Measurements of adipose tissue respiration in a closed chamber using an oxygen sensor: methodological considerations.

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

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Metabolic adaptations in brown adipose tissue of the hamster in extreme ambient temperatures

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.1.153 ◽

1976 ◽

Vol 231 (1) ◽

pp. 153-160 ◽

Cited By ~ 11

Author(s):

T Rabi ◽

Y Cassuto

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Protein Content ◽

Cold Acclimation ◽

Mitochondrial Protein ◽

Heat Acclimation ◽

Fat Content ◽

Tissue Respiration ◽

Cytochrome Oxidases ◽

Brown Adipose

Cold acclimation caused the following changes in the brown adipose tissue (BAT) of the hamster: the relative weight of the tissue increased, it color darkened, the multilocular structure predominated, and tissue protein content increased while fat content decreased. There was also an increase in the mitochondrial protein content. Heat acclimation had the opposite effects, i.e., the color became lighter, total and mitochondrial protein decreased, fat content increased, and tissue structure was mostly unilocular. Accordingly, cold acclimation was accompanied by increased tissue respiration in the presence of chi-glycerophosphate (chi-GP) and succinate, whereas heat acclimation reduced the respiratory activity of the tissue with these substrates. Isolated BAT mitochondria from cold-acclimated animals increased activities of chi-GP and NADH oxidase, whereas the activities of succinic and cytochrome oxidases and the amount of mitochondrial cytochromes were unchanged. The effects of heat acclimation were more pronounced: there was a decrease in the activities of chi-GP, succinic, NADH, and cytochrome oxidases, as well as in the cytochrome a and a3 content. When respiration of tissue slices on succinate was compared to the maximal potential respiration, as measured with mitochondria disrupted by freezing and thawing, it was found that the relative activity (slices vs. disrupted mitochondria) was highest in cold-acclimated animals and decreased progressively with increasing acclimation temperatures. It is suggested that the differences in the apparent activity of the mitochondria were due to changes in the conformation of the mitochondria as a result of acclimation.

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Reply to: Activation and quantification of human brown adipose tissue: Methodological considerations for between studies comparisons

European Journal of Internal Medicine ◽

10.1016/j.ejim.2017.03.003 ◽

2017 ◽

Vol 41 ◽

pp. e41-e42

Author(s):

Lonneke Bahler ◽

Frits Holleman ◽

Hein J. Verberne

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Brown Adipose ◽

Methodological Considerations

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Reversible temperature-dependent differences in brown adipose tissue respiration during torpor in a mammalian hibernator

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00316.2016 ◽

2017 ◽

Vol 312 (3) ◽

pp. R434-R442 ◽

Cited By ~ 4

Author(s):

Sarah V. McFarlane ◽

Katherine E. Mathers ◽

James F. Staples

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Mitochondrial Respiration ◽

Enzyme Activities ◽

Energy Savings ◽

Tissue Respiration ◽

Membrane Phospholipids ◽

Respiration Rates ◽

Bat Mitochondria ◽

Brown Adipose

Although seasonal modifications of brown adipose tissue (BAT) in hibernators are well documented, we know little about functional regulation of BAT in different phases of hibernation. In the 13-lined ground squirrel, liver mitochondrial respiration is suppressed by up to 70% during torpor. This suppression is reversed during arousal and interbout euthermia (IBE), and corresponds with patterns of maximal activities of electron transport system (ETS) enzymes. Uncoupling of BAT mitochondria is controlled by free fatty acid release stimulated by sympathetic activation of adipocytes, so we hypothesized that further regulation at the level of the ETS would be of little advantage. As predicted, maximal ETS enzyme activities of isolated BAT mitochondria did not differ between torpor and IBE. In contrast to this pattern, respiration rates of mitochondria isolated from torpid individuals were suppressed by ~60% compared with rates from IBE individuals when measured at 37°C. At 10°C, however, mitochondrial respiration rates tended to be greater in torpor than IBE. As a result, the temperature sensitivity (Q10) of mitochondrial respiration was significantly lower in torpor (~1.4) than IBE (~2.4), perhaps facilitating energy savings during entrance into torpor and thermogenesis at low body temperatures. Despite the observed differences in isolated mitochondria, norepinephrine-stimulated respiration rates of isolated BAT adipocytes did not differ between torpor and IBE, perhaps because the adipocyte isolation requires lengthy incubation at 37°C, potentially reversing any changes that occur in torpor. Such changes may include remodeling of BAT mitochondrial membrane phospholipids, which could change in situ enzyme activities and temperature sensitivities.

