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)

Cholecystokinin (CCK) secreted from the duodenum during feeding has been shown to elicit satiety and stimulate growth of the pancreas in addition to affecting gastrointestinal function. In previous experiments hyperphagic Zucker obese rats were less sensitive to the effects of CCK on satiety and had a smaller pancreas than normal-weight rats. In the present experiments with hyperphagic lactating Zucker rats, the food intake response to exogenously administered CCK and the size and composition of the pancreas were measured. Food intakes after a 2-h fast were not decreased by 4.0 or 8.0 micrograms/kg CCK-8 during wk 1, 2, or 3 of lactation. However, in the same rats 2 wk after pups were weaned, 4.0 and 8.0 micrograms/kg CCK-8 decreased food intake 32% (2.1 +/- 0.4 vs. 3.1 +/- 0.3 g, paired t = 2.33, P less than 0.03) and 52% (1.5 +/- 0.2 vs. 3.1 +/- 0.5 g, paired t = 3.48, P less than 0.006). On day 18 of lactation, pancreas weight was increased 41% (1.38 +/- 0.05 vs. 0.98 +/- 0.02 g, paired t = 2.68, P less than 0.02) and contents of DNA, RNA, and protein were increased 57, 57, and 73%, respectively. Thus, hyperphagia in lactating female rats was associated with 1) decreased sensitivity to the satiety effect of CCK similar to that in hyperphagic obese rats and 2) hypertrophy of the pancreas in contrast to decreased pancreas size in obese rats.
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PMID:Hyperphagia during lactation: satiety response to CCK and growth of the pancreas. 618 5

Obese Zucker rats exhibit marked hyperphagia when compared to lean littermates but deposit a smaller percentage of total dietary energy as body protein. This study was designed to determine the roles of skeletal muscle protein synthesis, protein degradation, RNA, or DNA in producing the lower muscle mass of obese rats. At 44 days, 3 hindlimb muscles, the extensor digitorum longus (EDL), the gastrocnemius and the plantaris were significantly smaller in the obese animals. At 72 days, the differences in weights of these muscles were more pronounced. Protein synthesis and degradation were determined in the soleus at 44 days of age using an in vitro whole muscle incubation technique. Protein synthesis rate was significantly decreased in the obese animals. These changes were accompanied by reductions in both RNA and DNA levels. Significant changes in nucleic acid levels were observed in both the red and white portions of the gastrocnemius muscle. These changes in the anabolic process of protein accretion appear to be sufficient to account for the reduced muscle mass in the obese Zucker rat.
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PMID:Skeletal muscle growth in lean and obese Zucker rats. 619 56

Male and female Holtzman rats were made hyperphagic and obese with bilateral radiofrequency heat lesions of the ventromedial hypothalamic (VMH) area. When VMH rats were maintained at 28 degrees C, their brown adipose tissue (BAT) DNA, protein, and cytochrome oxidase contents were normal although more stored lipid was present, as judged from a threefold increase in wet weight. Thermogenic activity of BAT mitochondria was normal in male VMH rats, as judged from the unchanged level of guanosine diphosphate (GDP) binding (known to be a sensitive index of the functional activity of the thermogenic proton conductance pathway), and reduced in female VMH rats. When rats with VMH lesions were exposed to cold (4 degrees C for 24 h), the visible hyperemia of their BAT and normal large increase in mitochondrial GDP binding indicated normal thermogenic responsiveness. We conclude that the medial nuclei of the hypothalamus and associated afferent or efferent nerve tracts do not represent an essential central nervous system link for cold-induced, sympathetic-mediated activation of BAT thermogenesis. It is possible, however, that diet-induced, sympathetic-mediated activation of BAT function and growth might require an intact VMH region because no enhancement of BAT mitochondrial function normally associated with hyperphagia was detected in these hyperphagic VMH-lesioned animals.
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PMID:Brown adipose tissue of rats with obesity-inducing ventromedial hypothalamic lesions. 628 74

