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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

The authors report a girl with acute lymphoblastic leukaemia presenting hypothalamic syndrome characterized by meningeal leukaemia, hyperphagia and obesity. Insulin and growth hormone secretion, studied with arginine and insulin stimulation tests, showed a high peak of serum insulin and no response of growth hormone. Insulin and growth hormone responses to these tests reverted to normal after intrathecal methotrexate.
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PMID:Insulin and growth hormone secretion in a leukaemic girl with hypothalamic syndrome. 26 33

Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. The glucose moiety of gold thioglucose is essential for production of the lesion. Glucose analogues (2-deoxy-glucose, sodium thioglucose and phlorizin) prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia. Insulin deficiency prevents the lesion. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Electron microscopic studies, in which general necrosis is avoided by administration of aspirin before gold thioglucose or by administration of subnecrotic doses of gold thioglucose, reveal that gold thioglucose primarily affects neural elements contiguous with capillaries in the ventromedial hypothalamus. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake.
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PMID:Gold thioglucose obesity syndrome. 32 50

A new strain of obese mouse, the PBB/Ld, has been studied in terms of fat pad cellularity, serum insulin and blood glucose levels, and response to gold thioglucose injections. Age-matched C57B1/6J mice were used as controls. Adipocyte size and number in the major fat depots were determined at various ages from weanling to maturity in the PBB/Ld and C57B1/6J strains. Results indicated that obesity in the PBB/Ld was due to hypertrophy of adipocytes in retroperitoneal and subcutaneous fat depots and to hypertrophy and hyperplasia in the epididymal fat pad. PBB/Ld mice also developed hyperinsulinemia and hyperglycemia and these findings have been discussed in terms of the developmental changes in fat pad cellularity. The injection of gold thioglucose led to increased food intake in both PBB/Ld and C57B1/6J mice. Hyperphagia was also present in the PBB/LD control group, but increased efficiency of converting calories to body weight was not observed in this group when compared to control C57B1/6J mice. The characteristics of obesity seen in the PBB/Ld mouse are discussed and comparisons are made to similar studies in other rodent models of obesity.
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PMID:Description of obesity in the PBB/Ld mouse. 34 7

Intravenous hyperalimentation allows complete nutrition and anabolism in patients who cannot be fed by the oral route. However, several complications have been reported, e.g. septicaemia and hyperglycaemina. In 51 intensive-care patients receiving hyperalimentation, 18% were found to be hyperglycaemic in spite of insulin administration. Hyperglycaemia was frequently associated with stress. In 8 patients undergoing major surgery, which was chosen as a stress model, decreased insulin and increased glucagon, growth hormone and cortisone levels were observed. These findings could explain stress-induced glucose intolerance. In a further experiment, 8 intensive-care patients were given alternative intravenous feedings with either 600g of a mixture of glucose, fructose and xylitol in a ration of 1:2:1 or 600g glucose per day. During both regimens insulin administration was required in 4 patients, but the insulin dosage was lower with the mixture. Plasma glucose during glucose infusion was 205+/-25mg/100ml(M+/-SEM) and the sum of plasma glucose, fructose and xylitol during infusion of the mixture was 176+/-33mg/100ml, the difference being of borderline significance (p less than 0.05). The advantages and disadvantages of infusable substrates are summarized on the basis of the available literature and it is concluded that, in general, glucose is preferable. However, if hyperglycaemia is difficult to control, partial replacement of glucose by glucose substitutes or fat emulsions may be advantageous. A routine infusion programme for central venous feeding is suggested. Causes and prevention of side-effects are reviewed. In many patients receiving central venous nutrition less hazardous and less expensive methods could be used such as nasogastric tube feeding, elemental diet or peripheral venous nutrition.
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PMID:[Parenteral hyperalimentation (author's transl)]. 40 48

Solutions of crystalline amino acids infused without dextrose produce a marked improvement in nitrogen balance. Increasing the infusion level of amino acid from 1.0 to 1.7 grams per kilogram further improves nitrogen balance. The addition of dextrose to the amino acid solutions did not affect nitrogen balance and proved that the role of insulin during protein sparing has been overemphasized. Nitrogen balance is slightly, but not significantly, superior when nonprotein dextrose calories are administered. However, amino acid solutions are isotonic and can be infused peripherally, whereas adding dextrose doubles the concentration and renders peripheral infusion more difficult. Protein sparing may be useful for short term nutritional support when the potential risks of total parenteral hyperalimentation are not justified. Endogenous body fat is mobilized. Hence, protein sparing also prevents the development of fatty acid deficiency and may be useful in treating fatty infiltration of the liver. Protein sparing provides suboptimal caloric replacement and should only be used for temporary nutritional support until oral alimentation is resumed or until there is an absolute indication for intravenous hyperalimentation. Expense and the fact that most patients do well after elective abdominal operations militate against the proposition that amino acids should become a routine substitute for 5 per cent dextrose therapy post-operatively.
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PMID:The current status of protein sparing. 40 22

