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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gold Thioglucose injections in mice are followed by a rapid accumulation of fat in the carcasses. The incorporation of an oral dose of [3H] glyceroyl tripalmitate in body fat stores showed after GTG-treatment a transient but significant increase and a return to normal values within 6 weeks. The rate of incorporation of dietary fat into the body was estimated from these values as well as from food intake and fat content of the diet (2.5 per cent). The resulting curve showed great similarity with the first differential of the curve of total body fat accumulated during that period. The rate of incorporation of dietary fat into body stores is apparently modified in GTG obesity in mice.
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PMID:Rate of incorporation of dietary fat in gold thioglucose obesity in mice. 5 61

A longitudinal in vivo and in vitro analysis of the genesis of insulin resistance has been carried out in mice made obese by chemical made obese by chemical lesion (goldthioglucose, GTG) of the hypothalamus. Six weeks after GTG administration, glycemia and glucose disposal were normal but associated with increased insulin concentration, suggesting incipient insulin resistance. The in vitro counterpart of the latter in obese mice was observed in soleus muscle that was somewhat less responsive to insulin than controls, in liver that had increased basal lipogenesis but was uninfluenced by insulin, and in hepatic plasma membranes in which a slight decrease of insulin binding was measured. At this stage of obesity, basal adipose tissue lipogenesis was increased but the tissue responded in a normal fashion to insulin. These relatively discrete early metabolic changes were corroborated in vivo by a normal hypoglycemic effect of exogenous insulin. Sixteen weeks after GTG administration, hyperglycemia and gross hyperinsulinemia were recorded. This insulin resistance was evidenced in vivo by the lack of hypoglycemic effect of exogenous insulin unless considerable amounts of the hormone were administered. It coincided in vitro with a poor response of soleus muscle to insulin, an absence of a stimulatory effect of the hormone upon both adipose tissue and liver tissue, and a marked decrease in insulin binding to liver plasma membranes. It appears that insulin resistance is a multifactorial and progressive abnormality that might involve both insulin receptor and intracellular metabolic alterations.
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PMID:Longitudinal study on the establishment of insulin resistance in hypothalamic obese mice. 36 21

Adenylate cyclase activity was determined in membranes of liver, muscle, white adipose tissue, and brown adipose tissue (BAT) of lean (Fa/) and obese (fa/fa) Zucker rats. Responses were monitored following beta-adrenergic receptor stimulation and addition of GTP, GTP gamma S, or forskolin. beta-Adrenergic responses in liver, white adipose tissue, and BAT were lower in obese than in lean animals. No such difference was observed in muscle membranes. Production of cAMP after addition of guanine nucleotides was lower in liver and white adipose tissue membranes from obese rats compared with their lean littermates. Synthesis of cAMP in muscle membranes of obese animals after addition of GTP was either not different, or slightly higher, than that observed in muscle membranes from lean animals. Furthermore, production of cAMP after forskolin addition to muscle membranes of obese rats was significantly higher than that observed from lean rats under the same conditions. Interestingly, BAT membranes of obese rats were significantly more sensitive to guanine nucleotide activation than those of lean animals. The results confirm recent findings indicating inferior function of G proteins in liver plasma membranes of obese Zucker rats, and extend this observation to adipose tissue. The present results further suggest that the "nonreceptor" components (e.g., G proteins) responsible for the activation of adenylate cyclase in BAT membranes of obese rats are more responsive to stimulation than those of lean animals. Such sensitivity may be related to and perhaps compensate for the reduced thermogenic activity in the obese Zucker rat during the development of obesity.
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PMID:Nonreceptor-mediated responses of adenylate cyclase in membranes from liver, muscle, and white and brown adipose tissue of obese (fa/fa) and lean (Fa/) Zucker rats. 217 38

The effect of oral administration of total soya saponins (TS) on the development of obesity induced by (GTG) injection was examined. In the GTG-obese group, the serum immunoreactive insulin (IRI) levels were significantly increased and food consumption was suggestively increased. In addition, sucrase activity in the intestinal mucosa was increased and the surface area of intestinal villi was significantly greater, suggesting enhanced gastrointestinal function. Oral administration of TS prevented development of obesity and prevented an increased level of IRI in GTG-obese animals. It also restored the sucrase activity and the surface area of intestinal villi to normal. Thus, TS may be effective in preventing development of obesity.
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PMID:Effect of soya saponins on gold thioglucose (GTG)-induced obesity in mice. 309 55

