Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this controlled trial we have studied the effect of anabolic steroid on ill surgical patients receiving intravenous hyperalimentation. Body composition, plasma proteins, and amino acids were compared in each of two groups of 12 patients before and after 14 days of intravenous feeding. The patients in one group were given 100 mg of nandrolone decanoate at the commencement of study and again one week later. Body weight, muscle (AMC), plasma transferrin, prealbumin, and retinol-binding protein were increased comparably in both groups. An apparent gain in total body nitrogen was not significant. However, anabolic steroid caused greater gain of water requiring a more liberal use of diuretics, but prevented the gains of fat, triglyceride and insulin that occurred in the control group. Most plasma amino acids increased due to intravenous hyperalimentation but decreased in patients given anabolic steroid. It is concluded that in patients who may be in the catabolic phase of recovery anabolic steroid probably enhances amino acid and water uptake by tissues and increases the utilization of fat but, does not promote any greater increase in "visceral" proteins than during intravenous hyperalimentation alone.
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PMID:Effects of an anabolic steroid on plasma amino acids, proteins, and body composition in patients receiving intravenous hyperalimentation. 640 71

To evaluate satiety in the hyperphagic, genetically obese Zucker "fatty" (fafa) rat, food-deprived fatty and lean (FaFa) control rats were given equicaloric intragastric infusions consisting largely of fat, carbohydrate, or protein. Relative to distilled water infusion, these infusions resulted in immediate reductions of food intake in both fatty and lean rats allowed to feed 20 min post-infusion. Cumulative food intakes remained reduced throughout the 2 hr period of observation. Thus, despite its hyperphagia, the fatty rat is responsive to the satiating effect of infused nutrients. However, the relative satiating effectiveness of the macronutrient infusions differed for the two genotypes. In lean rats, the different macronutrient infusions resulted in equivalent reductions of feeding. In contrast, in fatty rats, fat was the least satiating and protein was the most satiating macronutrient. Moreover, compared to lean rats, fatty rats displayed less initial suppression of feeding after fat infusion and greater overall suppression after protein infusion. These effects are consistent with the long-term feeding behavior of the fatty rat for the different macronutrients and may be related to pre- and postabsorptive metabolic alterations that have been documented in this animal.
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PMID:The satiety effects of intragastric macronutrient infusions in fatty and lean Zucker rats. 641 87

Goodson and Hunt showed that wound healing is impaired in streptozotocin (Sz) diabetic rats; we speculated that this impairment results from defective early inflammatory responses to wounding. Because we had shown that supplemental vitamin A stimulates the early inflammatory response to wounding in nondiabetic rats, we studied the effect of supplemental vitamin A on wound healing in rats with Sz-induced diabetes. Male Sprague-Dawley rats were fed a commercial rat chow containing twice the amount of vitamin A recommended by the NRC for healthy rats. The rats ate and drank (tap water) ad libitum. Two-thirds of the rats were injected (intravenously) with Sz 60 mg/kg body weight. All of these rats became diabetic (hyperglycemia greater than 350 mg/dl, hyperphagic, polydipsic, polyuric, glycosuric greater than 2%). Seven days later, half of the Sz-injected rats were continued on the chow (Group 2) while the other half (Group 3) were switched to the chow supplemented with 150,000 units of vitamin A/kg chow. The next day, all were wounded (7 cm skin incisions and s.c. polyvinyl alcohol sponge implants). Similarly wounded saline injected nondiabetic rats ingesting the unsupplemented chow served as controls (Group 1). The wounds of Group 2 rats healed poorly compared to Group 1 (breaking strength of skin incisions, 308 +/- 19 g vs 584 +/- 23 g, p less than 0.001; hydroxyproline of the sponge reparative tissue, 0.87 mg vs 2.40 mg/100 mg sponge p less than 0.001). Supplemental vitamin A (Group 3) did not affect the hyperglycemia, hyperphagia, polydipsia or glycosuria, but increased the breaking strengths of the incisions of the diabetic rats (468 +/- 40 g, p less than 0.001), and the sponge hydroxyproline (2.38 mg/100 mg sponge, p less than 0.001). In another experiment, in which the wounding and start of supplemental vitamin A were delayed until 28 days after streptozotocin administration (50 mg/kg body weight), similar results were obtained. Streptozotocin diabetes also caused a decrease in the cross-linking of reparative collagen as judged by the ratio of breaking strengths of skin incisions before and after formalin fixation. Supplemental vitamin A did not influence this defect. Sz also caused peripheral lymphocytopenia, adrenal hypertrophy and thymic involution which responded to the supplemental vitamin A. Based upon experimental data and theoretical considerations we conclude Sz diabetes causes two defects in wound healing: a) quantitatively (reduction in reparative collagen accumulation) and b) qualitative reduction in the degree of cross-linking of reparative wound collagen. The action of supplemental vitamin A in correcting the impaired wound healing, adrenal enlargement, thymic involution and lymphocytopenia of Sz-diabetic rats is independent of an effect on their disturbed carbohydrate metabolism.
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PMID:Impaired wound healing in streptozotocin diabetes. Prevention by supplemental vitamin A. 645 99

