rates. As a result, like-minded physicians formed a society that created training programs and encouraged formation of hospital nutrition teams. Industry produced nutrition formulas and catheters. Complications in sick hospitalized patients plummeted while survival rates rose, and California passed legislation to mandate nutritional support. Tough the health care industry recognized the importance of nutrition in patient care, Congress failed to pass fiscal support for nutrition teams. As a result, hospitals disbanded their newly created nutrition teams, nutrition education and skills declined, and hospital complications and death rates have risen again (AU)

Special postoperative diet orders: Irrational, obsolete, and imprudent.

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.

Metabolically healthy obese individuals: Key protective factors.

OBJECTIVES: Obesity is a significant quality of life-impairing health problem affecting industrialized nations. However, despite carrying a large fat mass, some very obese individuals exhibit normal metabolic profiles (metabolically healthy obesity). The physiological factors underlying their protective and favorable metabolic profiles remain poorly defined. METHODS: A search of the National Library of Medicine PubMed database was performed using the following keywords: Metabolically healthy obese, metabolically normal obese, insulin resistance, metabolically unhealthy normal weight, and uncomplicated obesity. RESULTS: This article reviewed factors associated with severe obesity that lacks complications, and suggests putative activities by which these obese individuals avoid developing the clinical features of metabolic syndrome, or the metabolic complications associated with severe obesity. CONCLUSIONS: Despite the knowledge that visceral fat deposition is the seminal factor that ultimately causes insulin resistance (IR) and the detrimental inflammatory and hormonal profile that contributes to increase risk for cardiovascular disease, it remains unknown whether metabolically healthy obesity (MHO) has genetic predisposing factors, and whether MHO ultimately succumbs to IR and the metabolic syndrome, indicating a need for prophylatic bariatric surgery.

Nutritional support in adults with chyle leaks.

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.

Addition of lipids to parenteral nutrition does not cause fungal infections.

Parenteral nutrition (PN) that includes lipid emulsion is considered to increase both bacterial and fungal central venous catheter-related bloodstream infections. This concept is based on several erroneous metrics: Reports in age-old literature at a time when preparing PN admixtures lacked stringent quality control, when its infusion, the techniques of insertion, maintenance of vascular access devices, and delivery systems were not well identified or enforced. Additionally, concepts of glucohomeostasis were different and higher glucose levels were accepted. We provide updated information with supporting literature to show that associating PN with lipids with an increase in bloodstream infections is not justified.

Renal glomerular and tubular injury after gastric bypass in obese rats.

OBJECTIVE: Roux-en-Y gastric bypass (RYGB) surgery is the most common surgical intervention for long-term weight loss in morbidly obese patients. By decreasing obesity-associated hyperfiltration, diabetes, and hypertension, RYGB is touted to stabilize, if not prevent, progression of chronic renal disease. To test this, the renal histology of diet-induced obese rats that underwent RYGB surgery was compared with that of pair-fed and sham obese controls. METHODS: Sprague-Dawley rats, fed a high-fat, low-oxalate diet to induce gross obesity, were randomized to RYGB (n = 6), gastrointestinal-intact sham-operated obese controls (sham, n = 4), or gastrointestinal-intact sham-operated obese pair-fed controls (fed, n = 8). Daily body weight and food intake were recorded. On postoperative day 42, renal histology and immunohistochemistry were examined. Renal pathology was assessed by a categorical glomerular lesion score and a quantitative glomerular/tubular scoring system by experienced veterinary pathologists. Osteopontin and ED-1 (monocyte/macrophage cell) stainings were estimated by the percentage of stained area and the number of counted cells/high-power field, respectively. RESULTS: Compared with sham and fed controls, RYGB rats had significant decreases in body weight (P < 0.001), more glomerular lesions (P = 0.02), and received higher glomerular and tubular lesion scores (P < 0.01). RYGB rodents had significantly stronger staining for osteopontin within the inner medullary region (P < 0.005) and ED-1 within the outer medullary region (P < 0.02) compared with sham and fed controls. CONCLUSION: In this diet-induced obese rat model, RYGB is associated with chronic glomerulosclerosis and tubulointerstitial nephritis, confirmed by histology and immunohistochemistry. Prospective studies to better define the injurious mechanisms in this model are underway.