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)

Multilumen catheters have been condemned for hyperalimentation based on reports of infection rates between 10% and 25% in uncontrolled studies. Because of the potential usefulness of multilumen catheters, we studied infection rates in a prospective, randomized trial. All patients requiring total parenteral nutrition were randomized to either single- or double-lumen catheters. Single-lumen catheters were used for dextrose-amino acids only. Medications or fat emulsions were given either by another central line or peripherally. Double-lumen catheters were used for dextrose-amino acid solutions, compatible medications, and fat emulsions. Catheters were cultured (48 single lumen and 53 double lumen) from 112 patients who successfully completed the study. No patients in either group developed catheter sepsis. We concluded that parenteral nutrition can be given as safely via double-lumen catheters as single-lumen catheters when strict protocols are established and followed.
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PMID:Single-lumen vs double-lumen catheters for total parenteral nutrition. A randomized, prospective trial. 211 19

Medium-chain triglycerides (MCT) are an important component of an enteral ketogenic diet for seizure control. Previously, it was difficult to maintain ketosis when parenteral (iv) nutrition therapy was necessary. The use of iv MCT in a 5-year-old girl with Lennox-Gastaut syndrome who had diarrhea and dehydration is reported. Conventional 20% iv fat emulsion (long-chain triglycerides, LCT) and dextrose free hyperalimentation (HAL) in a 4:1 ketogenic ratio did not maintain adequate ketosis during bowel rest. Compassionate use of iv MCT (Clintec Nutrition) infused as a 70:30 MCT/LCT ratio plus HAL maintained moderate ketosis. Seizures were well controlled during the iv MCT regimen, which allowed normal daily functioning. Complications included abnormal liver function tests and severe iron deficiency anemia of unknown etiology. Serum triglyceride and cholesterol levels increased to 1717 mg/dl and 614 mg/dl, respectively, but decreased with a reduction of lipid infusion and use of an antihyperlipemic drug. Nutritional status was maintained. In this case, iv MCT proved to be a relatively safe and effective short-term method of continuing parenteral nutrition while maintaining ketosis for seizure control.
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PMID:Use of parenteral medium-chain triglyceride emulsion for maintaining seizure control in a 5-year-old girl with intractable diarrhea. 212 29

1. The effects of streptozotocin-induced diabetes mellitus on active jejunal glucose uptake in vivo, and on galactose movement across the brush-border (phlorhizin-sensitive) and basolateral (phlorhizin-insensitive) membranes of isolated upper and mid-villus enterocytes has been studied. 2. Chronic diabetes increased unidirectional phlorhizin-sensitive galactose uptake by mid-villus but not upper villus cells. In contrast, phlorhizin-insensitive uptake by both cell populations was enhanced by diabetes. 3. Diabetes increased glucose absorption in vivo by mechanisms which were unrelated to hyperphagia. Mucosal hyperplasia acting together with an epithelium containing a higher proportion of mature enterocytes is the most likely explanation for the response. 4. We conclude that, during diabetes, the mid-villus region is an important site of adaptation with functional changes occurring at both the brush-border and basolateral membranes. The increased hexose transport ability of the basolateral membrane is retained during cell transit along the villus.
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PMID:Diabetes mellitus and sugar transport across the brush-border and basolateral membranes of rat jejunal enterocytes. 214 23

