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

Long-term cafeteria feeding, cold exposure, and the combination of treatments increased energy intake in female Wistar rats by 25%, 113%, and 150%, respectively, in comparison with controls (P less than 0.01). Although cafeteria feeding at room temperature markedly increased the insulin response to an intravenous glucose tolerance test (IVGTT), glucose tolerance was deteriorated (P less than 0.01). In contrast, cold exposure significantly improved glucose tolerance in the presence of a reduced insulin response in Purina- and cafeteria-fed animals. Moreover, cold exposure also decreased body weight gain and increased brown adipose tissue mass, total cytochrome-oxidase activity, and cellularity by approximately 600-800%. The results suggest that cold exposure enhances insulin sensitivity of peripheral tissues, whereas hyperphagia on a high-fat, low-protein diet leads to insulin resistance. In addition, the results demonstrate that prolonged stimulation of energy expenditure by cold exposure not only reverses the diabetogenic effects of cafeteria feeding but also improves glucose tolerance. This phenomenon could result from a combination of two factors: (1) a cold-induced prevention of obesity; and (2) an enhanced disposal of circulating glucose into peripheral tissues, including brown adipose tissue.
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PMID:Cold exposure reverses the diabetogenic effects of high-fat feeding. 300 94

Rats with obesity-producing, hypothalamic knife cuts were fed a high fat diet and placed in the cold (2 degrees C) for six days starting 3, 11, or 24 days after surgery. Between surgery and cold exposure, knife-cut rats consumed 90% to 122% more energy and gained more weight (32 +/- 4, 112 +/- 5, and 241 +/- 9 g) than sham-operated rats (15 +/- 2, 34 +/- 2, and 58 +/- 3 g). When exposed to cold, sham-operated rats increased (22% to 30%) energy intake whereas knife-cut rats decreased (5% to 51%) intake. After 24 hours at 2 degrees C body temperatures of knife-cut rats were 1.2, 0.7, and 0.7 degrees less than those of control rats; body temperatures continued to decrease to 2.9, 3.0 and 2.5 degrees less than control rats after six days at 2 degrees C. Fasting for 12 hours at 2 degrees C caused a further reduction in body temperature to 4.9, 4.8, and 5.9 degrees less than in control rats. Cold exposure increased urinary excretion of norepinephrine and epinephrine (indicators of sympathoadrenal activity) in all rats. Guanosine diphosphate (GDP) binding to brown adipose tissue (BAT) mitochondria (an indicator of the thermogenic capacity of the tissue) was similar in cold-exposed, knife-cut, and sham-operated rats. Cold acclimation before hypothalamic knife-cut surgery prevented the cold-induced decrease in body temperatures of knife-cut rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired thermoregulation in cold-exposed rats with hypothalamic obesity. 302 Mar 46

A cloned cDNA sequence for the unique mitochondrial uncoupling protein of rat brown adipose tissue has been used to assay the corresponding mRNA in several situations. When thermogenesis in brown adipose tissue is stimulated (exposure of adult rats to the cold, birth) a rapid and prolonged increase in the level of uncoupling protein mRNA is observed. Such an increase can be mimicked by injection of animals with a new beta-adrenoreceptor agonist BRL 26830A. Conversely it is known that mice and rats with genetic or surgical obesity have a weakly thermogenic brown adipose tissue with a reduced norepinephrine turnover. A reduced level of uncoupling protein mRNA was measured in obese fa/fa rats 10 days or 10 weeks old and in obese rats with a lesion of the ventromedial hypothalamic area but not in obese ob/ob mice. Moreover, exposure of obese animals to cold or dosing with BRL 26830A strikingly increased the level of uncoupling protein mRNA. Measurement of the relative concentration of nascent Ucp transcripts in nuclei isolated from brown adipose tissue indicates that Ucp gene is acutely (within 15 min) regulated at the level of transcription and is controlled via activation of beta-adrenoreceptors of plasma membrane. Ucp gene transcription is decreased in obese fa/fa rats but can be fully and rapidly turned on after injection of BRL 26830A.
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PMID:Expression of uncoupling protein mRNA in thermogenic or weakly thermogenic brown adipose tissue. Evidence for a rapid beta-adrenoreceptor-mediated and transcriptionally regulated step during activation of thermogenesis. 302 20

The energizing balance of the body is the result of intake and output of energy. Intake corresponds to eating and output corresponds to basal metabolism, physical exercise and heat production. Recent studies conducted on man suggest that obesity could be associated with a lack of heat production. Thus, a decreased thermogenic consumption associated with eating could contribute to the development of obesity. This hypothesis seems valid as far as obese rodents are concerned. In this case, it is a known fact that a specific organ, the brown fatty tissue, main effector of the thermogenesis induced by cold and eating. The molecular mechanisms of heat production by the brown fatty tissue, have been recently explained. Brown adipocytes are present in man, but their specific contribution to the energizing balance or imbalance is not yet established. This will be subject of further studies.
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PMID:[Thermogenesis and obesity: molecular aspects]. 322 99