Rats treated with a sublethal dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 15 micrograms/kg) exhibited reduced feed intake and loss of body weight for the first 3 weeks after treatment. During the next 10 weeks, TCDD-treated rats maintained their body weight at a lower nearly constant percentage of that of control rats fed ad libitum. At no time did rats treated with TCDD exhibit hyperphagia which would have returned their weight to a normal level. Control rats pair-fed to TCDD-treated rats for more than 7 weeks displayed compensatory hyperphagia when permitted to feed ad libitum and their weight recovered to a near-normal level. The lower level of body weight in TCDD-treated animals was apparently due to a reduction in the regulation level or "set-point" for body weight. The following findings in TCDD-treated and control rats fed ad libitum supported this idea. First, when the reduced weight of the TCDD group was challenged by changes in the caloric density or palatability of the diet, TCDD-treated rats exhibited adjustments in feed intake and body weight that were essentially identical to those of control rats. Second, when body weight was manipulated by feeding a high-calorie diet or by restricting feed intake, both TCDD-treated and control rats quickly returned to weight levels from which they had been displaced. Third, carcass analyses conducted 7 weeks after treatment revealed that TCDD-treated rats had lower absolute amounts of body fat, protein, and water. However, when these constituents were expressed as percentages of total body weight no remarkable differences from the control were observed. Fourth, when TCDD-treated rats were induced to overeat and restore body weight to the same level as control rats fed ad libitum. TCDD-treated animals did not reassume a normal body composition but became obese. Obesity was also observed when control rats were induced to overeat. Thus, TCDD-treated rats regulate their body weight in the same fashion as control rats but at a weight regulation level or set-point that is markedly reduced.
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PMID:Body weight regulation in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin. 650 77

The hyperphagia/obesity syndrome produced by paraventricular hypothalamic (PVH) lesions and that produced by medial hypothalamic (MH) knife cuts were compared in adult female rats. Each treatment produced hyperphagia and overweight on a chow diet, although the PVH effect was less than the knife-cut effect. Each treatment also produced qualitatively similar ingestive responses to unpalatable quinine- and sucrose octaacetate-adulterated diets and to palatable dextrose and fat diets during the dynamic and static weight-gain phases. The PVH lesions and MH cuts disrupted day/night feeding patterns and elevated water intakes but not water/food intake ratios. However, PVH lesions, unlike MH cuts, did not increase emotional reactivity. The relation of the PVH syndrome to the classic hypothalamic hyperphagia syndrome is discussed. Also considered is the neuroanatomical substrate responsible for the PVH hyperphagic effect.
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PMID:Paraventricular hypothalamic lesions and medial hypothalamic knife cuts produce similar hyperphagia syndromes. 665 67

Six adult dogs were implanted stereotaxically with chronic indwelling Medtronic platinum-tipped electrodes in the left ventromedial hypothalamic area (VMH); two dogs with electrodes placed in the subcortical white matter served as controls. Following 24 hours of food deprivation, VMH-stimulated dogs delayed their next meal for a period ranging from 1 to 18 hours. When not stimulated, however, each dog ate immediately upon receiving its food and consumed greater than average daily intake (p less than 0.005). The two control dogs ate immediately upon receiving food regardless of whether they were stimulated or not. Dogs that received 1 hour of VMH stimulation every 12 hours for 3 consecutive days maintained an average daily food intake of 35% of normal baseline levels (range 13% to 51%), and water consumption averaged 50% of baseline intake (range 29% to 67%). Both of these results were statistically significant (p less than 0.01). After cessation of stimulation, food and water intake returned to normal within 6 to 9 days, with no observable "rebound hyperphagia." The two animals that received subcortical electrodes showed no change in food or water intake with stimulation. Blood pressure, pulse, respiration, temperature, and gross behavior were not altered during or after stimulation. These results suggest that the use of electrical stimulation of the VMH may be a useful modality for regulating food intake, and deserves further examination as a potential alternative therapy for human morbid obesity.
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PMID:Changes in food intake with electrical stimulation of the ventromedial hypothalamus in dogs. 672 69

