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)

beta-Aspartyl-methionine, -aspartic acid and -glutamic acid and gamma-glutamyl-threonine and -glycine were isolated and identified in human urine by ion-exchange chromatography, high-voltage paper electrophoresis, acid hydrolysis and determination of N-terminal amino acids of the isolated compounds, and comparison of their behaviors in paper electrophoresis and chromatography with those of the authentic compounds. The concentrations of acidic beta-aspartyl dipeptides in human urine were determined using an amino acid analyzer. Their concentrations were as follows: beta-aspartyl-glycine, male, 44.4 +/- 8.5, female, 61.4 +/- 18.9, child, 83.7 +/- 27.1; -alanine, male, 11.0 +/- 4.9, female, 20.7 +/- 12.0, child, 25.3 +/- 9.1; -glutamic acid, male, 10.0 +/- 3.7, female, 23.0 +/- 8.5, child, 20.4 +/- 7.5; -serine, male, 9.9 +/- 2.8, female, 13.6 +/- 3.8, child, 14.9 +/- 4.7; -aspartic acid, male, 4.3 +/- 1.0, female, 9.1 +/- 2.2, child, 18.4 +/- 6.5; -threonine, male 3.9 +/- 0.9, female, 5.8 +/- 1.1, child, 13.2 +/- 4.9 mumol/g creatinine (mean +/- S.D.). The order of the sum of their concentrations tended to be child greater than female greater than male. Patients receiving intravenous hyperalimentation also excreted acidic beta-aspartyl dipeptides into urine in amounts similar to those in females and in a pattern similar to that observed in healthy persons. This finding indicates that urinary beta-aspartyl dipeptides were probably of endogenous origin because oral nutrition was stringently excluded in these patients.
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PMID:Isolation and identification of urinary beta-aspartyl dipeptides and their concentrations in human urine. 3 58

Obese Zucker rats were either pair-fed to their lean litter-mates or fed ad lib, to determine the effect of hyperphagia on serum hormone levels and tissue metabolism as indicated by enzyme activities and in vitro metabolite flux. Hyperphagia was shown to be non-essential for the elevation in serum insulin and suppression in serum growth hormone and prolactin in the genetically obese rat. It was also shown that the increased liver cell lipogenic rate was not dependent on hyperphagia in the obese rat and that adipose cell lipogenesis was not significantly altered in the pair-fed obese rat. The utilization of alanine for glucose synthesis in vitro was similar for both lean and obese rats, but its utilization for fatty acid synthesis was higher in the obese rat. Data is presented which suggest that the inhibitory effect of glucagon on liver lipogenesis is blunted in the obese rat.
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PMID:Serum hormone levels and tissue metabolism in pair-fed lean and obese Zucker rats. 19 81

1. Lactation is associated with an increase in the arterial blood concentration of L-alanine and L-glutamate, but a decrease in that of L-glutamine compared with the corresponding values for virgin rats. 2. Virgin rats fed a 'cafeteria diet' that induces hyperphagia have increased arterial concentrations of L-alanine, L-glutamate and L-glutamine. During lactation L-alanine and L-glutamate concentrations are even higher. 3. The removal of L-alanine is decreased in hepatocytes from lactating rats fed either a chow or cafeteria diet. 4. Measurements of arteriovenous differences across lactating mammary glands indicate that appreciable amounts of L-glutamine and L-alanine are extracted by the gland. 5. A high proportion of the L-alanine metabolized by isolated acini from fed lactating rats is converted into lipid. 6. Metabolism of L-alanine in acini from starved lactating rats is limited by the activity of pyruvate dehydrogenase. 7. It is concluded that L-alanine and certain other amino acids taken up by the gland in excess of the requirements for protein synthesis can be converted into lipid.
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PMID:Utilization of L-alanine and L-glutamine by lactating mammary gland of the rat. A role for L-alanine as a lipogenic precursor. 731 14