Mild cold exposure (22 degrees C, with reference to 28 degrees C, thermoneutral) was studied by overnight whole-body indirect calorimetry in euthyroid women. Basal, sleeping, energy expenditure (EE) was significantly increased (+3.8%, P less than 0.05) in six normal weight women but reduced (-3.5%, P less than 0.05) in five obese type II diabetic women. Mixed responses were found in five women with simple obesity. Biochemical measurements were made on fasting blood samples taken at 0900 h after 12 h exposure to the two temperatures. Serum T4, free T3 and TSH were within the normal reference range in all subjects. Serum T4 did not show any differences between the groups, nor any effect from temperature. There was a significant increase in free T3 (P less than 0.05) at 22 degrees C in the control subjects, but no differences in the obese diabetic women. Serum thyroglobulin fell significantly in the diabetic group. Both TSH and free T3 responses to mild cold were significantly different between the groups, but both correlated positively (P less than 0.05) with the changes in sleeping energy expenditure at 22 degrees C with reference to 28 degrees C. Changes in TSH and free T3 were themselves significantly correlated within individuals (P less than 0.01). The normal physiological non-shivering thermogenesis of adult humans on exposure to a cool environment may thus be mediated by a pituitary-thyroid mechanism. The abnormal response of obese diabetic women was associated with impaired TSH and thyroid hormone responses, and may be a factor contributing to weight gain.
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PMID:Metabolic and thyroidal responses to mild cold are abnormal in obese diabetic women. 325 62

The effects of cold acclimation on cellularity, lipoprotein lipase (LPL) activity and lipolysis were studied in white adipose tissue of rats fed a high fat diet. Male Osborne-Mendel rats (7 weeks old) were exposed at either 28 or 5 degrees C for 10 weeks. The rats were fed a semipurified diet (normal fat (NL): 5% lard, high fat (HL): 54% lard) for the last 9 weeks. Caloric intake with NL and HL diets were comparable and cold exposure led to the same increase with both diets. At 28 degrees C, HL diet initiated both hypertrophy and hyperplasia; however, at 5 degrees C only hyperplasia was observed. Total LPL activity showed high stimulation both in 28 and 5 degrees C HL rats. In vitro lipolytic stimulation by norepinephrine was lowered at 5 degrees C and abolished at 28 degrees C in HL-fed rats. HL diet resulted in enhanced lipid deposition without an increase in caloric intake. Even in cold-adapted Osborne-Mendel rats a relative obesity could be produced by a HL diet.
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PMID:Effect of environmental temperature on dietary obesity in Osborne-Mendel rats. 325 90

We have previously shown that normal chicken serum (NCS) is able to interfere with the IL 2 promoted incorporation of DNA precursors into T lymphoblasts and that serum derived from autoimmunity prone Obese strain (OS) chickens is deficient in this respect. This "defect in non-specific suppression" has been speculated to be one of the causes for T cell hyperreactivity in the OS. In this study we present several lines of evidence that the suppressive effect of normal chicken serum (NCS) on 5-(125Iodo)-2-deoxyuridine (125IUdR) uptake into chicken T blasts is a competition artefact due to cold thymidine (TdR) present in NCS. Inhibition of 125IUdR required the continuous presence of NCS and suppression of 3H-TdR incorporation could be competed for by increasing the dose of the radiolabel. Molecular sieve chromatography followed by reversed phase high performance liquid chromotagraphy revealed the "inhibitory" activity to co-elute with TdR. Moreover, NCS did not suppress protein synthesis by chicken T cells growing with IL 2 and did not affect oxidative metabolism, cell viability, expression of IL 2 receptors, or percentages of cells in the S phase of the cell cycle. In accordance with these data, OS-sera suprisingly contain less TdR than those from normal controls. Experiments involving crosses of the OS with the normal inbred CB strain, revealed that the subnormal serum TdR level of the OS is an autosomally dominant trait which, however, segregates from T cell hyperreactivity. These findings falsify our previous hypothesis that a defect in specific IL 2 antagonists might be involved in T cell hyperfunction of the OS and indicate that NCS is devoid of factors which neutralize IL 2 function.
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PMID:Decreased level of thymidine in the serum of obese strain (OS) chickens with spontaneous autoimmune thyroiditis. 326 15