Twenty-seven patients with the presumed diagnosis of Prader-Willi syndrome (PWS) were studied clinically and cytogenetically. The patients were classified into three study groups on the basis of their clinical pictures: group 1 with 12 children meeting the strict diagnostic criteria for PWS; group 2 with nine floppy infants and young children, aged 3 years or less, without obesity and hyperphagia; and group 3 with six older children in whom some characteristic features of the syndrome were absent. High-resolution GTG banding of prometaphase chromosomes revealed del(15)(q11.1;q12) in eleven and t(15;15)(qter----p11.2::q12----qter) in one of the twelve group 1 patients. In group 2, four patients had del(15)(q11.1; q12), one had t(15;15)(qter----p11.1::q13----qter), and the remaining four had normal karyotypes. The deleted segment common to the 17 patients with the chromosome aberrations was confined to subband 15q11.2. On the other hand, all six group 3 patients had normal karyotypes. These findings indicated that when strictly defined PWS is absolutely correlated with chromosome 15 aberrations, i.e., there is a positive phenotype-karyotype correlation, and that the aberrations are etiologically related to the syndrome. Parental origin of the deleted chromosome was determined in seven patients, with QFQ-heteromorphisms being used as hereditary markers. The deleted chromosome originated from the paternal chromosome 15 in six patients and from the maternal 15 in one.
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PMID:Clinical and cytogenetic studies of the Prader-Willi syndrome: evidence of phenotype-karyotype correlation. 790 98

Defective BAT thermogenesis is associated with obesity in all the different types of obese animal so far studied. The deficit in normal energy expenditure may be presumed to contribute to the high metabolic efficiency and, together with the hyperphagia, to the obesity of these animals. In two types of obese animal (the ob/ob mouse, the db/db mouse) an increased propensity to become torpid provides an additional energy conserving mechanism that contributes to the high metabolic efficiency. In all these animals an abnormality of hypothalamic function appears likely. Obviously animals with induced hypothalamic lesions (the VMH-lesioned rat, the GTG-obese mouse) have an interruption in the normal pathway that links diet and the sympathetic innervation of BAT. The fa/fa rat resembles these animals in failing to activate BAT thermogenesis in response to diet: the lesion may lie in the hypothalamus itself or elsewhere in the food-intestine-hypothalamus-BAT axis, for example in intestinal peptide hormones. The ob/ob mouse has a peculiar hypothalamic defect that interferes with control of thermogenesis in BAT as well as impairing or exaggerating some aspects of thermoregulation. The db/db mouse resembles the ob/ob mouse but, since the defect is genetically distinct, presumably has a different lesion at the molecular level.
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PMID:Defective brown adipose tissue thermogenesis in obese mice. 406 36

The present experiments were carried out to elucidate the effect of mazindol feeding on obese mice made by gold-thioglucose injection. Mazindol was added to the diet at the level of 0.5, 2, 10 mg/kg body weight. It was found that oral administration of mazindol reduced the body weight gain and perimetrial adipose tissue weights increased in GTG-obese mice. Decreased adipose tissue weights were correlated with the decreased level of size and volume of fat cells. Basal lipolytic activity and adrenaline-induced lipolysis were also significantly decreased in mazindol groups as compared to those in GTG-obese mice that were not administered mazindol. These results indicate that the weight reduction induced by mazindol administration might not be due to increase in fat mobilization. The increased level of liver and serum lipid induced by GTG-obesity was also found to be improved by mazindol. Scanning electron micrographs indicated that the villous width of the small intestine were significantly smaller in the mazindol group that those in the GTG-obese group. Sucrase and esterase activities of the small intestine were also decreased by mazindol feeding as compared to those in the GTG-obese mice. based on these results mechanisms of action of mazindol were discussed.
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PMID:[Effect of mazindol on obesity induced by administration of gold thioglucose]. 643 Jul 60

