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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The central control of brown fat thermogenesis was evaluated in seventeen rats with moveable electrodes implanted in the ventromedial hypothalamus (VMH) and adjacent structures. Brown adipose tissue and core body temperatures were monitored in response to VMH stimulation; sites which elicited a rise in brown fat temperature were observed in the dorsomedial and anterior ventromedial hypothalamus, with BAT temperature profiles varying widely in duration and peak values. Given the complexity of BAT responses to endogenous VMH signals, these varied profiles may be mediated by dissimilar VMH signals, which remain to be characterized.
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PMID:Ventromedial hypothalamic regulation of brown adipose tissue. 176 48

1. Groups of lean and corpulent LA/N-cp rats were fed isoenergetic diets containing, 54% carbohydrate as maize starch (MS) or sucrose (SU), 20% protein, 16% mixed fats, plus other essential nutrients and fiber from 1.5-9 months of age. Final body weights of corpulent rats were 2-3 times those of their lean littermates, and were greater with SU than MS diet in both phenotypes. 2. Interscapular brown adipose tissue (IBAT) mass was greater in corpulent than lean and was greater with SU than MS diet in lean but not corpulent rats. IBAT cell diameters and adipocyte volumes were generally similar in both phenotypes, and were not markedly affected by dietary carbohydrate type. 3. Brown adipocyte locularity profiles were qualitatively similar in both phenotypes, and were morphologically indicative of thermogenic activity in both phenotypes. Locule profiles of corpulent animals contained a greater proportion of thermogenically less active types IV and V brown adipocytes than similarly fed lean animals, however, and locule distribution profiles were not influenced by diet. 4. Serum T3 concentrations were similar in both phenotypes, were greater in SU than MS lean rats and were not influenced by diet in the corpulent phenotype. In contrast, serum thyroxine concentrations and percent thyroxine uptake were not influenced by diet or phenotype. 5. These results are consistent with a partial impairment in BAT-mediated thermogenic activity in the corpulent phenotype and suggest that obesity in this strain may be due to factors other than biochemically defective brown adipose tissue thermogenesis.
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PMID:Effects of dietary carbohydrate and phenotype on thyroid hormones and brown adipose tissue locularity in adult LA/N-cp rats. 257 70

To determine the effects of cafeteria feeding on brown (BAT) and white (WAT) adipose tissue cellularity, thermogenesis and body composition, male Sprague-Dawley rats were fed a cafeteria or a Purina chow diet for 52 days postweaning. Interscapular BAT (IBAT) was removed from subgroups of rats on each diet, and the animals continued on the same regimens. The IBAT weight of rats fed cafeteria diets was 160% of controls after 3 days and 220% after 52 days of the dietary regimens, and brown adipocyte numbers were 130 and 300% those of stock diet-fed rats, respectively, during the same period. Brown adipocyte diameters were initially greater in rats fed cafeteria diet than in rats fed stock diet but were similar after 52 days. Norepinephrine-stimulated thermogenesis was greater in rats fed cafeteria diets than in rats fed stock diet and was intermediate between the two in the IBAT-lipectomized group fed cafeteria diet. Surgical reduction of IBAT resulted in hypertrophy of WAT and an improved efficiency of weight gain, whereas body composition, WAT cellularity, and the efficiency of weight gain of similarly operated rats fed stock diet were unaltered from those of unoperated animals fed stock diet. These results are consistent with the development of a nutritionally induced hyperplasia and/or differentiation of BAT similar to that which follows cold acclimatization. BAT may play an active role in the expenditure of excess energy during periods of overnutrition, and thereby influence an animal's propensity for fatness.
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PMID:Effect of cafeteria feeding on brown and white adipose tissue cellularity, thermogenesis, and body composition in rats. 714 7

Nothing has significantly checked the growth of the tobacco industry since the introduction of smoking to Europe, and the industry has easily survived the 40 years since the first authoritative revelations about the health effects of smoking. Some explanations are offered and the tactics of the industry and the response of the UK Government are reviewed. The policies of British-American Tobacco and its subsidiaries, especially Brown and Williamson in the USA, are considered in detail, including the rejection of an early proposal for a pragmatic but honest deal. In particular, an internal document from 1970 is examined in which BAT purports to set policy for the whole industry. The document is revealed as showing far-sighted but cynical calculation, for instance, in limiting concessions to those countries where public and government awareness requires them. Examples of BAT activities are quoted to illustrate key points.
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PMID:Forty years on: a war to recognise and win. How the tobacco industry has survived the revelations on smoking and health. 874 5

