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

A new program of total parenteral nutrition (TPN) for surgical neonates has been described an investigated. The program is based on the use of fat emulsion as the major source of calories and infusion of large volumes of the solution via peripheral veins. This program has three main advantages over conventional hyperalimentation using a central venous catheter: (1) it avoids complications such as septicemia, thrombosis of large vessels, and metabolic complications such as hyperglycemia or osmotic diuresis; (2) it provides physiological nutritive elements containing a normal composition of glucose, protein, and fat; and (3) it is easy to start and manage the TPN using a peripheral vein. Thirty-four neonatal surgical patients with life-threatening gastrointestinal anomalies have been placed on this TPN program. Infusion of fat emulsion and large volumes of fluid were well tolerated and all patients gained weight during the period of observation.
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PMID:Total parenteral nutrition using peripheral veins in surgical neonates. 40 73

Urinary outputs of amino acids in nine patients receiving intravenous hyperalimentation were estimated for evaluating adequacy of dosage and composition of the infusage for the maintenance of normal metabolism of tissue proteins in the subjects. The daily outputs of the methylated amino acids (3-methylhistidine, epsilon-N-methylated lysines and guanidino-N-methylated arginines), which are thought to be derived from tissue proteins, remained in the normal ranges, suggesting that the normal metabolism of tissue proteins was sustained during intravenous hyperalimentation. Relatively large urinary excretion of threonine, serine and glycine might reflect the large dosage of glucose in the infusate and disuse of these amino acids during the treatment, especially in the patients with hepatic dysfunction. Diurnal rhythms in urinary outputs of amino acids in patients receiving intravenous hyperalimentation were not observed, except for the outputs of threonine, serine and glycine, which were large during the 3.00-9.00 h and 15.00-21.00 h periods. The absence of daily fluctuations of the methylated amino acids in urine suggested that there were no diurnal rhythms in the metabolism of tissue proteins in the subjects.
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PMID:Urinary excretion of amino acids in patients receiving intravenous hyperalimentation. 41 73

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

The acute effect of bilateral electrolytic ventromedial hypothalamic lesions (20-25-m Coulomb stainless steel electrodes) on plasma levels of insulin and glucose was studied in anesthetized rats to determine early effects that would occur before hyperphagia and obesity. In rats fed ad libitum, lesions in the ventromedial hypothalamus (VMH) but not in the cortex produced a marked increase in circulating insulin levels (starting at 20 min postlesion) and a small increase in glycemia which, however, was not significant and could therefore not be the cause of increased insulin secretion. Hyperinsulinemia after VMH lesions was more pronounced when glucose was infused iv at a rate of 7-8 mg/kg . min. Bilateral subdiaphragmatic vagotomy, performed 50 min after VMH lesions, immediately and completely reversed the observed hyperinsulinemia. With the exception of a tendency of lesions producing the highest degree of hyperinsulinemia to be slightly larger than the lesions not producing any hyperinsulinemia, no statement about the critical involvement of a specific hypothalamic locus can be made. It is concluded that electrolytic VMH destruction causes immediate hypersecretion of the pancreatic B cell, an effect that requires the integrity of the vagus nerves. Further localization of the central circuitry responsible for this mechanism, however, will require more specific methods than electrolytic lesions.
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PMID:Acute hyperinsulinemia and its reversal by vagotomy after lesions of the ventromedial hypothalamus in anesthetized rats. 44 4

