Protein synthesis in liver, skeletal muscle, and brown adipose tissue of rats fed a protein-deficient diet

Feeding protein-deficient diets to rats is known to stimulate diet-induced thermogenesis and activate brown adipose tissue (BAT). The fact that BAT protein content, unlike that of other tissues, is unnaffected by protein deficiency prompted us to measure tissue protein synthesis in vivo in animals maintained on normal- (18.8%) and low- (7.6%) protein (LP) diets. Protein synthesis was depressed in the liver of the LP rats due to a fall in RNA activity, with no change in RNA content, and synthesis was also reduced in skeletal muscle from the LP group, but this was due to decreased RNA content with no change in RNA activity. Conversely, protein synthesis, RNA, DNA, and protein content of interscapular BAT were all unaltered in protein-restricted animals. These data indicate that, unlike liver, skeletal muscle, and whole carcass, BAT protein synthesis is not reduced in protein-restricted rats, and this may be related to activation of thermo-genesis in the tissue.

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Cell-autonomous activation of Hedgehog signaling inhibits brown adipose tissue development

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1420978112 ◽

2015 ◽

Vol 112 (16) ◽

pp. 5069-5074 ◽

Cited By ~ 18

Author(s):

LaGina Nosavanh ◽

Da-Hai Yu ◽

Eric J. Jaehnig ◽

Qiang Tong ◽

Lanlan Shen ◽

...

Keyword(s):

Skeletal Muscle ◽

Adipose Tissue ◽

Brown Adipose Tissue ◽

Hedgehog Signaling ◽

Primary Cilia ◽

Brown Adipose ◽

Adipose Tissue Development ◽

Poorly Differentiated ◽

Hh Signaling

Although recent studies have shown that brown adipose tissue (BAT) arises from progenitor cells that also give rise to skeletal muscle, the developmental signals that control the formation of BAT remain largely unknown. Here, we show that brown preadipocytes possess primary cilia and can respond to Hedgehog (Hh) signaling. Furthermore, cell-autonomous activation of Hh signaling blocks early brown-preadipocyte differentiation, inhibits BAT formation in vivo, and results in replacement of neck BAT with poorly differentiated skeletal muscle. Finally, we show that Hh signaling inhibits BAT formation partially through up-regulation of chicken ovalbumin upstream promoter transcription factor II (COUP-TFII). Taken together, our studies uncover a previously unidentified role for Hh as an inhibitor of BAT development.

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Functional characterization of human brown adipose tissue metabolism

Biochemical Journal ◽

10.1042/bcj20190464 ◽

2020 ◽

Vol 477 (7) ◽

pp. 1261-1286 ◽

Cited By ~ 3

Author(s):

Marie Anne Richard ◽

Hannah Pallubinsky ◽

Denis P. Blondin

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Functional Characterization ◽

Human Infants ◽

Positron Emission ◽

Brown Adipose ◽

Treatment Of Obesity ◽

And Function

Brown adipose tissue (BAT) has long been described according to its histological features as a multilocular, lipid-containing tissue, light brown in color, that is also responsive to the cold and found especially in hibernating mammals and human infants. Its presence in both hibernators and human infants, combined with its function as a heat-generating organ, raised many questions about its role in humans. Early characterizations of the tissue in humans focused on its progressive atrophy with age and its apparent importance for cold-exposed workers. However, the use of positron emission tomography (PET) with the glucose tracer [18F]fluorodeoxyglucose ([18F]FDG) made it possible to begin characterizing the possible function of BAT in adult humans, and whether it could play a role in the prevention or treatment of obesity and type 2 diabetes (T2D). This review focuses on the in vivo functional characterization of human BAT, the methodological approaches applied to examine these features and addresses critical gaps that remain in moving the field forward. Specifically, we describe the anatomical and biomolecular features of human BAT, the modalities and applications of non-invasive tools such as PET and magnetic resonance imaging coupled with spectroscopy (MRI/MRS) to study BAT morphology and function in vivo, and finally describe the functional characteristics of human BAT that have only been possible through the development and application of such tools.