Plasma amino acid profiles along with hemoglobin, hematocrit, albumin, protein, blood urea nitrogen and serum creatinine values for ten patients undergoing abdominal operations were studied before operation and for 16 days there-after at different intervals. Six patients in the control group were studied in a similar manner. From the observations obtained, we concluded that total amino acid valued are a more sensitive reflection of patient nutrition in both the preoperative and postoperative periods. In future, total amino acid levels may become part of the nutritional assessment of a patient undergoing an operation. The histidine levels in plasma remain low for the longest period of time, an indication of a great need for histidine. Hence, greater attention should be paid to the histidine content of a diet or solution administered parenterally, or both. In addition, branched chain amino acids, alanine, glycine, cystine, arginine, lysine, tryptophan and threonine are required in greater quantity than the other amino acids as a result of the increased catabolism and partial starvation of the patients postoperatively. In formulation hyperalimentation solutions, an increased need for these amino acids should be kept in mind.
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PMID:Changes in plasma amino acid profiles following abdominal operations. 746 77

Diet protein increases whereas carbohydrates decrease urea synthesis. Traditionally, these effects have been explained by changes in substrate supply. Diet protein intake increases whereas carbohydrate decreases blood amino acid concentration. However, glucose also decreases urea synthesis by a hepatic mechanism independent of the decrease in blood amino acid concentration. Whether this is due to an effect of glucose in itself, or whether the fall in glucagon or the rise in insulin is responsible, was not known. This survey deals with the effect of an increase in diet protein intake and of the separate effects of glucose, glucagon and insulin on functional hepatic nitrogen clearance in normal man and in patients with cirrhosis of the liver. The functional hepatic nitrogen clearance is calculated as the slope of the linear regression analysis of alanine-stimulated urea synthesis rate and blood alpha-amino nitrogen concentration, and expresses urea synthesis independent of changes in blood amino acid concentration. In patients with cirrhosis, hepatic nitrogen clearance is reduced in parallel with liver cell mass, despite high glucagon concentration that would normally up-regulate the process. In both healthy subjects and in patients with cirrhosis, an increase in diet protein intake (plus approximately 50 g/day) for 14 days increases hepatic nitrogen clearance by 40%. Thus, in addition to the substrate effect, protein intake increases urea synthesis by an effect in the liver, probably by enzyme formation. What induces this is not clear but high postprandial levels of glucagon may be involved. Although the effect is qualitatively intact in the patients, the response relative to the increase in protein intake is reduced by two-thirds. The effect may be important to control blood amino acid concentration during a high protein diet and may partly explain why patients with cirrhosis usually tolerates protein hyperalimentation without developing hepatic encephalopathy. It is shown that the reduction of hepatic nitrogen clearance by glucose depends on hyperglycaemia, and is accomplished by the additive effects of a direct hormone-independent action of glucose, and indirectly via suppression of glucagon. Insulin is not a direct controller of hepatic nitrogen clearance, but is still considered an important regulator of urea synthesis by its reducing effects on blood amino acid concentration. High experimental glucagon levels overrule the normal suppressive effect of glucose. In contrast, it is shown that the sugar-alcohol xylitol normalises the glucagon induced increase in hepatic nitrogen clearance. During normal glucagon levels xylitol exerts only a very little decrease in hepatic nitrogen clearance. In patients with cirrhosis, glucose does not down-regulate hepatic nitrogen clearance. However, when the spontaneous high glucagon levels are normalised by somatostatin, glucose decreases hepatic nitrogen clearance. This shows that the direct hormone-independent effect of glucose is intact. These findings indicate that the high glucagon levels during spontaneous hormone responses overrule the suppressive effect of glucose. Incomplete glucose suppression of glucagon secretion during alanine infusion contributes to the high glucagon levels. The removal of the high glucagon levels decreases hepatic nitrogen clearance in itself. Thus, the hyperglucagonaemia may be a compensatory mechanism by which the cirrhotic liver to some extent reestablishes its capacity to produce urea. The consequence is the defective down-regulation of hepatic nitrogen clearance by glucose. The reduction in urea synthesis by glucose, i.e. its nitrogen sparing effect, is accomplished by two different mechanisms: A hepatic component (reduction of the hepatic nitrogen clearance) and a peripheral component (reduced substrate availability mediated by the insulin response). This is an extension of former thoughts according to which glucose reduces urea synthesis due solely to
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PMID:Regulation of urea synthesis by diet protein and carbohydrate in normal man and in patients with cirrhosis. Relationship to glucagon and insulin. 923 44