Brown adipose tissue (BAT; brown fat) is the principal site of adaptive thermogenesis in the human newborn and other small mammals. Of paramount importance for thermogenesis is vascular perfusion, which controls the flow of cool blood in, and warmed blood out, of BAT. We have developed an optical method for the quantitative imaging of BAT perfusion in the living, intact animal using the heptamethine indocyanine IR-786 and near-infrared (NIR) fluorescent light. We present a detailed analysis of the physical, chemical, and cellular properties of IR-786, its biodistribution and pharmacokinetics, and its uptake into BAT. Using transgenic animals with homozygous deletion of Type II iodiothyronine deiodinase, or homozygous deletion of uncoupling proteins (UCPs) 1 and 2, we demonstrate that BAT perfusion can be measured noninvasively, accurately, and reproducibly. Using these techniques, we show that UCP -1/-2 knockout animals, when compared to wild-type animals, have a higher baseline perfusion of BAT but a similar maximal response to beta 3-receptor agonist. These results suggest that compensation for UCP deletion is mediated, in part, by the control of BAT perfusion. Taken together, BAT perfusion can now be measured noninvasively using NIR fluorescent light, and pharmacological modulators of thermogenesis can be screened at relatively high throughput in living animals.
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PMID:Quantitation of brown adipose tissue perfusion in transgenic mice using near-infrared fluorescence imaging. 1292 36

Brown (BAT) and white (WAT) adipose tissues play a key role in the body energy balance orchestrated by the central nervous system. Hibernators have developed a seasonal obesity to respond to inhospitable environment. Jerboa is one of the deep hibernator originated from sub-desert highlands. Thus, this animal represents an excellent model to study cold adaptation mechanism. We report that the adipogenic factor PPARgamma exhibits a differential expression between BAT and WAT at mRNA level. A specific induction was only seen in WAT of pre-hibernating jerboa. Interestingly, PPAR beta/delta is specifically induced in BAT and brain of pre-hibernating jerboa, highlighting for the first time the possible key role of this ubiquitous isoform in the cold adaptation of this true hibernator. Inductions of PPARgamma(2) in WAT and PPAR beta/delta in BAT are blunted by a hypolipemic drug, the ciprofibrate. These changes may be correlated with hibernation arrest and death of treated jerboa. Mitochondrial acyl-CoA dehydrogenase and peroxisomal acyl-CoA oxidase activities in brown and white adipose tissues are decreased up to 85% during cold acclimatization (without food privation). These enzyme activities are subject to a strong induction in BAT and in WAT (3.4-7.5 fold) during the hibernation period. The BAT thermogenesis marker is also largely induced (approximately 4 fold of UCP1 mRNA level) during pre-hibernation period. Unexpectedly, treatment with ciprofibrate deeply affects lipolysis in BAT by increasing acyl-CoA dehydrogenase activity (3.4 fold) and acyl-CoA oxidase at both activity and mRNA levels (2.8 and 3.8 fold, respectively) and enhances strongly UCP1 mRNA level (9.5 fold) during pre-hibernation.
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PMID:Peroxisome proliferator-activated receptors as regulators of lipid metabolism; tissue differential expression in adipose tissues during cold acclimatization and hibernation of jerboa (Jaculus orientalis). 1558 84

Brown adipocytes increase energy production in response to induction of PGC-1alpha, a dominant regulator of energy metabolism. We have found that the orphan nuclear receptor SHP (NR0B2) is a negative regulator of PGC-1alpha expression in brown adipocytes. Mice lacking SHP show increased basal expression of PGC-1alpha, increased energy expenditure, and resistance to diet-induced obesity. Increased PGC-1alpha expression in SHP null brown adipose tissue is not due to beta-adrenergic activation, since it is also observed in primary cultures of SHP(-/-) brown adipocytes that are not exposed to such stimuli. In addition, acute inhibition of SHP expression in cultured wild-type brown adipocytes increases basal PGC-1alpha expression, and SHP overexpression in SHP null brown adipocytes decreases it. The orphan nuclear receptor ERRgamma is expressed in BAT and its transactivation of the PGC-1alpha promoter is potently inhibited by SHP. We conclude that SHP functions as a negative regulator of energy production in BAT.
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PMID:The orphan nuclear receptor SHP regulates PGC-1alpha expression and energy production in brown adipocytes. 1621 25

