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)

Ten women with low estriol excretion received hyperalimentation prior to induction of labor. Six received an amino acid mixture (5% Aminofusin) and 25% dextrose, two received the amino acid mixture, and two received 25% dextrose. Amniotic fluid obtained before and after hyperalimentation was assayed for fetal surfactant production, thyroid, pituitary, and carbohydrate regulating hormones. In the combined amino acid/dextrose infusion group the amniotic fluid palmitic acid levels increased significantly post infusion; rT3 also increased significantly but T3 and T4 showed no significant change. The pituitary hormones growth hormone, prolactin, and ACTH showed no significant change, but beta-endorphin-like activity was significantly elevated. No thyroid-stimulating hormone was detected in any of the samples. All the carbohydrate regulating hormones, insulin, cortisol, and cAMP, showed significant increases but cGMP showed a significant decrease. The amino acid and dextrose only groups gave similar results. Seven of the infants showed some degree of intrauterine growth retardation but no neonatal complications attributable to the hyperalimentation.
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PMID:Amniotic fluid endocrine changes during maternal hyperalimentation. 608 68

Opiate receptor blockade, or forced imbibition of 2% NaCl to deplete pituitary dynorphin decreases 2-deoxy-D-glucose (2-DG), but not insulin-induced hyperphagia, indicating a possible role for dynorphin in the eating associated with endogenous opiates. Beta-adrenergic receptor blockade decreases vasopressin release induced by 2-DG but not by insulin. Because vasopressin and dynorphin are sometimes co-localized, it was hypothesized that naloxone-sensitive feeding might be selectively inhibited by beta-adrenergic blockade with propranolol. Propranolol in doses as low as 2.5 mg/kg inhibited 4 hr feeding induced by 2-DG (400 mg/kg). Propranolol did not significantly affect feeding induced by ketocyclazocine administration (3.0 mg/kg) or by 24 hr food deprivation. Feeding stimulated by insulin (10 U/kg) was significantly inhibited by propranolol (2.5 mg/kg) only when the propranolol was reinjected during the period 2 hr after insulin injection, when the induced feeding was greatest. In summary, propranolol inhibited opiate-related (2-DG) as well as opiate-independent (insulin) hyperphagias. It also failed to inhibit food intake resulting from the opiate related stimulus of 24 hr food deprivation. Therefore, naloxone sensitive hyperphagias were not specifically inhibited by beta-adrenergic blockade, indicating that vasopressin-associated dynorphin is not involved in opiate related feeding.
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PMID:Differential inhibition by propranolol of feeding induced in rats by various stimuli. 609 26

The effects of glucoprivation on the food intake have been determined in infant rats up to weaning. It was found that insulin reduced the milk intake of 9, 13 and 17-day-old males and females for three hours after treatment. In 24-day-old pups food intake increased for three hours after insulin administration, and decreased during the next 21-hour period. 2-deoxy-D-glucose increased the food intake in 28-day-old rat pups only. It was concluded that the inability of rat pups to correct glucoprivation by a subsequent increase of food intake is a consequence of the inadequate development of hypothalamic regulatory mechanisms. Glucoprivation stimuli are ineffective inducers of short-term hyperphagia of rat pups until the age of 24-28 days.
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PMID:Effect of insulin and 2-deoxy-d-glucose on the food intake of infant rats. 621 8

1,5-Anhydroglucitol (1-DG) has been known as an antimetabolic glucose analogue. Using gas chromatography, 1-DG was found to be physiologically present in rat serum. In order to investigate its direct and long-term effects on feeding, 1-DG was infused during the light period into the rat third ventricle in doses of 3.0, 6.0 and 12.0 mumol/rat. Its effects were then compared to those of similarly applied 2-deoxy-D-glucose (2-DG). Following initial hyperphagia, both of these glucose-analogues produced suppressive effects on feeding during the subsequent day throughout the light and dark periods. On the third day after 2-DG injection reduction of feeding did not recover completely to the pretreatment baseline levels, but it did recover after 1-DG. Both 1-DG and 2-DG caused linear dose-related hypophagia, with the slope for 1-DG being about half of that for 2-DG. It is suggested that the delayed hypophagia which followed the initial hyperphagia produced by deoxyglucose was a result of sustained inactivation of the Na-pump due to intracellular ATP deficiency caused by accumulation of deoxy-glucose-6-phosphate.
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PMID:Feeding suppression induced by intra-ventricle III infusion of 1,5-anhydroglucitol. 631 43