Agrimony eupatoria (agrimony) has been documented as a traditional treatment of diabetes. Here, the effects of dietary administration of agrimony on streptozotocin (STZ)-diabetic mice and on in vitro glucose uptake and glucose metabolism, and on insulin secretion by BRIN-BD11 cells were investigated. Agrimony incorporated into the diet (62.5 g/kg) and drinking water (2.5 g/l) countered the weight loss, polydipsia, hyperphagia and hyperglycaemia of STZ-diabetic mice. Aqueous extract of agrimony (1 mg/ml) stimulated 2-deoxy-glucose transport (1.4-fold), glucose oxidation (1.4-fold) and incorporation of glucose into glycogen (2.0-fold) in mouse abdominal muscle comparable with 0.1 microM-insulin. In acute 20 min tests, 0.25-1 mg/ml aqueous extract of agrimony evoked a stepwise 1.9-3.8-fold stimulation of insulin secretion from the BRIN-BD11 pancreatic B-cell line. This effect was abolished by 0.5 mM-diazoxide and previous exposure to extract did not adversely affect subsequent stimulation of insulin secretion by 10 mM-L-alanine, thereby indicating that there was no detrimental effect of the extract on cell viability. The effect of extract was glucose-independent and was not evident in BRIN-BD11 cells exposed to a depolarizing concentration of KCl. The ability of agrimony extract to enhance insulin secretion was dependent on use of heat during extract preparation. These results demonstrate the presence of antihyperglycaemic, insulin-releasing and insulin-like activity in Agrimony eupatoria.
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PMID:Actions of the traditional anti-diabetic plant, Agrimony eupatoria (agrimony): effects on hyperglycaemia, cellular glucose metabolism and insulin secretion. 979 50

The mouse agouti-related protein (AGRP) is a powerful appetite effector that results in hyperphagia and the development of obesity when administered intracerebroventricularly or when overexpressed in transgenic mice. Animal studies have also shown that exogenous administration of AGRP predisposes toward hedonic intake of high fat and high sucrose diets. The human ortholog (hAGRP) maps on chromosome 16q22 and has similar physiological properties, as tested in animal models. A polymorphism was identified in the third exon of hAGRP, c.199G-->A, that resulted in a nonconservative amino acid substitution, Ala(67)Thr. Computational analysis of the protein showed significant differences in the coils of the two polymorphic isoforms of the protein. Human studies showed no genotype effects in individuals with a mean age of 25 yr. However, the G/G genotype was significantly associated with fatness and abdominal adiposity in the parental population with a mean age of 53 yr. The c.199G-->A polymorphism in hAGRP could, therefore, play a role in the development of human obesity in an age-dependent fashion.
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PMID:A polymorphism in the human agouti-related protein is associated with late-onset obesity. 1221 71