The ability of nanomolar concentrations of guanine, but not adenine, nucleotides to inhibit specific 125I-Bolton-Hunter CCK binding to ligated rat vagus nerve demonstrated that vagal CCK binding sites were linked to G-proteins during axonal transport. The GTP analogue, GTP[S], reduced specific binding to both anterogradely and retrogradely transported binding sites by more than 90% at 1 microM. Transport of these putative receptor-G-protein complexes was examined under conditions of food deprivation or physiological hyperphagia induced by either lactation or genetic obesity. None of the physiological or imposed manipulations of food intake had any effect on the axonal transport of CCK binding sites. Transection of the cervical vagus resulted in an accumulation of binding sites at the lesion site that was indistinguishable from that seen following ligation for the same period.
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PMID:G-protein coupling of vagal CCK binding sites and comparisons of transport rates. 768 78

The association of obesity and hypertension is well documented, and the combination is important as a coronary risk factor, but its non-pharmacological management is very difficult. Japanese hypertensive obese subjects (HO, n = 95) selected from 321 non-medicated obese subjects with a body mass index > 25 kg/m2 were characterized by the clinical features of significant diaphragmatic elevation, higher heart rate (HR), fasting blood glucose (FBS), total cholesterol (Tch), uric acid and gamma GTP values and lower vital capacity (VC) compared to those of normotensive-obese subjects (NO, n = 226) (p < 0.01). During a diet therapy program (about 1,200 kcal/day) for HO (n = 55), 25 subjects were treated with a non-drug-dependent pulse-synchronized transpercutaneous electric abdominal muscle stimulator (PEM) (ca. 30,000 muscle contractions/day) for 4 weeks. These subjects showed significant improvement with reduction in body weight (9.4%, 7.4 kg), intra-abdominal visceral fat (VF) CT scan area (29%), abdominal subcutaneous area (10%) at the level of the umbilicus, blood pressure (BP), HR, FBS, gamma GTP, Tch, plasma norepinephrine, plasma renin activity and plasma insulin, an increase of VC and lowering of the diaphragm (p < 0.05). The reductions in weight, BP, FBS and Tch in the diet group (n = 30, 1,200 kcal/day for 4 weeks) were smaller than those in the PEM-diet group (p < 0.05). The Japanese hypertensive obese patients had complications of many other coronary risk factors, and the reduction in weight and VF with PEM-diet therapy seems to be effective for improving these risk factors.
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PMID:Improvement of multiple coronary risk factors in obese hypertensives by reduction of intra-abdominal visceral fat. 789 17

N(2S)-7-carbethoxymethoxy-1,2,3,4-tetrahydronaphth-2-yl]-(2R )-2-hydroxy-2-(3-chlorophenyl)ethanamine hydrochloride (SR 58611A) increased cyclic AMP levels in membrane homogenates from rat interscapular brown adipose tissue with an EC50 of 20 +/- 2 nM. Substitution of GTP with the GDP analog, guanosine-5'-O[thiodiphosphate], in the incubation medium suppressed the stimulation of adenylyl cyclase activity by SR 58611A. This compound also stimulated glycerol release from the brown fat cells, with an EC50 of 11 +/- 0.4 nM. Only at doses higher than 10 microM did the non-selective beta-adrenoceptor antagonists, propranolol and alprenolol, as well as the selective beta 1- and beta 2-adrenoceptor antagonists, (+-)-[2-(3-carbamoyl-4-hydroxy-phenoxy)- ethylamino]-3-[4(1-methyl-4-trifluoromethyl-2-imidazolyl)-phenoxy]-2 propanol (CGP 20712A) and erythro-(+-)-1-(7-methylindan-4-yloxy)-3-iso-propylamino butan-2-ol-hydrochloride (ICI 118,551), antagonize the SR 58611A-induced stimulation of both adenylyl cyclase activity and lipid metabolism. Since, at high doses, all these beta-adrenoceptor antagonists lack selectivity for beta 1- or beta 2-adrenoceptors, these results suggest that the beta-adrenoceptor agonist, SR 58611A, activates thermogenesis by acting on brown fat cell beta 3-adrenoceptors. This implies that this compound might be useful for treatment of obesity.
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PMID:SR 58611A: a novel thermogenic beta-adrenoceptor agonist. 795 12


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