Hyperalimentation solutions have been shown to increase aminoglycoside nephrotoxicity in rats and rabbits. Lysine is a major constituent of hyperalimentation solutions and is known to inhibit tubular reabsorption of protein. To test the effects of lysine on renal function and structure and on aminoglycoside nephrotoxicity, three groups of rats were prepared. Groups 1 and 2 were infused with lysine (55 mumol/kg/min, 1.9 gm/kg total) for 4 hours. In group 2, gentamicin (60 mg/kg) was also infused during the third hour. In group 3, dextrose was given instead of lysine, and gentamicin was given as in group 2. In group 1 (lysine-saline solution), there was a decrease in glomerular filtration rate (GFR) and an increase in 125I-albumin clearance factored by GFR. In group 2 (lysine-gentamicin), the same effects were seen, but the reduction in GFR was significantly greater. Group 3 (dextrose-gentamicin) showed no change in GFR over the 4-hour period, but did show an increase in 125I-albumin clearance factored by GFR. Fractional excretion of sodium rose in group 2 but not in groups 1 and 3. A gradual mild (20%) and nonsignificant fall in renal blood flow followed the combined administration of lysine and gentamicin. In separate 20-hour studies, lysine (1.9 gm/kg intraperitoneally) or gentamicin or tobramycin (60 mg/kg subcutaneously) produced mild renal failure, but the combination of lysine and an aminoglycoside produced substantially greater renal failure. Serum creatinine in experimental groups was significantly correlated with medullary cast formation and tubular necrosis (p less than 0.001). Giant lysosomes with crystalloid inclusions in proximal tubular cells, individual cell necrosis in the pars recta, and casts in the thin limb of the loop of Henle were seen in rats given lysine. We conclude that lysine alone and single large doses of aminoglycosides alone are nephrotoxic, and when the two are combined, toxicity is additive. The nephrotoxicity of lysine may be related to direct tubular toxicity and to tubular obstruction.
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PMID:Nephrotoxicity of lysine and of a single dose of aminoglycoside in rats given lysine. 642 41

Trauma victims often suffer immune system failure. Oral arginine has strong immune-enhancing properties. The metabolic, hormonal, and immune effects of increasing concentrations of arginine as part of post-trauma intravenous hyperalimentation (IVH) were studied. Groups of 11-14 rats, 275-350 g, underwent jugular vein catheterization and bilateral closed femoral fractures under anesthesia. IVH was started immediately postinjury at a rate of 0.8-1 ml/100 g body wt/hr and continued for 5 days. Twenty percent dextrose and three different amino acid mixtures were given as follows: (A) FreII (1.55 g ARG/1); (B) FreIII (4.05 g ARG/1); (C) modified FreIII (7.9 g ARG/1). All rats lost weight over the 5-day postinjury period; however, rats in groups B and C lost significantly less weight than rats in group A (-3.4 +/- 0.8% of initial body weight and -3.6 +/- 0.9% vs -6.1 +/- 1.2%, P less than 0.05). Rats in group A had negative cumulative nitrogen balance, while those in groups B and C were in highly positive balance. No significant difference in body weight change or nitrogen balance was noted between groups B and C. Trauma-induced thymic involution as assessed by thymic weight and lymphocyte content was greatest in group A, which received the lowest amount of arginine, and was linearly abrogated by increasing the amount of arginine administered (A less than B less than C). Thymocyte immune responsiveness increased with the amount of arginine given as assessed by mitogenesis in response to Con A (stimulation index: A--151.3 +/- 28.8 vs B--243.6 +/- 29.2, P less than 0.01 vs C--321.8 +/- 22.3, P less than 0.001 vs A and P less than 0.02 vs B) and PHA (A--65.0 +/- 14.3 vs B--67.7 +/- 15.3, NS, vs C--117 +/- 14.0, P less than 0.005 vs A and B).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High arginine levels in intravenous hyperalimentation abrogate post-traumatic immune suppression. 642 25

