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

Obese patients were admitted to a metabolic unit for weight loss. On two paired-test days subjects were given disguised preloads of 100 kcal (0.42MJ) or 300 kcal (1.26MJ). When presented with a meal one hour after the preload, subjects salivated more and reported more hunger, but not appetite, after the low compared to the high preload. A different group of 14 subjects were given preloads of the same energy content (200 kcal, 0.84MJ) on paired-test days. On one day they took 1 g methyl cellulose with 100 ml water drink immediately before the preload. Neither the energy-dilution effect of the water, nor the effect of the methyl cellulose caused a significant decrease in salivation, hunger or appetite scores one hour after the preloads of equal energy content. These results show that salivation and hunger are inversely related to short-term changes in energy intake in obese subjects. Alterations in energy density without changing energy intake or the ingestion of methyl cellulose have no effect on salivation, hunger or appetite.
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PMID:Short-term effects of energy density on salivation, hunger and appetite in obese subjects. 52 33

The methods utilized in our laboratory for a biochemical approach of obesity include dietary manipulations, fatty acid analysis of tissue lipids, in vivo lipogenesis from [3H H2O and [1-14C] acetate, in vitro utilization of [3H] H2O, [U-14C] glucose, [U-14C] fructose, [U-14C] alanine and [1-14C] acetate by adipose tissue fragments, hormone sensitivity (to insulin and catecholamines), and the activity of enzymes such as fatty acid synthetase and adenylate cyclase in adipose tissue extracts. With these methods at hand, it is possible to estimate the major biochemical factors responsible for fat accumulation in adipose tissue. As an example, the case of obese (ob/ob) homozygotic animals of the C57BL/6J strain of Bar Harbor, which suffer from an autosomal recessive obese-hyperglycemic (O-H) syndrome, is compared to that of control nonobese (ob+/ob+) mice from the same strain. The hereditary O-H syndrome in ob/ob mice is characterized by obesity, resistance to the action of insulin, and hyperinsulinism. The development of obesity depends on high lipogenesis in fat depots. Contribute also to obesity a large influx of fatty acids of hepatic and dietary origin, and reduced lipolysis. In these mice, a high fat diet is more propitious to fat accretion than a high-carbohydrate diet.
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PMID:Experimental basis of obesity. 62 36

1. The body compositions of obob and lean (ob+ and ++) mice at 10, 12, 17 and 28 d of age were investigated using a 'cold stress' test to identify the two groups. 2. At each of these ages the obob mice were found to contain significantly more fat than the lean. At 10 d 20% more fat was present and by 17 d the increase was 72%. The obob mice at 28 d contained nearly three times as much fat as the lean. 3. Carcass energy was significantly higher in obob mice at all ages investigated. 4. Other changes in body composition found in the 28 d obob mice, i.e. a reduction in total carcass nitrogen and water content, were already established in the 17-d-old mice but differences at 10 and 12 d were not apparent. 5. The livers of obob mice were significantly heavier than those from lean control mice at 28 d but no differences were detected at the earlier ages. 6. The results are discussed with reference to the early origin of obesity in obob mice.
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PMID:The development of obesity in preweaning obob mice. 62 27

Colchicine, a drug which produces a reversible inhibition of intraaxonal transport and synaptic transmission, was used as a reversible neural blocker to investigate the role of the ventromedial hypothalamus (VMH) in the control of ingestive behavior and body weight regulation. Male Sprague-Dawley rats received intracranial microinjections of colchicine into the VMH. Volume and concentration of the colchicine solution were varied to assess specificity of action and dose-response relationship. When colchicine (2 and 4 microgram) was microinjected bilaterally into the VMH, there was a dose-dependent increase in food and water intakes and body weight gain which lasted several days. The acute period of hyperphagia was followed by a marked depression in feeding which persisted until body weight was lowered to control levels. This suppression of feeding appeared to be a consequence of the preceding period of hyperphagia and obesity, since colchicine-treated rats which were pair-fed with controls to prevent obesity continued to maintain normal food intake and body weight gain when later fed ad libitum. The results of this study confirm the importance of the VMH in the long term regulation of feeding, and indicate that reversible neuronal blocking with colchicine is a useful technique for investigating the neural substrates of feeding and other behaviors.
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PMID:Reversible hyperphagia and obesity following intracerebral microinjections of colchicine into the ventromedial hypothalamus of the rat. 67 51

The M16 line of mice, selected for rapid postweaning gain, exhibits polygenically controlled obesity and hyperphagia. The effect of limiting postweaning energy intake on the subsequent growth and development of obesity in M16 mice was investigated. Male mice from M16 and an unselected line (ICR) were provided either ad libitum or limited (congruent to 70% of ad libitum) feed during the rapid postweaning growth period from 4 to 6 weeks of age. Body weights (g) at 6 weeks of age were: ad libitum ICR (31.0 +/- 0.6), restricted ICR (23.8 +/- 0.7), ad libitum M16 (45.0 +/- 0.6) and restricted M16 (30.1 +/- 0.6). In both lines, restricted feed intake severely depressed body fat, lean, ash, and water at 6 weeks. In addition, percent triacylglycerol, fat cell size and number in the epididymal fat pads were lower. Restricted M16 and ICR mice showed a marked compensatory gain in all body components when subsequently fed ad libitum for 10 weeks. All measurements of adiposity at 16 weeks were similar for the restricted and ad libitum regimens within each line. The relative amounts of energy deposited as fat and lean between 4 and 16 weeks were not influenced by restricted feeding, but M16 mice deposited a larger proportion of energy as fat than as lean when compared with ICR mice. The results suggest that fat cell number is determined at a relatively early age in mice and is primarily under genetic control.
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PMID:Effect of postweaning feed restriction on adipose cellularity and body compositon in polygenic obese mice. 70 8

