Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mouse ob mutation has been mapped relative to a series of RFLPs among the progeny of three separate mouse crosses: an intraspecific backcross, an intraspecific intercross, and an interspecific intercross. Genotypic assignment at the ob locus was made by making use of measurements of body mass index and the plasma concentrations of glucose and insulin. These data have suggested that the development of diabetes in these animals is a consequence of unlinked polygenes. There was also evidence that unlinked Mus spretus alleles can diminish the obesity of ob/ob mice. From these data we have mapped several markers on chromosome 6 with the following order: cen-Cola-2-Met-ob-Cpa-Tcrb. The homologs of markers that flank ob map to human chromosome 7q, suggesting that if there is a human homologue of ob, it maps to 7q31.
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PMID:Molecular mapping of the mouse ob mutation. 168 14

Histological study of biopsy specimens taken from the liver of 96 patients during operation for formation of a "small stomach" revealed fatty dystrophy of the liver in 93 patients (96.9%) which was attended by marked inflammatory and fibrous changes in 68 (70.8%) of them and by disturbed lobar structure of the liver (cirrhosis) in 2 patients (2.1%). Biochemical blood tests failed to show the pattern of the pathological changes before the operation. Study of the hepatobiliary system with methionine-75Se was the only method by which protein and pigment metabolism in the liver could be appraised. Examination of patients during 3 postoperative years showed a positive dynamics of changes in biochemical blood tests and improved protein metabolism in the hepatocytes according to the results of scanning of the liver with methionine-75Se. Thirteen repeated studies of the hepatic tissue collected from patients in different periods after operation for the formation of a "small stomach" showed a significant diminution of fatty dystrophy and inflammation of the parenchyma. The level of portal tract inflammation and portal fibrosis did not change. The findings suggest that there is an improved functional and morphological condition of the liver in weight loss caused by operation for the formation of a "small stomach", which allows this type of surgical intervention to be recommended for the treatment of patients with alimentary-constitutional obesity and initially diminished compensatory capacities of the liver.
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PMID:[State of the liver in patients with obesity at distant periods after formation of a "small stomach"]. 177 62

Insulin resistance is frequently associated with acanthosis nigricans and hyperandrogenism. In patients with type A insulin resistance, this has been shown to be due to genetic defects in insulin receptor function. However, other patients with a similar clinical syndrome have been reported to have a variant of this syndrome, in which assays of insulin receptor function were normal. We have sequenced a portion of the insulin receptor gene in one such patient, a 29-yr-old woman with obesity and insulin resistance. The patient is heterozygous for a mutation substituting isoleucine for methionine at position 1153. Met1153 is located in the intracellular domain of the receptor near the cluster of tyrosine phosphorylation sites at positions 1158, 1162, and 1163. Studies of the mutant receptor expressed in NIH-3T3 cells demonstrated that the Ile1153-mutation impairs the ability of insulin to stimulate autophosphorylation of solubilized insulin receptors. In addition, the mutation impairs the ability of insulin to stimulate receptor tyrosine kinase activity to phosphorylate an artificial substrate [poly(Glu-Tyr)]. It seems likely that this defect in receptor tyrosine kinase activity explains the defect in the ability of the patient's insulin receptors to mediate insulin action in vivo. Furthermore, this patient provides a paradigm in which genetic factors act in concert with other risk factors, such as obesity, to cause clinically important insulin resistance.
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PMID:A mutation in the tyrosine kinase domain of the insulin receptor associated with insulin resistance in an obese woman. 189 Jan 61