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Mechanisms of stimulus-calorigenesis coupling in brown adipose tissue

Canadian Journal of Biochemistry and Cell Biology ◽

10.1139/o84-083 ◽

1984 ◽

Vol 62 (7) ◽

pp. 623-630 ◽

Cited By ~ 14

Author(s):

Ludwik J. Bukowiecki

Keyword(s):

Fatty Acids ◽

Adipose Tissue ◽

Brown Adipose Tissue ◽

Mitochondrial Respiration ◽

Uncoupling Protein ◽

Relative Mass ◽

Tissue Respiration ◽

Beta Oxidation ◽

Brown Adipose ◽

Hormone Sensitive

The sequence of metabolic events leading to increased calorigenesis in brown adipose tissue has been reviewed. The first step of this sequence consists in the binding of norepinephrine to adrenergic receptors of the beta1 subtype. This results in the stimulation of adenylate cyclase and activation of lipolysis via the system of protein kinases. Hormone-sensitive lipases represent the "flux-generating" step regulating mitochondrial respiration. Fatty acids released from intracellular triglyceride droplets in consequence of lipase activation play a messenger role between lipolysis and mitochondrial respiration. They stimulate respiration by serving as substrates for beta oxidation (via carnitine-dependent pathways) and (or) by simultaneously increasing mitochondrial permeability to protons (physiological "loose coupling"). The control of brown adipose tissue respiration by lipolysis represents a self-regulatory process, as excessive concentrations of fatty acids retroinhibit lipolysis. At the mitochondrial level, fatty acids appear to interact with an "uncoupling" protein (thermogenin or 32 000 relative mass protein) localized in the inner membrane that confers upon brown adipose mitochondria a unique sensitivity for fatty acid uncoupling. This explains that, contrary to other tissues, respiration is principally controlled in brown adipose tissue by substrate supply (mainly long-chain fatty acids), rather than by the phosphorylation state ratio.

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Thyroid hormone-sensitive brown adipose tissue respiration in the newborn rabbit

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1981.241.6.e449 ◽

1981 ◽

Vol 241 (6) ◽

pp. E449-E453

Author(s):

A. H. Klein ◽

J. J. Jenkins ◽

A. Reviczky ◽

D. A. Fisher

Keyword(s):

Adipose Tissue ◽

Thyroid Hormone ◽

Brown Adipose Tissue ◽

Hormone Treatment ◽

Cellular Respiration ◽

Tissue Respiration ◽

Newborn Rabbit ◽

Glycerophosphate Dehydrogenase ◽

Brown Adipose ◽

Hormone Sensitive

The effects of thyroid hormone treatment on brown adipose tissue (BAT) and liver metabolism were assessed by measuring oxygen consumption, sodium-potassium adenosine triphosphatase (Na-K-ATPase), and mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) activities in tissues from triiodothyronine- (T3) and vehicle-injected (for 3 days) newborn and adult rabbits. In the newborns, basal BAT cellular respiration was increased [mean (%/- SE) = 119 +/- 18 vs. 65 +/- 4 microliter O2/10(6) cells-1 . h in controls (P less than 0.005)], whereas hepatic respiration was unchanged. Ouabain had no effect on basal BAT cellular respiration, but suppressed hepatic respiration by 30% in both newborn groups. T3 treatment had no effect on NE- (10(-6) M) stimulated BAT respiration, whereas adult hepatic respiration was increased almost twofold. alpha-GPD activities were increased in both newborn BAT and adult liver but not in newborn liver. Na-K-ATPase activity was significantly increased only in newborn liver. In conclusion, 1) both BAT and liver are thyroid-hormone sensitive in the newborn rabbit, but the responses to T3 treatment are different in the two tissues; 2) the failure to stimulate both hepatic alpha-GPD and respiration in the newborn appears to be a developmental phenomenon characteristic of the rabbit; 3) thyroid hormones have little effect on sodium transport-dependent respiration in either BAT of liver in the newborn rabbit.

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