We measured the serum GH responses to GHRH (1 micrograms/kg) in six normal men who had been rendered hyperinsulinemic and hypolipidemic by 10 days of total parenteral nutrition (TPN subjects) with a 25% dextrose-amino acid solution. The men underwent GHRH testing after 3 h of infusion of NaCl or Met-human (h) GH (2 micrograms/kg.h). The results of these tests were compared with those of five men tested in the post-absorptive state (PA subjects). The serum GH response to GHRH during NaCl infusion was significantly lower in the TPN subjects than in the PA subjects. During the Met-hGH infusion, the serum GH response to GHRH in the PA subjects was significantly lower than that after the NaCl infusion, whereas in the TPN subjects the response was similar to that during the NaCl infusion. The mean integrated areas under the GH response-time curve after GHRH treatment were 3963 +/- 2086 min/micrograms.L following NaCl infusion and 413 +/- 64 min/micrograms.L following Met-hGH infusion in PA subjects; they were 1127 +/- 500 min/micrograms.L following NaCl infusion and 1456 +/- 682 min/micrograms.L during Met-hGH infusion in the TPN subjects. The Met-hGH infusions resulted in a significant increase in serum FFA concentrations in the PA, but not the TPN, subjects. These results suggest that hyperalimentation induces a metabolic background which inhibits GH secretion, as manifested by a diminished serum GH response to GHRH administered after NaCl infusion. The absent FFA response to Met-hGH infusion in the TPN subjects may explain why the Met-hGH infusion in them did not result in a reduced serum GH response to GHRH as occurred in the PA subjects. Hence, FFA may play an important role in the effects of short term Met-hGH infusion on GH secretion.
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PMID:Intravenous refeeding blocks growth hormone (GH)-provoked rises in serum free fatty acids and blunting of somatotroph response to GH-releasing hormone in normal men. 250 53

Hyperglycaemic hyperosmolar non-ketotic syndrome (HHNS) is a life-threatening complication of uncontrolled diabetes mellitus. This syndrome is characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, beta-blockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular and extracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. Therefore, correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities. Appropriate management of precipitating illnesses will limit the high mortality associated with HHNS. This review discusses the current state of knowledge concerning the pathogenesis of HHNS, the clinical features of the disorder, and a systematic approach to treatment.
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PMID:Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome. 268 Apr 38

Individuals with cystic fibrosis have a 1% to 7% incidence of insulin-dependent diabetes mellitus. The occurrence of diabetic microangiopathy in patients with cystic fibrosis has been reported recently. From 1978 to 1987, 19 patients with cystic fibrosis and diabetes mellitus were followed up. Four patients (21%) had evidence of diabetic microangiopathy. In one, peripheral neuropathy developed 5 years after the onset of diabetes mellitus, and the other 3 patients each had complications of retinopathy, nephropathy, and neuropathy which developed 10 years after the onset of diabetes mellitus. All were poorly compliant in their medical care. Significant morbidity was seen in the 3 patients with multisystem involvement--blindness, glaucoma, hypertension, and renal failure. The combination of long-standing diabetes mellitus, poor glycemic control, plus pathophysiologic features associated with cystic fibrosis may have contributed to the development of microangiopathy. The use of steroids in 4 other patients and dextrose infusions (as part of hyperalimentation) in another 4 patients precipitated or exacerbated diabetes. The data indicate that diabetic microangiopathy can occur in the individual with cystic fibrosis. Routine screening for diabetes and its complications in the population with cystic fibrosis, as well as optimal control of hyperglycemia, is warranted.
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PMID:Diabetic microangiopathy in patients with cystic fibrosis. 278 Jan 26

The glucose antimetabolite 2-deoxy-D-glucose (2DG) reliably causes hyperphagia in rats, but has consistently proven ineffective in producing overeating in golden hamsters. It was hypothesized that hamsters do not overeat following 2DG administration because of unusually strong aversive effects of the drug in this species. To test this hypothesis, rats and hamsters were tested in a conditioned taste aversion (CTA) paradigm, in which a novel 0.1% saccharin solution was paired on three occasions with intraperitoneal injections of either saline, lithium chloride (LiCl; 50 mg/kg), or 2DG (either 350 or 750 mg/kg). CTA was measured in 16 twenty-minute, two-bottle preference tests which were conducted at 2-3 day intervals following conditioning. LiCl and 2DG both produced strong and long-lasting aversions to saccharin solution in rats. However, 2DG was significantly less effective than LiCl in producing CTA in hamsters. It is unlikely, therefore, that the failure of 2DG to produce hyperphagia in hamsters is due primarily to an unusual sensitivity to the aversive effects of the drug.
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PMID:Conditioned taste aversion produced by 2-deoxy-D-glucose in rats and hamsters. 285 80