With the combination of a noninvasive saturation measurement and plethysmography, pulse oximetry has become an important monitoring method for peripheral perfusion and oxygen supply. Indications for pulse oximetry is practically every anaesthesia especially in geriatric patients and patients with one-lung-anaesthesia, obesity, asthma and emphysema. Pulse oximetry has proved its worth in the transport of emergency patients. Sources of error are a bad perfusion at the site of measurement (hypotension, hypothermia), dyshaemoglobinaemia (Met-carboxy-haemoglobin) and interference of colours (dark skin, intravenous colours, high light intensity). Accuracy of response of most currently available pulse oximeters lies between 2-3% (SD) with oxygen saturations between 80-100%. Deviations increase at lower oxygen saturations. Pulse oximetry will soon be regarded as minimal monitoring standard worldwide together with the ECG, blood pressure, pulse and respiratory monitoring.
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PMID:[The importance of pulse oximetry for anesthesia]. 204 38

We have shown in earlier studies, that the development of spontaneous autoimmune thyroiditis (SAT) in chickens of the Obese strain (OS) depends on the presence of both, two dominant genes coding for an altered immune regulation and one recessive gene responsible for the susceptibility of the target organ for the autoimmune attack. The product(s) of the latter is (are) still not known. The present study was aimed at identifying possible candidates of cellular components of the thyroid gland of OS chicken and its SAT susceptible parental Cornell C-strain (CS) by high resolution 2-dimensional (2D) gel electrophoresis. For this purpose organ cultures of the thyroid, bursa, thymus and liver were established and the synthesized polypeptides were labelled by 35S-methionine. OS and CS organs were compared with those of healthy normal White Leghorn (NWL) controls. The autoradiographs of the 2D-gels obtained from individual samples after various labelling periods were subjected to comparative analysis. We have found both quantitative and qualitative differences of polypeptide spots between OS/CS and NWL organ samples, some of them specific for the thyroid gland. Although one has to be aware that in this multidimensional analytical approach numerous, still elusive pattern differences are revealed, the thyroid specific phenomena will be further scrutinized.
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PMID:Molecular analysis of genetically determined target organ abnormalities in spontaneous autoimmune thyroiditis. 209 9

The hyperphagia and obesity induced by ventromedial hypothalamic (VMH) electrolytic lesions in female rats were associated with a 70-94% decrease in the level of beta-endorphin (beta-E) in the hypothalamus and other regions of brain, but not in the pituitary. Dynorphin (Dyn) and methionine-enkephalin (ME) levels were also decreased. Rats with VMH lesions were less sensitive to the inhibitory effect of naloxone on their food-intake. Mice injected with gold thioglucose (GTG) also showed a decrease in the hypothalamic content of beta-E and Dyn and exhibited 30% less analgesia compared to control mice after cold swim stress.
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PMID:Effect of electrolytic and chemical ventromedial hypothalamic lesions on food intake, body weight, analgesia and the CNS opioid peptides in rats and mice. 289 79

We have recently shown that in addition to beta-endorphin the opioid peptides Met- and Leu-enkephalin and their apparent precursors are localized in islet endocrine cells of the rat pancreas. To begin evaluating a possible role for these pancreatic opiates in the pathophysiology of genetic diabetes in rodents, immunoreactive beta-endorphin and Met- and Leu-enkephalins were measured in acetic acid extracts of pancreas and pituitary of C57BL/KsJ db/db mice and their lean littermates. Groups of animals were studied during three phases of development of the diabetic syndrome in the mutant mice: at 4 (hyperinsulinemic and prediabetic); 6, 9, and 12 (frankly obese and diabetic); and 30 (hypoinsulinemic) wk of age. Elevations or decreases (P less than .05) were found in db/db mice (vs. lean littermates) as follows: pituitary content of Met-enkephalin was twofold higher at all ages studied; pituitary free Leu-enkephalin was lower at 4 wk and reversed to higher at 6-30 wk; pancreatic beta-endorphin was 30% lower at 4 wk and reversed to threefold higher at 6-12 wk; Met- and Leu-enkephalin-containing larger peptides were elevated at one or more points between 6 and 12 wk in both the pancreas and the pituitary. Thus, the onset of overt obesity between 4 and 6 wk of age was accompanied by a marked rise in both pancreatic beta-endorphin and pituitary Leu-enkephalin; similar elevations in these parameters have been reported previously in C57BL/6J ob/ob mice at approximately 12 wk of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered beta-endorphin, Met- and Leu-enkephalins, and enkephalin-containing peptides in pancreas and pituitary of genetically obese diabetic (db/db) mice during development of diabetic syndrome. 294 83

