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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

This study evaluates the correlation between long-term weight history and health risks. One thousand three hundred and sixteen male subjects of normal weight (-5%(-)+5% by Broca's obesity index) at age twenty, were studied. The average age of the subjects was 43.7 +/- 6.5 (M. +/- S.D.) years old. According to their long-term weight history, the subjects were classified into four groups: weight lost (N = 35), weight stable (N = 502), mild weight gain (N = 187), severe weight gain (N = 592). Odds ratios for systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, uric acid, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, hyperperspiration, angina pectoris, and hypertension were significantly higher in the severe weight gain group than in the stable weight group. Stepwise logistic regression analysis was performed by choosing weight history, obesity index, age, and smoking and drinking habits as the independent variables. Weight history was shown to be a significant variable in systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, chronic hepatitis and liver cirrhosis. Odds ratios for factors suspected of promoting atherosclerosis were significantly higher in the severe weight gain group. Results of this study indicate that a weight gain of over 7 kilograms appears to be the critical level that is associated with health risks.
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PMID:[Health risk assessment of long-term weight history]. 213 52

The purpose of this study is to evaluate waist size as an indicator of health risk among subjects considered to have normal body construction based on height-weight obesity indices. For estimating standard waist sizes based on height, a regression equation was formulated from 46 male subjects who had no abnormal findings in their health checkups. The regression equation was as follows: Standard waist size (cm) = 0.8 X height (cm)-57.7. The ratio of measured waist size to standard waist size was defined as the "waist ratio". The correlation coefficient between the waist ratio and the modified Broca's obesity index was 0.898 (N = 207, p less than 0.01). To clarify the meaning of the waist ratio, 95 male subjects were divided into three groups on the basis of the difference between their waist ratio and their obesity index. The group whose waist ratios were larger than their obesity indices had significantly worse findings than the group whose waist ratios were not in the following medical categories: systolic blood pressure, glutamic oxaloacetic transaminase levels, gamma glutamyl transpeptidase levels, uric acid levels, total bilirubin, electrocardiogram readings and optic funduscopic observation. Accordingly, the waist ratio derived from waist size might be useful for assessing obesity-related health risks even for subjects judged to be normal from the height-weight obesity index.
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PMID:[Evaluation of waist size as a health risk indicator for obesity]. 221 94

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 insulin secretory response to an intravenous glucose load was examined in chronically catheterized, conscious mice 2, 5, and 10 wk after induction of obesity by a single injection of gold thioglucose. At 2 wk after administration of gold thioglucose, a significant increase in both the insulinemia and incremental area under the curve of insulin release after intravenous glucose were observed (incremental area under the curve for 2-wk control mice, 852 +/- 54 min/pM; incremental area under the curve for 2-wk GTG-injected mice, 1140 +/- 114 min/pM; P < 0.05). At this stage, no significant difference existed in the glucose tolerance or body weight of control and gold thioglucose-injected mice. By 5 wk, the gold thioglucose-injected mice were approximately 33% heavier than their lean controls and showed a marked glucose intolerance. This was accompanied by overt hyperinsulinemia in both the basal state and also in response to an intravenous glucose bolus as indicated by the increase in the incremental area under the curve of insulin (5-wk control mice, 816 +/- 114 min/pM; 5-wk gold thioglucose-injected mice, 1374 +/- 156 min/pM; P < 0.05). At 10 wk after gold thioglucose administration, body weight and the degree of glucose intolerance were increased. Although 10-wk gold thioglucose-injected mice showed basal hyperinsulinemia, an intravenous glucose bolus elicited a smaller insulin secretory response than that observed in the age-matched lean control animals (10-wk control mice, 672 +/- 54 min/pM; 10-wk gold-thioglucose-injected mice 186 +/- 42 min/pM; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin response to an intravenous glucose load during development of obesity in gold thioglucose-injected mice. 832 46

To investigate associations of alcohol intake to constitutional and biochemical variables, cross-sectional studies of men aged 40-59 years from six geographical and occupational populations with varied lifestyles were conducted in the 1990's. Systolic and diastolic blood pressures, glutamic oxaloacetic transaminase, gamma glutamyl transpeptidase, HDL-cholesterol, and uric acid were linearly associated with alcohol intake in all six populations. Drinkers of 2+ drinks (46 g ethanol or more) per day showed higher levels of triglyceride, glutamic pyruvic transaminase than never-drinkers. In two urban occupational populations, men who mainly drank beer had higher uric acid levels; men mainly drinking sake had higher blood pressures and lower serum total cholesterol; men mainly drinking whiskey had higher obesity indices. These differences in constitutional and biochemical variables related to type of alcoholic beverage consumed may be due to differences in lifestyles such as diet and physical activity.
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PMID:[The relation of alcohol intake to constitutional and biochemical variables in Japanese populations]. 890 Dec 13


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