Hyperalimentation solutions, with low protein content but rich in amino acids, have been more frequently used as a dietary treatment for renal terminal patients, with the purpose to increase their survival. However, the literature in this respect is contradictory. Some authors justify the use of amino acids due to the fact that they seem to regenerate damaged tubular cells (glycine, for example). Other authors, on the contrary, do not agree with this position, since some amino acids, like L-Serine and Lysine, are nephrotoxic. In 1977, it was demostrated that Lysine and Arginine inhibited protein tubular reabsorption, inducing proteinuria, while Glycine, Alanine, Asparagine and Glutamic Acid did not. In order to clarify this issue, we carried out a controlled animal study using uninephrectomized rats fed during nine weeks, with different hypoproteinic diets (4% protein content), enriched individually with five different amino acids. The hypoproteinic diets were enriched with Lysine and Arginine (essential amino acids) and Proline, Glutamic Acid and Asparagine (non essential amino acids). Assays for serum biochemical markers and renal function were carried-out pre-nephrectomy, two weeks after nephrectomy (post-nephrectomy control) and nine weeks post-diet for all the animals, no matter the diet to which they were subjected, the serum biochemistry results showed that all the hypoproteinic diets, enriched with amino acids, affected the renal function. The nephrotoxicity of the tested amino acids, followed this decreasing order: Glutamic Acid > Proline > Lysine > Asparagine > Arginine. hypoproteinic diets enriched with Lysine, Asparagine and Arginine, produced glomerular hyperfiltration, without proteinuria. In summary, our results point towards the idea that, contrarily to what has been described in the literature by some authors: enrichment of hypoproteinic diets with certain amino acids does not seem to protect against progression of renal disease in physiologically compromised kidneys.
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PMID:[Effect of hypoproteic diets enriched with essential and non-essential amino acids on the uninephrectomized rat ]. 1221 96

Otsuka Long-Evans Tokushima fatty (OLETF) rats lack the CCK-1 receptor, are hyperphagic, progressively become obese, and develop type-2 diabetes. We recently demonstrated an increased preference for both real and sham feeding of sucrose in this strain, suggesting altered orosensory sensitivity. To investigate taste functions, we used an automated gustometer with 10-s access to different concentrations of various sapid stimuli. Tests were repeated at 10 and 18 wk of age to assess the early and advanced stages of prediabetes, respectively. Compared with age-matched, nonmutant controls, the OLETF rats showed higher avidity for sucrose at both ages. This difference increased as a function of age and tastant concentration. An exaggerated response also occurred for saccharin, alanine, and fructose, but not for Polycose. Similarly, OLETF rats consumed monosodium-glutamate more at the lower concentrations compared with controls, an effect that age also accentuated. In contrast, there was no statistical strain or age differences in responses to NaCl, MgCl2, citric acid, quinine-HCl, and the trigeminal stimulus capsaicin. These findings demonstrate that compared with controls, OLETF rats differ in their gustatory functions with an overall augmented sensitivity for sweet that progresses during prediabetes. This effect explains their overconsumption of sweet solutions and may contribute to the overall hyperphagia and obesity in this strain.
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PMID:Altered taste sensitivity in obese, prediabetic OLETF rats lacking CCK-1 receptors. 1608 77

Medical records of 16 cats diagnosed with exocrine pancreatic insufficiency (EPI) were reviewed. The diagnosis was confirmed with either a serum feline trypsin-like immunoreactivity (fTLI) concentration <or=12 microg/l or a fecal proteolytic activity (FPA) <6mm for three consecutive days. The majority of cats were castrated male domestic shorthairs. The median age of cats affected was 7 years. The most common clinical sign was weight loss followed by diarrhea, polyphagia and vomiting. Concurrent disease was present in 10/16 (63%) cats. The most common laboratory abnormalities were normocytic normochromic anemia, lymphopenia, neutrophilia, increased alanine transferase activity, hyperglycemia and increased bilirubin concentrations. All 10 cats that were tested for serum cobalamin levels were found to be deficient. All 10 cats that were tested for serum folate concentrations had normal or increased levels. Ten out of 11 cats had at least a partial response to treatment. All cats were discharged from the hospital alive. Results suggest that EPI should be considered a differential diagnosis in any cat with weight loss or poor growth after more common diseases have been ruled out. Concurrent disease is common in feline EPI. Cobalamin deficiency is common in cats with EPI and cats should receive cobalamin supplementation to improve response to treatment. Cats in this study had a good prognosis.
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PMID:Feline exocrine pancreatic insufficiency: 16 cases (1992-2007). 1955 51


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