UMLS:C0020505 - FACTA Search

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

In this study, the protective effects of L-arginine treatment in vivo on vascular reactivity of streptozotocin (STZ)-induced 12-week-old diabetic rats were examined. Loss of weight, polydipsia, polyphagia, hyperglycemia, hypoinsulinemia, and elevated levels of plasma cholesterol and triglyceride were observed in diabetic rats. L-arginine treatment (1 mg/mL in drinking water) did not significantly affect these metabolic and biochemical abnormalities. Plasma malondialdehyde (MDA) levels in untreated diabetic rats were also significantly higher than untreated controls. However, L-arginine treatment prevented the increase in MDA level of plasma of diabetic rats. Contractile responses, but not sensitivity to noradrenaline (NA), were significantly increased in diabetic rats compared to controls. Treatment of diabetic rats with L-arginine completely prevented the increase in NA responses. Relaxation response to acetylcholine (ACh), but not to sodium nitroprusside (SNP), in diabetic aorta has been found to be significantly decreased as compared with controls. However, there were no significant differences in pD2 values of acetylcholine in either of the groups. L-arginine treatment increased the ACh responses to the control level. All effects of L-arginine on vascular reactivity were found to be specific for diabetic rats and not controls. These results suggest that functional abnormalities occurred in aorta from diabetic rat might at least in part result from L-arginine deficiency, and the lipid peroxidation-lowering effect of L-arginine may account for its protective effect on vascular reactivity of diabetic rats.
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PMID:The effects of chronic L-arginine treatment on vascular responsiveness of streptozotocin-diabetic rats. 1052 67

Effects of nitric oxide synthase(NOS) inhibitors on 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT)-induced hyperphagia which is mediated by the 5-HT autoreceptor were investigated. The non-selective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI) clearly suppressed increases in food intake by 8-OH-DPAT. Both hypophagic effects of L-NAME and 7-NI were reversed by the nitric oxide precursor, L-arginine. The findings suggest that nitric oxide formed in the brain is involved in 8-OH-DPAT-induced hyperphagia.
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PMID:Involvement of nitric oxide in the 5-HT1A autoreceptor-mediated hyperphagia in rats. 1072 Oct 47

In rats, a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) inhibited the hyperphagia induced by the 5-hydroxytryptamine (5-HT)(1A) autoreceptor agonist, 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT). 8-OH-DPAT reduced 5-HT metabolism in the hypothalamus, and this was not blocked by pretreatment with L-NAME. L-NAME also did not affect basal hypothalamic 5-HT metabolism or reverse the decreases in 5-HT synthesis in hypothalamus. These results suggest that the hypophagic effects of L-NAME, which inhibits NO formation, are independent of 5-HT metabolism in the hypothalamus.
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PMID:A nitric oxide synthase inhibitor reduces hyperphagia induced in rats by the 5-HT(1A) receptor agonist, 8-OH-DPAT, independently of hypothalamic serotonin metabolism. 1095 91

We investigated the effects of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) on hypophagia in rats elicited by alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT) and 5-carboxamidotryptamine (5-CT) which are suggested to be mediated by the peripheral 5-HT2A and 5-HT7 receptor, respectively. Both alpha-methyl-5-HT and 5-CT apparently inhibited food intake in food-deprived rats. L-NAME significantly enhanced alpha-methyl-5-HT-elicited hypophagia, while it inhibited 5-CT-elicited hypophagia. These results suggest that NO is differentially related to alpha-methyl-5-HT and 5-CT-induced hypophagia and that NO may play a role in hypo- and hyperphagia.
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PMID:Effects of a nitric oxide synthase inhibitor on hypophagia induced by the peripheral 5-HT receptor agonists, alpha-methyl-5-hydroxytryptamine and 5-carboxamidotryptamine in rats. 1114 88