Thermogenesis of brown adipose tissue (BAT) of genetically obese mice, KKAY mice, was examined by measuring the BAT mitochondrial guanosine diphosphate (GDP) binding as an index of thermogenesis and comparing it with that of normal C57BL mice. No great difference in GDP binding was observed in KKAY and C57BL mice fed a stock diet. However, when they were given a sucrose solution, the increase in BAT mitochondrial GDP binding of KKAY mice (+22%) was much lower than that of C57BL mice (+106%). A high fat diet increased BAT mitochondrial GDP binding in KKAY mice to the same extent (+82%) as in C57BL mice. When the mice were fasted for 48 h, BAT mitochondrial GDP binding of C57BL mice decreased by 70%, while that of KKAY mice showed no change. Both acute exposure to cold and norepinephrine injections increased GDP binding in KKAY mice by 90% and 131%, respectively. These results indicate that low BAT thermogenesis in response to sucrose intake may be a cause of obesity in KKAY mice, and this may be brought about by defects in the central nervous system.
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PMID:Thermogenesis in brown adipose tissue of genetically obese, diabetic (KKAY) mice. 339 15

The aim of the present work was to elucidate the importance of brown adipose tissue (BAT) and skeletal muscle for ephedrine-induced thermogenesis, and to examine the effect of chronic ephedrine treatment on energy expenditure. The investigations were carried out in vivo on humans, as well as on rats and dogs. In rodents BAT is the major site of cold-induced nonshivering thermogenesis and of facultative thermogenesis: the component of food-induced thermogenesis storage of nutrients. BAT thermogenesis is mediated through an activation of the sympathetic nervous system. Via a sustained stimulation of the sympathetic nervous system, acclimation to cold and overfeeding induces hyperplasia of BAT, and subsequently an increased thermogenic capacity. In a number of obesity syndromes in rodents the sympathetic mediation is defective, and this leads to extreme sensitivity to cold and to obesity. BAT has been reported to be present also in humans, and there has been focused mainly on the interscapular subcutaneous tissue. An ephedrine-induced increase of the interscapular skin temperature has been interpreted as evidence of the presence of thermogenic BAT. This lead to the assumption that BAT, also in humans, plays a significant role in the regulation of energy balance. Likewise, the hypothesis has been advanced that a diminished thermogenesis in BAT may be the cause of some types of human obesity. After validation of the xenon clearance method in rats for blood flow measurements in BAT, the method was applied on humans to examine the ephedrine-induced increase in the interscapular temperature. The warmest interscapular skin area was localized by thermography during ephedrine stimulation. In a second study subcutaneous blood flow and temperature were measured in this area during ephedrine stimulation and compared to the response of white adipose tissue in the lumbar area. The results showed that the increases in blood flow and temperatures were of similar magnitude in the two locations. Biopsies taken from the warmest interscapular spots did not contain brown adipocytes. A histological study on human autopsies confirmed that BAT is rare in the interscapular tissue, but frequently occurring in the perirenal depot. In the next study, the thermogenic function of the perirenal BAT was examined by measurements of blood flow and local temperature. Perirenal BAT thermogenesis was uninfluenced by ephedrine in 4 of 5 subjects. It was estimated that BAT thermogenesis in the single responding subject could account for maximally 15% of the ephedrine-induced increase in whole body oxygen consumption.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thermogenesis in human brown adipose tissue and skeletal muscle induced by sympathomimetic stimulation. 346 54

Previous studies on obese strains of rats (e.g., Zucker and LA/N cp) have shown that they are deficient in nonshivering thermogenesis and poor in cold tolerance. Our earlier studies have established that aminophylline (AMPY; 85% theophylline-15% ethylenediamine) is effective in significantly improving cold tolerance in the lean Sprague-Dawley rat regardless of age or thermogenic capacity. The present study tested whether AMPY may be also effective in improving cold tolerance in both young (12-18 wk) and older (36-42 wk) lean and corpulent LA/N cp rats. Contrary to previous reports, however, the norepinephrine (NE)-stimulated nonshivering thermogenesis was not only present but also equal in magnitude in the corpulent rats to that of their lean controls. Further, no difference in cold tolerance was observed between the two groups regardless of age. Similarly, AMPY (18.7 mg/kg ip) significantly improved thermogenesis and cold tolerance in both lean and corpulent rats, again without any age-related difference in response. These results indicate that, despite the existence of obesity, no difference in thermogenic capacity to either NE or cold stimulation is evident in the LA/N cp rats. Thus the ontogeny of obesity in this strain may be caused by factors other than deficiency in NE- or cold-stimulated thermogenesis at the end-organ level.
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PMID:Enhancement of cold-stimulated thermogenesis in the corpulent rat (LA/N cp) by aminophylline. 356 4


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