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Faculty Opinions recommendation of Cold but not sympathomimetics activates human brown adipose tissue in vivo.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.723897883.793548350 ◽

2018 ◽

Author(s):

Michael Symonds

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Brown Adipose

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TAF7L modulates brown adipose tissue formation

eLife ◽

10.7554/elife.02811 ◽

2014 ◽

Vol 3 ◽

Cited By ~ 12

Author(s):

Haiying Zhou ◽

Bo Wan ◽

Ivan Grubisic ◽

Tommy Kaplan ◽

Robert Tjian

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Core Promoter ◽

Uncoupling Protein ◽

Dna Looping ◽

Chromatin Interactions ◽

Brown Adipose ◽

Important Regulator

Brown adipose tissue (BAT) plays an essential role in metabolic homeostasis by dissipating energy via thermogenesis through uncoupling protein 1 (UCP1). Previously, we reported that the TATA-binding protein associated factor 7L (TAF7L) is an important regulator of white adipose tissue (WAT) differentiation. In this study, we show that TAF7L also serves as a molecular switch between brown fat and muscle lineages in vivo and in vitro. In adipose tissue, TAF7L-containing TFIID complexes associate with PPARγ to mediate DNA looping between distal enhancers and core promoter elements. Our findings suggest that the presence of the tissue-specific TAF7L subunit in TFIID functions to promote long-range chromatin interactions during BAT lineage specification.

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The Effects of Thyroxine and Isopropylnoradrenaline on Cytochrome Oxidase Activity in Brown Adipose Tissue

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y73-114 ◽

1973 ◽

Vol 51 (10) ◽

pp. 751-758 ◽

Cited By ~ 26

Author(s):

H. M. C. Heick ◽

C. Vachon ◽

Mary Ann Kallai ◽

Nicole Bégin-Heick ◽

J. LeBlanc

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Protein Content ◽

Cytochrome Oxidase ◽

Cold Adaptation ◽

Metabolic Response ◽

Mitochondrial Enzymes ◽

Cold Adapted ◽

Brown Adipose ◽

Hormonal Treatments

Groups of animals were treated with injections of isopropylnoradrenaline, thyroxine, or both hormones together. The effects of these hormonal treatments on the size, protein content, and level of some mitochondrial enzymes, in particular the cytochrome oxidase, were determined and compared to the effect on these parameters produced by cold adaptation. The changes observed were correlated with the resistance of the animals to cold stress and with their metabolic response to injections of isopropylnoradrenaline. All treatments increased the size of the brown adipose tissue. Whereas thyroxine had little effect on the protein content and cytochrome oxidase, both isopropylnoradrenaline and cold adaptation produced increases in these parameters. It appears that the isopropylnoradrenaline-treated animals mimic more closely the cold-adapted animals than do those with thyroxine treatment. However, the isopropylnoradrenaline-treated animals are not as resistant to cold as the cold-adapted animals.

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Noradrenaline-induced calorigenesis in warm- or cold-acclimated rats. In vivo estimation of adrenoceptor concentration of noradrenaline effecting half-maximal response

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y80-161 ◽

1980 ◽

Vol 58 (9) ◽

pp. 1072-1077 ◽

Cited By ~ 9

Author(s):

Florent Depocas ◽

Gloria Zaror-Behrens ◽

Suzanne Lacelle

Keyword(s):

Adipose Tissue ◽

Steady State ◽

Brown Adipose Tissue ◽

Maximal Response ◽

Brown Adipose ◽

Acclimation Group ◽

Arterial Plasma ◽

State Concentration ◽

Na Uptake

Desmethylimipramine (DMI, 1 mg DMI∙HCl kg−1) and normetanephrine (NMN, 1 μg min−1 g−0.74) were used to inhibit, respectively, neuronal and extraneuronal uptakes of noradrenaline (NA) during calorigenesis induced in barbital-sedated warm-acclimated (WA) or cold-acclimated (CA) rats by infusion of NA, a procedure which mimics the effects of NA released within calorigenic tissues in response to cold exposure. The doses of the inhibitors were selected for maximal effectiveness in potentiating calorigenic response and for minimal side effects. For rats of either acclimation group treated with DMI and NMN, with DMI only, or with neither inhibitor the doses of NA required to evoke approximately half-maximal calorigenic responses were, respectively, 0.5, 1.0, and 3.5 ng min−1 g−0.74. The corresponding steady-state concentrations of NA in arterial plasma averaged 14.3, 21.7, and 43.2 nM in the three groups of WA rats and 10.0, 14.8, and 31.9 nM in the three groups of CA rats. Reduction by NA uptake inhibitors of the circulating levels of NA necessary to stimulate calorigenesis, half-maximally, presumably in brown adipose tissue, indicates a reduction in the steepness of the NA concentration gradient between capillary plasma and synaptic clefts in that tissue. The steady-state concentration of NA in blood plasma of rats treated with DMI and NMN and infused with NA at a dose of 0.5 ng min−1 g−0.74 (~1 × 10−8 M) is a good estimate of the NA concentration required at calorigenic adrenoceptors to effect half-maximal activation. Presumably, this concentration is also an estimate of that resulting from NA released at nerve endings during cold-induced activation of nonshivering thermogenesis at half-maximal rates in brown adipose tissue.

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