Young genetically obese (fatty, fa/fa) rats (7-8 wk old) maintained on a chow diet at 28 degrees C have a relatively normal amount of brown adipose tissue (BAT) (normal protein content, normal noradrenaline content, normal or slightly reduced cytochrome oxidase content, 30% reduction in DNA content) with cells grossly hypertrophied by accumulation of lipid. The binding of purine nucleotides by BAT mitochondria is lower in fa/fa rats than in lean rats, suggesting a lesser thermogenic activation of this tissue. Acute exposure to cold (24 h at 4 degrees C) activates BAT thermogenesis (visible hyperemia, marked increase in mitochondrial binding of purine nucleotides, depletion of noradrenaline content) in fa/fa rats as in lean rats. In contrast, feeding a cafeteria diet to young fa/fa rats fails to activate BAT (no increase in mitochondrial binding of purine nucleotides) as it does in lean rats, and these rats accumulate more extra fat (increase in weight of gonadal white adipose tissue) than do cafeteria diet-fed lean rats. It is concluded that the young fa/fa rat has normal cold-induced nonshivering thermogenesis in BAT but defective diet-induced thermogenesis in BAT and that the consequent reduction in energy expenditure, coupled with hyperphagia, contributes to the development of its obesity. The most probable location for the defect is suggested to be associated with the hypothalamus.
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PMID:Brown adipose tissue in genetically obese (fa/fa) rats: response to cold and diet. 629 7

Serum factors which stimulate DNA synthesis were investigated in patients with anorexia nervosa. The factors were assayed by examining [3H]-thymidine incorporation into the nuclei of human fibroblasts in culture using autoradiography. The mean percentage of labeled nuclei (labeling index) induced by serum was significantly lower (p < 0.005) in 5 patients with anorexia nervosa (21.0 +/- 5.9 percent, mean +/- S.D.) than in 5 normal adult subjects (33.9 +/- 3.3 percent). Two of the patients with anorexia nervosa were treated with intravenous hyperalimentation (IVH). In one of the IVH treated patients, the labeling index increased from 17.4 to 32.8 percent at the 6th week of treatment, and in the other increased from 19.4 to 29.8 percent at the 4th week. In both patients, body weight increased by 1.5 to 2 kg. IVH in these patients increased DNA-synthesis-stimulating activity.
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PMID:DNA-synthesis-stimulating activity in the sera of anorexia nervosa. 678 Mar 32

Feeding a "cafeteria" diet for 2 wk to male Holtzman rats resulted in a weight gain that was, on average, only slightly more than that of control rats fed a regular chow diet. Wet weight, DNA, and total protein content of interscapular brown adipose tissue were more than doubled in the cafeteria-fed rats and proliferation of mitochondria paralleled tissue growth. After 2 wk of recovery from cafeteria feeding, the expanded size of the tissue had completely regressed to a normal level. Brown adipose tissue mitochondria of cafeteria-fed rats bound 3 times more purine nucleotides than mitochondria of chow-fed control rats, but no change in the proportion of polypeptides with molecular weight in the region of 32,000 could be detected. The changes in brown adipose tissue and its mitochondria in cafeteria-fed rats correspond to those seen previously in noradrenaline-treated rats, i.e., tissue growth accompanied by mitochondrial proliferation and an unmasking of proton conductance pathways. The increase in 32,000-mol-wt polypeptides seen in brown adipose tissue mitochondria of cold-acclimated rats does not occur in the cafeteria-fed rats. Control mechanisms are presumed to differ, either quantitatively or qualitatively, in the two situations, cold exposure and overeating, which both cause growth of brown adipose tissue.
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PMID:Brown adipose tissue of cafeteria-fed rats. 727 Jun 79

A six-month prospective survey was carried out in a university hospital to assess the incidence of Acinetobacter baumannii cross-contamination and to identify risk factors for colonization. Clinical isolates obtained during the study period were biotyped and genotyped by pulsed-field gel electrophoresis after ApaI macrorestriction of total DNA. Case-control univariate and multivariate analyses were performed to identify risk factors for Acinetobacter baumannii colonization. One hundred forty-seven patients hospitalized in 36 units were colonized or infected, of whom 52 were in three intensive care units. The urinary (29%) and bronchopulmonary tracts (26%) were the most frequently colonized sites. Nine major restriction patterns were identified: two were exhibited by epidemic multi-resistant strains of biotype 9 which were isolated from 65 patients hospitalized in ten units. Multivariate analysis showed that case-patients were (a) more likely than non-infected controls to be male, to have been previously hospitalized in another unit and to have had longer stays in the unit before colonization and hyperalimentation; and (b) more likely than controls colonized with other gram-negative bacilli to be male, to have had longer hospitalization, to have received treatment with third-generation cephalosporins and to have had a urinary catheter. The high incidence of colonization with Acinetobacter baumannii can thus be attributed to frequent cross-contamination and the use of broad-spectrum antibiotics. Colonized patients appear to be the major source of cross-contamination as epidemic strains spread throughout the hospital.
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PMID:Risk factors for nosocomial colonization with multiresistant Acinetobacter baumannii. 758 40