In 1994, Zhang et al. of Rockefeller University in New York reported the first successful complementary DNA (cDNA) cloning of leptin by the positional cloning method. Leptin was identified as the gene of ob/ob mouse in genetic obesity syndromes. It has very strong food intake control, and body weight and energy expenditure. The name "leptin" derived from the Greek word leptos, meaning "thin." We hereby review major advances leading to our current finding of leptin, leptin receptor and its structure, the outline of homozygote, and also influence of leptin in the pituitary. (The structure of leptin) The mouse obese gene has been localized to chromosome 6. With human leptin gene on chromosome 7q31.3, its DNA has more than 15000 base pairs and consists of three exons and two introns. For bioactivation of leptin the importance of disulfide-binding site is suggested. Human leptin which replaced the 128-th arginine with glutamine has the function of an aldosteron antagonist, which is reported to have the function of athrocytosis inhibition. The resemblance of leptin precursor of human, mouse and rat is very high, i.e., mouse and rat homology is 96% and mouse and human homology is 83%. (The structure of leptin receptor) The mutant gene, which is the cause of obesity, was shown on map on diabetic mouse (db/db) chromosome 4, and it was proven to be the same as the leptin receptor gene cloned by Tartaglia et all. Further studies have found the Zucker fatty rat (fa/fa) to be incorporated into a linkage map of rat chromosome 5, whose region of rat is the equivalent to the region of conserved synteny of the db/db mouse gene. The leptin receptor is glycoprotein consisting of a single transmembrane-spanning component. The primary structure of leptin receptor belongs to the cytokine-class1 family, the single membrane-spanning receptor, and is highly related to the gp130 signal-transducing component of the interleukin-6 (IL-6) receptor, the granulocyte colony-stimulating factor (G-CSF) receptor, and the leukemia inhibitory factor (LIF) receptor. The leptin receptor is known to have at least six existing isoforms (Ob-Ra, b, c, d, e, f) from the difference in splicing. (Homozygote Mutation of Leptin and Leptin Receptor :Hormone Secretion Disorders) The point mutation of ob/ob mouse and the splicing mutation of db/db mouse show remarkable obesity and hyperphagia. These obesity models show a reproduction disorder with both the male and the female, and they develop with homozygote. The cause is thought to be the gonadotropin secretory abnormality in pituitary. Three family lines report the cases of this deficiency, and it is considered that the secretory abnormality in pituitary develops into hypogonadotropic. These patients show low value in plasma FSHbeta (follicle stimulating hormone-beta and LHbeta (luteinizing hormone-beta which are produced from pituitary, and the plasma GnRH (gonadotropin releasing hormone) level is also low. Furthermore, the leptin receptor deficient family line was reported in 1998, in which case only the homozygote developed. The plasma leptin concentration of normal human is about 8.0 ng/ml, and this case with leptin receptor deficiency has high value of 500-700 ng/ml, which is the equivalent to the db/db mouse. (Role of Leptin in Hypothalamus-Pituitary-Periphery Function) The role of leptin which regulates pituitary hormones suggests the promotion the GHRH (growth hormone releasing hormone) secretion in hypothalamus-pituitary axis, with the possibility of the rise in secretion of GH (growth hormone) in pituitary, i.e. effects of icv (intracerebroventricular) infusion of leptin has spontaneously stimulated GHRH, which promotes GH secretion in the normal rats. On the other hand, topical treatment of GH3 (derived from a rat pituitary GH-secreting cell line) with leptin directly inhibits cell proliferation. The obesity model animals (ob/ob, db/db, fa/fa) have equally plump body compared to the normal models, which shows signs of sufficient growth. (Localization and Functional Relevance of Leptin and Leptin Receptor in Rodents Pituitary) Aside from being the food intake inhibitor and the energy control factor, leptin takes part in controlling the pituitary hormones. Promoting the secretion of GH, PRL (prolactin), TSHbeta (thyroid stimulating hormone-beta, FSHbeta/LHbeta, and inhibiting the secretion of ACTH (adrenocorticotropic hormone) are the major changes of pituitary hormones which are brought on by leptin. The expressive localization is specific, and immunohistochemistry (IHC) method recognized leptin in granular state in FSHbeta, LHbeta and TSHbeta positive cells. In our biochemical examination, the bulk of the expression of leptin is recognized in fraction of the secretory granule. In particular, FSHbeta cells had the highest percentage rate of colocalized leptin in rat pituitary. On the other hand, leptin receptor has been reported to be found only in normal rat pituitary, human pituitary adenoma, and respective cell lines in pituitaries by the RT-PCR method until now, but we disclosed for the first time the localization of leptin receptor on the plasma membrane of GH-secreting cells with the IHC method that has not been cleared so far. These findings show that leptin and leptin receptor have been expressed in different cells, and that the rat pituitary glands entertain paracrine mechanism between leptin (FSHbeta/LHbeta cells) and leptin receptor (GH cells). The function of paracrine in this pituitary suggests a new point of view in hypothalamus-pituitary axis, and it shall be concerned with many aspects such as hormone secretions and proliferation/inhibition. (Human Pituitary Adenoma) Preliminary report of leptin and leptin-receptor relationship with pituitary adenoma that has secretion abnormality has been filed, and its manifestation is being observed by the RT-PCR. Leptin and leptin receptor are expressed in most adenoma, and it is thought to function by autocrine and paracrine pathway in the adenomas. Leptin has been located in ACTH-secreting adenoma most frequently, especially in ACTH carcinoma. The leptin receptor is detected in all adenomas with high percentage rate, with both long and short forms, and then many cases of nonfunctioning pituitary adenomas, compared with other adenomas, have been reported to be positive with both long and short forms of leptin receptor as detected by RT-PCR. The HP75 cell line is derived from the nonfunctioning pituitary adenoma, which produces FSHbeta and LHbeta. The expression of leptin receptor in nonfunctioning pituitary adenoma, and the suppression of HP75 multiplication may lead to the possible hypothesis of leptin becoming one factor for the treatment of pituitary adenoma, especially in gonadotropin adenomas.
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PMID:Leptin and the pituitary. 1182 4