Neonatal administration of monosodium glutamate (MSG) produces in rats neurotoxic degeneration of the circumventricular system, including the medial-basal hypothalamus, depleting several neuropeptides and neurotransmitters in this area. In addition, a number of behavioral and neuroendocrine responses are impaired, including a significant decrease in the analgesic response to cold-water swims (CWS). The present study examined whether the alterations in the analgesic responses following CWS and 2-deoxy-D-glucose (2-DG) induced by neonatal MSG treatment were due either to direct alterations in a pain-inhibitory system, or alternatively, to alterations in a system that processes the stressful consequences or properties of a stimulus. To accomplish this, the analgesic, hypothermic, and locomotor responses following CWS and the analgesic, hyperphagic, and locomotor responses following 2-DG were assessed in rats treated neonatally (days 2, 4, 6, 8, and 10) with either MSG or a vehicle solution. MSG-treated rats displayed significant reductions in both their analgesic and hypothermic responses following CWS, suggesting that MSG treatment impairs an animal's ability to process sufficiently the stimulus properties of the swim as stressful. While MSG treatment potentiated 2-DG analgesia, it reduced 2-DG hyperphagia, suggesting that MSG treatment also impairs coping responses to glucoprivation. These data indicate the importance of the circumventricular system in the coding of stimuli as potential stressors and in the subsequent activation of requisite systems necessary to provide a sustained, coordinated, and synchronous coping response.
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PMID:Impairments in analgesic, hypothermic, and glucoprivic stress responses following neonatal monosodium glutamate. 673 8

Management of protein-calorie malnutrition found in 32 patients with severe liver diseases such as fulminant hepatitis and cirrhosis of the liver was carried out using 2 types of synthetic amino acid solution (Hep-OU and Fischer solution) for intravenous and enteral alimentations with rapid monitoring of serum aminogram. Intravenous hyperalimentation of these cases resulted in maintenance of nutritional status with improvement of nitrogen balance and normalization of impaired serum aminogram. During this study, however, nutritional support was initiated only when intractable ascites, upper gastrointestinal bleeding and hepatic encephalopathy were observed. In 2 cases of fulminant hepatitis with sepsis and 3 hepatoma patients with ascites, elemental diet containing maltose and amino acids was used to supply sufficient amounts of nutrients in a minimum volume of water. These techniques with simultaneous monitoring of urinary excretion of 3-methylhistidine and creatinine height index as nutritional parameters make nutritional management easy for patients with liver disease.
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PMID:Nutritional management of patients with severe liver disease by using intravenous hyperalimentation and elemental diet. 676 41

Available enteral hyperalimentation solutions used to treat undernourished cirrhotic, ascitic patients with protein intolerance are excessive in water, sodium, and in some cases protein. This study investigated the use of enteral formulae tailored to the water, sodium, and protein tolerance of 10 undernourished subjects with ascites due to alcoholic liver disease (n = 8) and postnecrotic cirrhosis (n = 2). During a 10- to 60-day (mean +/- 80 = 37 +/- 19) hyperalimentation period, three subjects were treated with a low Na (1g Na/2000 kcal), high caloric density formula (2 kcal/ml); previous encephalopathy in seven remaining subjects required infusion of a low Na, low protein (40 g/day) modular high caloric density formula. The high caloric density formula protein content in 6/7 subjects was increased to 80 to 143 g without adverse effect. Nine subjects tolerated the program well and showed improvement in the following indices: serum albumin, creatinine/height, and midarm muscle and fat areas. In selected cases, enteral hyperalimentation solutions with appropriate composition can be safely and effectively administered to cachectic cirrhotic subjects with ascites.
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PMID:Enteral hyperalimentation in undernourished patients with cirrhosis and ascites. 680 58

The effects of combined nutritional support (parenteral, enteral, and oral) were measured in cancer patients unable to maintain normal alimentation. Changes in body composition were quantified by measurement of total body levels of nitrogen, potassium, water, and fat. The protein-calorie intake of the patients was also evaluated by dietary survey (4-day recall). Standard anthropometric and biochemical measurements for nutritional assessment were obtained for comparison. The dietary evaluation indicated that the dietary supplementation for all patients was more than adequate to meet their energy requirements. Almost all patients gained weight on the combined nutritional support regimens. Determination of body composition indicated that change in body weight was equal to the sum of the changes in body protein, total body water, and total body fat. The findings from the anthropometric nutrition indices (arm muscle circumference and triceps skinfold) were consistent with the results of the body composition study. Information on the nature of the tissue gained was obtained by comparison of body composition data with the ratio of protein:water:lean body mass for normal tissue. The mean gain of protein in the cancer patients was quite small (0.3-0.6 kg). The main change in body weight appeared to be the result of gains in body water and body fat. The total body nitrogen to potassium ratio served to define the extent of tissue anabolism following hyperalimentation. The ratio dropped in the cancer patients following hyperalimentation toward the value of the control subjects on ad libidum diets. The body compartment techniques described have demonstrated their usefulness in determining the effects of hyperalimentation on cancer patients.
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PMID:Changes in body composition of cancer patients following combined nutritional support. 681 45


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