Safe and consistently reliable parenteral hyperalimentation in the care of the critically ill or injured remains an unrealized expectation. Our experience with critically ill patients managed with standard 25% dextrose/4.25% protein hyperalimentation solution (S.H.A.) delivered through a centrally placed catheter demonstrated that S.H.A. was associated with a high catheter infection rate, fluctuations in hyperosmolar tolerance, unstable insulin requirements, and a high discontinuation rate. In retrospect this unsatisfactory experience resulted from the inappropriate assumption that a single type of nutritional support and delivery system could meet the varying metabolic requirements of the critically ill or injured. In an effort to reduce these complications, we have recently utilized a system of selective hyperalimentation in managing 25 consecutive patients. We now identify specific risk factors for groups of patients and use these factors to select the appropriate rout and solution. Selective hyperalimentation has resulted in a lowering of infusion complications and an improvement in completion rate, with satisfactory weight gain and protein response. These results suggest that our approach is sucessful in meeting the nutritional requirements of differing groups of critically ill patients without exposing upsuitable candidates to the potential risks of standard hyperalimentation.
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PMID:Selective hyperalimentation: a new look at an old problem. 40 8

Using intravenous saline as a control, the kinetics of insulin in protein hydrolysate (hyperalimentation) solutions in glass bottles with and without the addition of albumin were studied using double radioisotope tags. Albumin is not a necessary additive to the solution. A technique for providing constant, predictable delivery of insulin is described. Albumin, when added to hyperalimentation and saline solutions with insulin, does not protectively coat plastic tubing or glass bottle surfaces to prevent insulin adsorption; some other mechanism is responsible for the increased insulin concentrations in intravenous solutions with added albumin.
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PMID:Insulin kinetics in hyperalimentation solution and routine intravenous therapy. 41 62

At the present time, two major factors limit further clinical application of islet cell transplantation in treatment of the insulin-deficient diabetic patient. First, the yield of islet tissue obtainable from a single donor pancreas is insufficient for adequate reconstitution of normal beta cell mass. The purification procedures required to eliminate acinar contamination and allow safe portal vein infusion cause large islet cell losses. Other procedures designed to minimize islet loss result in crude preparations containing substantial acinar tissue. In dogs and rats, crude preparations have been inoculated with safety into the spleen and function well in this location, but such a procedure might not be feasible in the human. Preliminary trials of these techniques in the monkey have not been successful. Second, dispersed and isolated islets inoculated into any site are exceptionally vulnerable to rejection and cease to function within a few days. Successful human islet allografting must await development of improved techniques of histocompatibility matching and/or immunosuppression. An additional question, unanswered in experiments to date, relates to the probable requirement for accuracy in replacement of alpha cells and beta cells for cure of the insulin-deficient juvenile diabetic patient. In rats, transplantation of large volumes of islet cells has resulted in hyperglucagonemia, hyperinsulinemia, and polyphagia, although the rats remain normoglycemic and have normal glucose tolerance tests. Bewick has elicited hyperinsulinemia in dogs by denervation and shunting the pancreatic venous drainage from portal to systemic. The metabolic effects of this abnormal state have not been adequately studied. These unresolved issues mandate that pancreatic transplantation remain an experimental procedure in humans. Whole or segmental pancreatic implants are technically feasible and are capable of function for extended periods of time. Islet implantation is reserved for carefully controlled experiments and in patients immunosuppressed for other organ transplants.
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PMID:Replacement of pancreatic beta cells as treatment for diabetes mellitus: a review. 41 7

The effects of training to various rhythms of intermittent total starvation (ITS) or intermittent protein starvation (IPS) on the plasma glucose and the plasma insulin levels were studied in the growing chicken. Both types of feeding improved the glucose tolerance in spite of a decrease in the insulin response. After an oral glucose load, plasma free fatty acids showed opposite variations to plasma insulin and plasma glucose. The insulin released in response to a test meal was unchanged. In the ITS 1-1 group (1 day fasting-1 day feeding cycles), low glycemia-low insulinemia were observed during the fasting period of the cycle and high glycemia-hyperinsulinemia during the repletion period in response to the "adaptive hyperphagia." In the IPS 1-1 group (1 day feeding with the protein free diet-1 day feeding with the balanced diet cycles), glycemia was sustained at a high level during both periods of the cycle and insulinemia was depressed by feeding with the protein-free diet and highly stimulated by refeeding with the balanced diet. Therefore, in the chicken, intermittent feeding increases the insulin sensitivity of target tissues and modifies the B-cell sensitivity to glucose. The highest decrease in B-cell sensitivity to glucose was obtained with the protein free diet which further emphasizes the glucose-amino acid synergism previously observed for insulin release.
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PMID:Effect of intermittent feeding on glucose-insulin relationship in the chicken. 43 Feb 64


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