Currently there is tremendous interest in obesity and its harmful donsequences. Height, weight and body mass index (BMI) along with waist girth are routinely used parameters. One snag in the interpretation of BMI >25 as a measure of obesity is the assumption that the increase is mainly due to fat. This review emphasizes the importance of assessing the muscle component of BMI (by simple somatoscopy or somatotyping). 75 percent of Indian T2DM patients have a normal or low BMI, only 25 percent have BMI >25, wherein muscle mass also contributes as well as fat. Hyperinsulinemia is anabolic to both fat and muscle. Since skeletal muscle is a primary site of insulin resistance, greater the muscle mass, greater the importance of physical exercise to overcome the insulin resistance and greater the importance of dietary supplement of n3-PUFA to optimize the phospholipid composition of the muscle membrane (increasing membrane fluidity and thereby permitting longer residence of GLUT-4 in the plasma membrane). I propose three testable hypotheses: (1) Brown fat (FDG-PET imaging) and UCP2 and UCP3 expression in muscle are positively correlated with ectomorphy and mesomorphy, and negatively correlated with endomorphy and obesity. BAT is absent in obese people. (2) Indian T2DM patients with normal or low BMI have increased UCP2 and UCP3 expession in their muscle, as well as increased high molecular weight adiponectin which promote fatty acid oxidation and prevent obesity. (3) Indian T2DM with BMI >25 and obesity have dysfunction of UCP2 and UCP3. They have high leptin with leptin resistance (induced by hyperinsulinemia) and low adiponectin. There is inverse relationship between adipose mass and adiponectin production.
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PMID:Fat and muscle component of body mass index (BMI): relation with hyperinsulinemia. 1759 32

The occurrence of cognitive and behavioral symptoms in patients with primary dystonia remains a matter of debate. We compared 45 patients with primary dystonia with 27 control subjects for performance on neuropsychological tasks with a load on executive-Wisconsin Card Sorting Test (WCST) and Stroop test, and visuospatial-Benton's visual retention test (BVRT) and Block assembly test from Wechsler Adult Intelligence Scale BAT-functions, as well as for intensity of obsessive-compulsive symptoms (Yale Brown Obsessive Compulsive Scale, Y-BOCS). Correlation analysis was performed between neuropsychological performance, dystonia characteristics (duration, age of onset) and severity (Unified Dystonia Rating Scale, UDRS), and Y-BOCS. Patients made more perseverative errors on the WCST (P = 0.042) and had a higher mean Y-BOCS (P = 0.003) score than controls. Timed tests (BVRT, BAT, Stroop test) correlated with UDRS. Y-BOCS, WCST, and UDRS scores were not significantly correlated with one another.These results suggest that patients with primary dystonia may have set-shifting deficits and a higher intensity of obsessive compulsive symptoms when compared to healthy subjects. This may reflect a pattern of complex neurophysiological dysfunction involving dorsolateral, orbitofrontal, and motor frontostriatal circuits.
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PMID:Set-shifting and behavioral dysfunction in primary focal dystonia. 1804 8

We have studied the effects of chronic peripheral infusion of Neuropeptide Y (NPY) and norepinephrine (NE) alone and together. Do these hormones additively affect the metabolic activity of Brown adipost tissue (BAT in obese animals? 20 obese (fa/fa) Zucker strain rats were studied. The diameter of the triglyceride droplets (TGDs) was measured as an indicator of the BAT metabolic activity. We confirmed that in these animals NE alone did not stimulated BAT metabolic activity. Neither did NPY alone. NPY and NE together caused significant induction of BAT metabolic activity as indicated by severe reduction in the TGD diameter.
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PMID:The effect of npy and norepinephrine on the triglyceride droplets in brown adipose tissue in obese warm acclimated rats. 1914 97


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