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

It is today's general medical opinion that children's diabetes mellitus was uncommon in the past. It was generally admitted at that time the initail stages were so sudden as to make difficut its early diagnosis. It's increased incidence is at present an alarming truth; however, a parallel increase of diabetic coma or of mulminant types has rather dropped. Diabetes may be diagnosed by just considering the main symptoms at the onset which are polydipsia, polyuria and weight loss. If an early diagnosis is not made, acidosis (abdominal pain, nausea, vomiting) may appear within a few days or weeks followed by coma (Kussamul's acidotic respiration and dehydration). Coma may be avoided by an early diagnosis and a life may be saved. It must be stressed that an important percentage of children and adolescents show a slow and gradual evolution (week or months) of their diabetes: gradual weight loss, sometimes with noticeable polyphagia, occasional enuresis, but without other associated symptoms. Asymptomatic, intermittent glucosurias are also frequent; they vary in magnitude an almost always they appear without ketonuria and with fasting normal glycemia. According to our experience they may precede in weeks or months the clinical manifestations of the disease. Postprandial glycemia is a sure diagnostic resource; it is of greater trustworthines than fasting glycemia; therefore we advise it as a routine diagnostic procedure which we recommend widely. In uncertain situations, the oral glucose tolerance test is advisable.
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PMID:[Diabetes mellitus in childhood and adolescence. Clinical types]. 48 58

The glucose analogue 2-deoxy-D-glucose (2DG) inhibits glucose metabolism and causes a rapid increase in food consumption in most species. This increase is most apparent during the first 6 postinjection hours, although it may persist as long as 10 hr. There are no published descriptions of alterations in food consumption subsequent to the hyperphagia. In the present study male and female rats were injected with 2DG (750 mg/kg IP), insulin (regular, 20 U/kg SC) or distilled water, and food intake was compared to baseline levels during the next 1, 6 and 24 hr. Results showed that food intake: (1) was not affected by injections of water: (2) was higher than normal during all 3 time periods following insulin injections: and (3) was higher than normal at 1 and 6 hr following 2DG, but significantly lower than normal by the end of 24 hr. The reasons underlying the development of hypophagia subsequent to the initial hyperphagia produced by 2DG are presently unknown.
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PMID:Hypophagia follows the initial hyperphagia produced by 2-deoxy-D-glucose in rats. 51 10

Obese (ob/ob) and diabetes (db/db) mice are genetic mutants that have been shown to have altered levels of central catecholamines as well as syndromes of obesity, hyperphagia, and hyperglycemia. Because of catecholamines, and particularly norepinephrine (NE), are implicated in the control of feeding, levels of central catecholamines were experimentally reduced in ob/ob and db/db mice to investigate the role of the catecholamines in these cases of spontaneously occurring obesity. Lesions produced by 6-hydroxydopamine (6-OHDA) were used to produce large depletions of NE and dopamine (DA) in both ob/ob and db/db mice and in lean control mice of the same background strains. In the db/db but not the ob/ob, central catecholamine depletion was accompanied by a significant and persistent weight loss and by a reduction in plasma glucose levels when compared with vehicle-infused controls. Treatment with the NE uptake blocker desmethylimipramine (DMI) prior to 6-OHDA infusions attenuated NE but not DA depletion. Diabetes mice that received DMI pretreatment showed a weight loss and decrease in plasma glucose proportional to the amount of NE depletion. Lean mice that received the 6-OHDA treatments showed only a transient weight loss and no significant change in blood glucose. It is concluded that abnormalities in central noradrenergic systems may account for part of the obesity syndrome observed in the diabetes mouse.
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PMID:Differential effects on body weight of central 6-hydroxydopamine lesions in obese (ob/ob) and diabetes (db/db) mice. 52 20

Alloxan-diabetic rats were hyperphagic when fed diets containing little fat, but they ate normal amounts of food when given diets rich in fat. Normal rats increased food intake to the same degree when the caloric density of their diet was decreased by reducing the content of fats or carbohydrates in isocaloric amounts. Diabetic rats did not respond substantially to changes in caloric density of their diet which were produced by altering the content of dietary carbohydrates, but they systematically increased food intake as the amount of fat in their diet was reduced. Diabetic rats ate normal amounts of a high-fat diet despite continued loss of nutrients in urine and persisting impairments in glucose utilization, fat storage, and liver glycogen deposition. These findings suggest that hyperphagia in experimental diabetes mellitus is a compensatory response to a lack of utiliziable fat fuels rather than the result of a metabolic disturbance per se.
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PMID:Hyperphagia in rats with experimental diabetes mellitus: a response to a decreased supply of utilizable fuels. 62 30


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