Dynorphin is one of the most potent appetite stimulants among the endogenous opioids. In this study, we describe the anorexic effects of 5 days of forced 2% NaCl drinking in rats, a regimen which depletes vasopressin as well as dynorphin in the neurohypophysis. Feeding induced by direct activation of kappa-opioid receptors with ketocyclazocine was unaffected by the NaCl regimen. However, 2% NaCl imbibition reduced 2-deoxy-D-glucose (2-DG) induced feeding by 65% and spontaneous nocturnal feeding by 38%. Feeding subsequent to 24 hour food deprivation was not decreased. Naloxone-resistant hyperphagia induced by insulin and spontaneous daytime feeding were also not reduced. The combination of naloxone (3.0 mg/kg) and the NaCl regimen produced an additional 50% reduction in 2-DG induced feeding and an extra 40% decrease in nocturnal feeding. Naloxone, given with 2% NaCl to food deprived animals, retained its appetite suppressing activity, indicating that the NaCl regimen did not deplete the endogenous opioid which mediates food deprivation hyperphagia. These results demonstrate that 2% NaCl imbibition suppresses certain opioid mediated hyperphagias. However, the failure of 2% NaCl to affect all of the naloxone-sensitive types of feeding and the independence of naloxone-sensitive and NaCl-sensitive components suggests that NaCl drinking does not deplete dynorphin in the brain areas which mediate opiate-sensitive hyperphagias.
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PMID:Effects of 2% sodium chloride imbibition on various opiate related hyperphagic conditions. 286 2

The present studies were undertaken to further assess the role of plasma beta-endorphin (beta-EP) in the hyperphagia induced by the glucose antimetabolite, 2-deoxy-D-glucose (2-DG). Plasma concentrations of immunoreactive beta-EP (ir-beta-EP) were measured at the end of the first hour of feeding in all animals treated with 400 mg/kg 2-DG. Previous studies had shown a consistent, positive association between 2-DG hyperphagia and plasma ir-beta-EP concentrations, but the present data revealed dissociations between hyperphagia and plasma ir-beta-EP. Dexamethasone administration blocked the 2-DG-induced rise in plasma ir-beta-EP, but had no effect on the 2-DG hyperphagia measured at 1 hour. Forced drinking of a 2% NaCl solution decreased 2-DG hyperphagia, but not the 2-DG induced rise in plasma ir-beta-EP. Thus, elevations in plasma ir-beta-EP are not necessary for the full expression of 2-DG-induced hyperphagia in dexamethasone-treated rats. Furthermore, decreased feeding responses to 2-DG could coexist with increased levels of plasma ir-beta-EP in NaCl-treated normal rats. Elevations in plasma ir-beta-EP do not appear to be the critical opiate link in 2-DG induced hyperphagia.
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PMID:Experimental dissociation of food intake and plasma beta-endorphin following 2-deoxy-D-glucose in rats. 293 39

Adult male rats were subjected to an acute bout of swimming exercise for 50 min during the early morning or late afternoon. Compared to nonexercised controls, all exercised groups showed an initial approximately 2-hr period of increased feeding (period I hyperphagia). A 50-min period of sham swimming (wading in water) was followed by period I hyperphagia but not period II hypophagia. Opioid modulation of period I hyperphagia was indicated by the ability of naltrexone to antagonize, in a dose-dependent manner, the postexercise hyperphagia. Furthermore, plasma concentrations of immunoreactive B-endorphin (Ir-B-ep) were increased during period I following exercise. Opioid modulation of the period II hypophagia was equivocal. Plasma Ir-B-ep was not altered in period II, and naltrexone did not modify period II hypophagia. The ability of 2-deoxy-D-glucose to induce feeding was slightly depressed (p less than 0.05) during period II after exercise, and the ability of exogenous insulin to induce feeding was not changed. These differential feeding responses to 2-deoxy-D-glucose (opioid-mediated) and insulin (relatively opioid-independent) suggest that an opioid deficiency may exist during period II and contribute to the hypophagia.
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PMID:Opioid modulation of feeding behavior following forced swimming exercise in male rats. 293 48


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