We reported recently that ventromedial hypothalamic (VMH) lesions increased the synthesis of DNA in the gastrointestinal tract of rats by the firing of vagus nerve activity, mainly via cholinergic receptor mechanisms. In the present study, we examined whether the mitotic response is due to proliferation of a cell population--mucosal, submucosal, or muscular layer. A monoclonal antibody to proliferating cell nuclear antigen (PCNA) has previously been shown to be capable of identifying proliferating cells. Samples of formalin-fixed gastrointestinal epithelium, taken before and after VMH lesioning, were immunostained with the anti-PCNA monoclonal antibody, and the labeling index (LI) was determined. To discriminate the effect of hyperphagia in VMH lesioned rats, we utilized the method of pair-feeding. Cell proliferation was examined by the PCNA-labeling technique 0, 1, 3, and 7 days after VMH lesioning. The increase in proliferation was confined to cells in the mucosa and did not involve the muscularis and serosa. Studies in control animals showed that the LI was higher in the small intestine than in other gut segments, and higher in the large intestine than in the stomach. The mean PCNA-LI began to increase at 1 day and continued to increase for 3 days, then decreased 7 days following the lesioning. Results indicate that the gastrointestinal mucosa is in a state of hyperproliferation after VMH lesioning.
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PMID:Ventromedial hypothalamic lesions induce the proliferation of gastrointestinal mucosal cells in the rat. 763 Mar 10

The metabolic properties of brown adipose tissue (BAT), liver, and skeletal muscles were compared in lean and obese diabetic SHR/N-cp rats (a new model of type II diabetes) to test whether the severe insulin resistance of obese animals is specifically associated with a thermogenic defect in BAT. The respiratory response of brown adipocytes to norepinephrine and to agents bypassing the adenylate cyclase complex (dibutyryl cyclic AMP and palmitate) was decreased by two-thirds in obese rats, thereby indicating the presence of a major postreceptor defect. Significantly, total BAT cytochrome oxidase activity, uncoupling protein content, and mitochondrial guanosine 5'-diphosphate binding (3 indexes of BAT thermogenic capacity) were also decreased by two-thirds. The specific activities of these parameters expressed per total BAT mitochondrial protein were not altered either. This indicates that the total number of mitochondria per cell is decreased in BAT of obese rats. In contrast, total tissue cytochrome oxidase activity, protein content, and DNA content all increased by two to three times in the liver of obese SHR/N-cp rats, but these parameters remained unchanged in skeletal muscles (vastus lateralis and soleus). Such a remarkable liver hypertrophy may have occurred as a consequence of the persistent hyperphagia-hyperinsulinemia of obese rats that induced a hyperplasia and/or a hepatocyte polyploidization. This observation together with the fact that daily energy expenditure associated with food intake was markedly increased in obese rats (representing as much as 25% of the total energy expenditure) strongly suggests that the liver plays a major role in energy balance in these animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific decrease of mitochondrial thermogenic capacity in brown adipose tissue of obese SHR/N-cp rats. 827 28

A special subphenotype of the fragile X syndrome is reported which is characterised by extreme obesity with a full, round face, small, broad hands/feet, and regional skin hyperpigmentation. It resembles the Prader-Willi syndrome (PWS) and might therefore be named 'Prader-Willi-like'. Unlike the PWS, these PW-like fragile X patients lack the neonatal hypotonia with feeding problems during infancy followed by hyperphagia from toddlerhood. We describe five new fragile X patients and present a clinical update of three previously described patients with the PW-like phenotype. In one family, segregation of either the classical Martin-Bell or the PW-like phenotype was observed and in another family there was repeated transmission of the PW-like phenotype. Previously, one of the patients had been misdiagnosed as having classical PWS, based on clinical findings. Molecular studies of the FMR-1 gene showed the typical full mutations as seen in fragile X syndrome males. Molecular analysis of the 15q11-13 region, which is deleted in the majority of classical PWS patients, did not show any detectable abnormalities. In a group of 26 patients with suspected Prader-Willi syndrome but without detectable molecular abnormalities of chromosome 15, one fragile X patient was found. These clinical and molecular findings illustrate the necessity to perform DNA analysis of the FMR-1 gene in mentally retarded patients presenting with a PW phenotype but without the PWS specific cytogenetic/molecular abnormalities of chromosome 15.
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PMID:Clinical and molecular studies in fragile X patients with a Prader-Willi-like phenotype. 801 84


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