We report a kindred with three cases of dementia. The proband presented with forgetfulness and personality changes at age 56, followed shortly thereafter by behavioral dyscontrol, hyperphagia, hypersexuality, delusions, illusions, disinhibition and double incontinence. Neuroimaging studies were consistent with frontotemporal dementia (FTD). In one allele, an arginine insertion at codon 352 in the presenilin 1 (PSEN1) gene was identified; no mutation was identified in the amyloid precursor protein or tau genes. We conclude that the clinical features of the Kluver-Bucy syndrome and FTD can be associated with PSEN1 mutations. Furthermore, presenilin analyses may be helpful to characterize kindreds with familial dementing illnesses regardless of the phenotype, particularly if no tau mutation is present.
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PMID:Familial frontotemporal dementia associated with a novel presenilin-1 mutation. 1205 27

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

Possible involvement of nitric oxide (NO) in lipoprivic feeding was investigated in nondeprived male ICR mice adapted to a high-fat diet in a within-subjects design. Lipoprivation was induced by blocking fatty acid oxidation with Na-mercaptoacetate (MA), which produces a short-term increase in feeding in mice and rats. Food intake, measured at 1, 2, and 4 h following injection of 70 mg/kg of MA, was attenuated in a dose related manner with increasing pretreatment dose (1,10, 25 and 50 mg/kg sc) of the NO-synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), reaching statistical significance at 10 mg/kg of L-NAME at h1 when compared to vehicle control condition. The inactive isomer, D-NAME, was ineffective, thereby supporting stereospecific drug action and directly implicating NO. A control experiment measured general locomotor activity (grid crossings and rears) in an open arena under 10-50 mg/kg of L-NAME in the same mice; both measures were significantly different from vehicle condition only at the highest dose. These findings support involvement of NO in lipoprivic hyperphagia; they are consistent with and extend research linking NO and ingestive behaviors through use of NOS inhibitors. Possible influences of confounds were discussed.
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PMID:A nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester, attenuates lipoprivic feeding in mice. 1456 10

Although nutritional support using nutrient enemas was recorded almost 3,500 years ago, the modern era of clinical dietetics commenced with the development of intravenous hyperalimentation by Dudrick et al. and the development of the chemically defined diet by Greenstein et al. Thereafter, clinical nutritional support became widely accepted as one of the basic tools of patient care, and knowledge of the metabolism of nutrients has been extended. In particular, the significance of micronutrients in systemic function, importance of gut function on the systemic metabolism and immune system, and involvement of amino acids and fat elements in the development and amelioration of specific disease status such as renal and hepatic failure have been recognized, and specific nutritional support has been created as a treatment strategy. In addition to knowledge of renal and hepatic failure or metabolic disorders, accumulated information on tumor metabolism and pathophysiology in cancer cachexia has also enabled cancer treatment using a nutritional approach. An enteral diet containing certain amino acids such as arginine or glutamate, omega-3 unsaturated fatty acids, and nucleic acids has been developed, and its clinical application under the new concept of "immunonutrition" has demonstrated reduction of the incidence of infection and shortening of hospital stay. Many questions on Immunonutrition remain to be answered such as its mechanism or optimal composition, although it is a promising field for future evolution. Currently, the assessment of nutritional status and gut function is required through lifelong education of medical doctors as well as the popularization of nutritional support teams. In the near future, tailor-made nutritional support will be required based on gene polymorphisms.
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PMID:[Advance and perspective of clinical nutrition]. 1502 60

Inhibition of hypothalamic nitric oxide (NO) decreases energy intake, and changes in hypothalamic NO synthase (NOS) have been observed in genetically obese rodents, but it is not known if NO is involved in the development of diet-induced obesity (DIO). We therefore measured changes in hypothalamic neuronal NOS (nNOS) in DIO and investigated effects of peripheral and central inhibition of NOS in this model. Expression of nNOS in relation to changes in nutritional state was measured by immunohistochemistry, with radiochemical detection. The effect of chronic intraperitoneal (i.p.) administration of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day) on energy intake, bodyweight and hypothalamic nitric oxide content was assessed in both chow-fed and DIO animals. Twenty-four hour energy intake after acute intracerebroventricular (i.c.v.) of L-NAME was also measured. Diet-induced obese animals had a statistically significant 32% reduction in the number of nNOS-immunolabelled cells in the ventromedial hypothalamus compared to chow-fed controls. Intraperitoneal administration of L-NAME decreased hypothalamic NO content in both chow-fed and DIO. Energy intake was reduced by 16% in DIO over 16 days, whereas energy intake was only reduced by 11% in chow-fed animals, although both were statistically significant. L-NAME significantly reduced body weight gain in DIO but not in chow-fed rats. L-NAME administered i.c.v. decreased 24 h energy intake to a greater extent in DIO rats, by 18%, compared with a 10% reduction in chow-fed rats. Ventromedial hypothalamic expression of nNOS is sensitive to changes in nutritional state. Despite having reduced nNOS, dietary obese rats were more sensitive to the effects of NOS inhibition than lean controls, suggesting a role for NO in the development of hyperphagia and obesity in rats fed a palatable diet.
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PMID:Reduced ventromedial hypothalamic neuronal nitric oxide synthase and increased sensitivity to NOS inhibition in dietary obese rats: further evidence of a role for nitric oxide in the regulation of energy balance. 1524 58

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