The optimal levels of arginine (Arg) for growth and immunity were studied in mildly depleted, noninjured rats maintained on intravenous hyperalimentation. Three groups of S-D rats (eight/group, weighing 275-300 g) underwent catheter insertion, 1 day of fasting, and then 7 days of intravenous hyperalimentation consisting of 20% dextrose, adequate minerals and vitamins, and three amino acid regimens: (1) FreAmine II (1.55 g Arg/liter); (2) FreAmine III (4.05 g Arg/liter); (3) experimental (7.5 g Arg/liter). The increase in arginine levels was achieved by lowering the glycine levels. There were no differences among the groups in terms of body weight gain (6.9 vs 8.3 vs 10.0 g) or in cumulative N balance (574 vs 660 vs 642 mg). Liver, spleen, and adrenal weights did not differ. Thymus weight was greater in groups B and C: (A) 345 +/- 27 mg vs (B) 445 +/- 34 mg, p less than 0.05, vs (C) 438 +/- 26 mg, p less than 0.05) as were the total number of lymphocytes/thymus (X 10(-9) (A) 0.93 +/- 0.12 vs (B) 1.37 +/- 0.18, p less than 0.05, vs (C) 1.46 +/- 0.15, p less than 0.05). Mitogen-induced thymocyte blastogenesis (cpm) was greatest in group C in response to phytohemagglutinin: (A) 9.558 +/- 3,799 vs (B) 20,088 +/- 5,890, NS, vs (C) 37,234 +/- 6,209, p less than 0.01 vs A and p less than 0.05 vs B) and Concanavalin A: (A) 71,035 +/- 15,228 vs (B) 111,734 +/- 15,021, NS, vs (C) 172,967 +/- 19,861, p less than 0.01 vs A and p less than 0.05 vs B). In the intravenous hyperalimentation-maintained noninjured rat ARG concentrations more than 1.55 g/liter do not enhance N retention or growth. Larger doses of ARG have strong thymic immunostimulatory effects without any toxicity or growth reduction.
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PMID:Optimal levels of arginine in maintenance intravenous hyperalimentation. 642 65

Intravenous (i.v.) infusion of excessive energy has been associated with hepatic steatosis. The time course of liver lipid accumulation was examined during 6 days of i.v. hyperalimentation with fat-free infusate. Adult male rats with indwelling superior vena cava cannulas received a dextrose-amino acid infusate for 0, 1/2, 1, 2, 4 or 6 days to provide 146% of nonprotein energy requirement [congruent to 350 non-protein kcal/(kg . day)] and 335% of nitrogen requirement [congruent to 2.7 g amino nitrogen/(kg . day)]. Significant hepatomegaly was apparent by day 1/2. Initially, glycogen deposition accounted for the liver enlargement, but after day 2, liver glycogen was declining and liver lipid was increasing. By day 4, liver lipid had increased fourfold and was the major contributor to hepatomegaly. Concurrent with fatty liver metamorphosis, hepatic essential fatty acid deficiency (EFAD) developed by day 4; liver linoleic acid levels had dropped from 20 to 1% of total fatty acids, and liver triene:tetraene ratio was 0.68. Similar changes in hepatic phospholipid fatty acids were observed. Enhanced lipogenesis and impaired lipid transport is known to accompany EFAD and may underlie the observed steatosis. A doubling of plasma cholesterol levels was also associated with steatosis. The mechanism leading to this increase in plasma cholesterol warrants further investigation.
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PMID:Development of hepatic steatosis and essential fatty acid deficiency in rats with hypercaloric, fat-free parenteral nutrition. 643 8

Intravenous hyperalimentation with dextrose can be associated with adverse respiratory and hepatic effects. The purpose of this study was to determine the respiratory and metabolic consequences of fat calories in excess of resting energy expenditure provided both continuously and discontinuously. No significant changes in respiratory mechanics, oxygen consumption, carbon dioxide production, resting energy expenditure, serum substrates, liver function, or nitrogen balance were noted by the addition of 500 kcal of lipid emulsion to dextrose calories sufficient to meet energy requirements. The respiratory quotient declined significantly with the 12- and 24-hour lipid infusions, but persisted for the entire 24 hours only in the latter instance. The sustained and increased (46% v 36%) oxidation of lipid with a 24-hour infusion suggests that a continuous infusion of lipid is preferable to a discontinuous infusion.
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PMID:Metabolic and respiratory effects of continuous and discontinuous lipid infusions. Occurrence in excess of resting energy expenditure. 643 73

5-Thio-D-glucose (200 and 500 mg/kg) produced hyperglycemia and significantly retarded emptying of the pregastric pouch of hamsters. 2-Deoxy-D-glucose did not affect stomach-emptying at either of the doses used (500 and 1000 mg/kg), but did cause hyperglycemia at the higher dose. These results are discussed in relation to the failure of these glucose analogs to produce hyperphagia in the golden hamster.
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PMID:Effects of 5-thio-D-glucose and 2-deoxy-D-glucose upon stomach-emptying in the golden hamster. 654 8


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