The weighing of the human body under water is an application of Archimedes' law. Fat being lighter than water or than the structures of lean body mass, body fat can be measured by determining the specific gravity of the human body; that is, by underwater weighing. Body fat has been determined in an "ideal" sample of 14 men and 23 women, all aged 20 years. Testing against a reference measure of body fat makes it possible to test the validity of some anthropometric measurements and of some indices of obesity. These indices offer no advantages over anthropometric measurements.
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PMID:[Measurement of human body fat by means of gravimetry. Application of Archimedes' principle]. 71 34

Isolated fat cells derived from 10-wk-old Zucker obese rats utilized substantially greater amounts of glucose per cell in the presence or absence of insulin than those from lean rats. Initial rates of deoxyglucose or 3-0-methylglucose uptake in fat cells from Zucker obese rats were also 5--10 times greater than those observed in cells from lean rats. However, while 240 microU/ml insulin elicited a maximal response in fat cells from lean rats, this dose of hormone was only about 50% as effective as 24 microU/ml insulin in stimulating glucose metabolism or hexose transport in obese rat cells. This apparent rightward shift in the dose response-relationship could not be adequately explained on the basis of decreased insulin receptors since (125I-) insulin binding per fat cell was increased 2.5--3-fold in obesity, while receptor density on the cell surface in obesity was decreased only slightly. Soleus muscles from obese Zucker rats exhibited decreased basal rates of D(5-3H)glucose conversion to glycogen and H2O compared to those of lean controls. While the percent increase in glucose metabolism due to a supermaximal dose of insulin was similar in soleus muscles of lean and obese Zucker rats, a blunted response to a submaximal insulin dose was observed in muscles from the latter animals. This rightward shift in the dose-response relationship was also observed when deoxyglucose uptake was monitored in soleus muscles from obese rats. Binding of (1251-) insulin to soleus muscles at a medium concentration of 57 microU/ml was significantly decreased in obese compared to lean rats. We conclude that (1) fat cells do not contribute to the insulin resistance of 10-wk obese Zucer rats since glucose utilization is higher in these cells at all concentrations of insulin tested, (2) obese Zucker rat soleus muscle metabolism is defective in two respects--imparied basal glucose utilization and a rightward shift in the insulin dose-response relationship with respect to hexose transport, and (3) this latter defect involving decreased sensitivity of muscle to insulin appears to result from a marked decrease in cell surface receptors for the hormone.
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PMID:Insulin response in skeletal muscle and fat cells of the genetically obese Zucker rat. 72 45

Effects of insulin (1 mU/ml) on diaphragms removed from older-obese (70--110 days, 350--520 g) male Sprague-Dawley rats were compared to responses on muscle removed from younger-lean (27--36 days, 80--150 g) animals. Insulin antagonism on glucose transport (2DG uptake), glucose uptake, glycogen synthesis, glycolysis (lactate production), and glucose oxidation was demonstrated in tissue from the older-obese rats. Extracellular water spaces (measured with inulin-H3) were significantly decreased in these tissue. To determine if insulin antagonism of glucose transport could be secondary to inhibition of a rate-limiting reaction in the Embden-Meyerhof pathway with a subsequent negative feedback on transport, both tissue levels of glycolytic intermediates and oxidation of intracellular lipids were measured. No free intracellular glucose was found in diaphragms from either group of rats. Levels of G-6-P, F-6-P, F-1, 6-diP, PEP, and pyruvate were all lower in muscle from the older-obese animals. Incorporation of C14-FFA into tissue TG was slightly, but significantly, lower in this same tissue. Oxidation of intracellular TG and PL was similar in the two groups. In conclusion, diaphragms from older-obese rats manifest insulin antagonism of glucose transport that is probably responsible for the diminished hormonal effect on glucose uptake and the intracellular pathways of glycogen synthesis, glycolysis, and glucose oxidation. This inhibition of insulin action cannot be accounted for by changes in glycolytic intermediates causing a negative feedback on transport or enhanced lipid oxidation and therefore should be considered primary. The relative effects of age and obesity will need to be evaluated in future studies.
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PMID:Primary insulin antagonism of glucose transport in muscle from the older-obese rat. 72 47

Despite frequently good early successes the several therapeutic methods of obesity show in general unsatisfactory long-term results with large numbers of recidivations. Considering non-existing causal-therapeutic possibilities in the present paper in reported on a complex and differentiated therapeutic programme in 549 obese persons. After an initial subtotal fasting cure of ca. 100 kcal/a day with gradual increase of diet in more than half the obese persons an additional differentiated pharmacotherapy was performed. The indications resulted above all from the frequent syntropy with diabetes mellitus (28%), arterial hypertension (23%) and hyperlipidaemia (14%). In 122 test persons (adipose patients with hyperlipoproteinaemia and extremely obese patients without essential factors of risk, respectively) a treatment with 2 x 50 microgram tri-iodothyronine--partly in combination with diuretics--was performed in intermittent and gradually decreasing dosage. Apart from a vast normalisation of the lipid parameters a reduction of weight from 32.6 +/- 14.8 kg could be achieved after 31 +/- 14 months. Of 131 adipose hypertensive patients 74 received additionally diuretics on account of increased water retention with also good long-term results concerning the reduction of weight and normalisation of blood pressure. The biguanides were a therapeutic enrichment particularly in the treatment of adipose elderly diabetics with obligatory diet. Apart from an improvement of the carbohydrate tolerance regularly a more intensive reduction of weight was obtained.
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PMID:[Indications and results of an additional differentiated pharmacotherapy of obesity]. 73 44

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48


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