In order to test the hypothesis that serotonergic activity is abnormal in the brains of genetically obese Zucker rats, levels of serotonin (5-HT); its amino acid precursor, tryptophan (Trp), and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were measured in eight brain regions in groups of obese and non-obese male rats. Plasma albumin levels as well as levels of amino acids and related compounds in plasma and in a cortical sample were also determined in the same animals. While Trp was lower in several brain regions of the obese animals, the only region showing a depressed level of 5-HT in the obese group was the mesencephalon. Obese animals also had a lower amount of 5-HIAA in the diencephalon, but no other differences were significant. Both elevations and depressions were observed in cortical amino acid levels in obese animals. The level of plasma albumin was increased in the obese group. Free Trp was decreased in the plasma of obese rats while levels of other amino acids (methionine, leucine, isoleucine, valine and phenylalanine) which compete with Trp for transport across the blood-brain barrier were elevated. Thus the combination of lower plasma free Trp and increased levels of competitive amino acids appears to contribute to decreased levels of Trp in the brain of genetically obese rats.
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PMID:Brain serotonergic activity and plasma amino acid levels in genetically obese Zucker rats. 618 36

A diet providing less than 20 mg of magnesium per 100 kcal that maintains urine pH near 6.0 3 to 5 hours after eating, or a diet providing this amount fo magnesium (see Table 2) with 1 gm of ammonium chloride or 1.5 gm of dl-methionine added daily, should be fed for 1 to 3 months to dissolve struvite uroliths (see Fig. 1). The low-magnesium diet should be fed indefinitely to prevent recurrence, because struvite urolithiasis and all of its effects (hematuria, pollakiuria, and/or complete to partial obstruction to urinary excretion) recurs repeatedly in cats that have previously experienced the condition if they are returned to regular cat food. In contrast, if a diet low in magnesium is fed, recurrence is uncommon. For cats that have never been affected, feeding a low-magnesium ration is unnecessary. For all cats, the following measures are recommended: encourage exercise, allow frequent urination, prevent obesity, decrease confinement, keep the litter box clean, and always have palatable water readily available.
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PMID:Treatment and prevention of feline struvite urolithiasis. 637 67

The effects of insulin and insulin-like growth factor I (IFG-I) on protein synthesis were compared in muscle isolated from lean and goldthioglucose (GTG)-obese mice. Two types of skeletal muscles, the red soleus and the white extensor digitorum longus (EDL) muscles, were studied. In muscles from lean mice, 6.7 nM insulin and 50 nM IGF-I caused a similar maximal stimulation of tyrosine incorporation in total proteins (40% increase). However, the potency of IGF-I was only 5-10% that of insulin both in soleus and in EDL muscles (EC50 approximately equal to 6 nM for IGF-I and 0.5 nM for insulin). Basal rate of protein synthesis was identical in muscles from GTG-obese and lean mice. Similarly, a comparable increase in the rate of protein synthesis was obtained using maximally effective concentrations of insulin and IGF-I in both lean and GTG-obese animals. SDS-polyacrylamide gel electrophoresis analysis of proteins labeled with 35S-methionine confirmed that, in muscles from lean and GTG-obese animals, insulin and IGF-I increased overall protein synthesis in a similar manner. These results suggest that the protein synthesis machinery is not impaired in GTG-induced obesity, which is therefore not associated with resistance to insulin for its effect on protein metabolism.
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PMID:Insulin and insulin-like growth factor I. Effects on protein synthesis in isolated muscles from lean and goldthioglucose-obese mice. 640 79


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