Melatonin increases brown adipose tissue mass and function in Zücker diabetic fatty rats: implications for obesity control

2018 ◽  
Vol 64 (4) ◽  
pp. e12472 ◽  
Author(s):  
Gumersindo Fernández Vázquez ◽  
Russel J. Reiter ◽  
Ahmad Agil
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Tissue Mass ◽  
Obesity Control ◽  
Brown Adipose ◽  
Zucker Diabetic Fatty Rats ◽  
Adipose Tissue Mass ◽  
And Function

Fibroblast Growth Factor-9 Regulates Adaptive Brown Adipose Tissue Mass Expansion

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 277-OR ◽  
Author(s):  
FARNAZ SHAMSI ◽  
TIAN LIAN HUANG ◽  
YU-HUA TSENG
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Brown Adipose Tissue ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Tissue Mass ◽  
Brown Adipose ◽  
Adipose Tissue Mass ◽  
Mass Expansion

Brown Adipose Tissue and Its Uncoupling Protein in Chronically Hypoxic Rats

1997 ◽  
Vol 93 (4) ◽  
pp. 349-354 ◽  
Author(s):  
Jacopo P. Mortola ◽  
Lina Naso
Keyword(s):  
Adipose Tissue ◽  
Ambient Temperature ◽  
Brown Adipose Tissue ◽  
Body Mass ◽  
Uncoupling Protein ◽  
Total Proteins ◽  
Tissue Mass ◽  
Brown Adipose ◽  
Adipose Tissue Mass ◽  
Old Rats

1. Hypoxia is known to decrease thermogenesis. We set out to determine whether this is accompanied by alterations in the brown adipose tissue, which is a major source of non-shivering thermogenesis. 2. Measurements were performed on 25- and 64-day-old rats, after 4 days of hypoxia (10% inspired O2), and on ∼3.5-month-old rats in hypobaric hypoxia since birth, at an ambient temperature of 25°C. 3. All hypoxic rats had higher haematocrit and lower body mass than corresponding controls. 4. In the 25-day-old rats, hypoxia had minimal and non significant effects on brown adipose tissue mass, proteins and DNA concentration. The content of the mitochondrial uncoupling protein thermogenin, evaluated by immunoblot after electrophoretic separation, relative to the cytoskeleton actin (UCP/Act), was not significantly altered. 5. In 25-day-old rats exposed for 4 days to cold (ambient temperature = 7–9°C), brown adipose tissue was hyperplastic, with increased UCP/Act; hypoxia did not appreciably alter the response to cold. 6. In the 2-month-old rats, after 4 days of hypoxia UCP/Act was reduced to about 40% of control. 7. In the 3.5-month-old rats maintained in hypoxia since birth, brown adipose tissue mass was reduced in proportion to body mass, with little effect on total proteins and DNA; UCP/Act was decreased to about 50% of control. 8. We conclude that chronic hypoxia had a minimal effect on brown adipose tissue total proteins and DNA content. However, the uncoupling protein content can be greatly reduced, depending upon age and duration of hypoxia.

scholarly journals Loss of ADAMTS5 enhances brown adipose tissue mass and promotes browning of white adipose tissue via CREB signaling

2017 ◽  
Vol 6 (7) ◽  
pp. 715-724 ◽  
Author(s):  
Dries Bauters ◽  
Mathias Cobbaut ◽  
Lotte Geys ◽  
Johan Van Lint ◽  
Bianca Hemmeryckx ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
Tissue Mass ◽  
Brown Adipose ◽  
Adipose Tissue Mass

Functional characterization of human brown adipose tissue metabolism

2020 ◽  
Vol 477 (7) ◽  
pp. 1261-1286 ◽  
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.

Effects of fasting and food restriction on brown adipose tissue composition in normal and dystrophic hamsters

1986 ◽  
Vol 64 (7) ◽  
pp. 970-975 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos ◽  
H. M. Yuen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Food Deprivation ◽  
Food Restriction ◽  
Tissue Mass ◽  
Tissue Protein ◽  
Guanosine Diphosphate ◽  
Isolated Mitochondria ◽  
Daily Food ◽  
Brown Adipose

Fasting for 36–48 h or food restriction (30% reduction of daily food intake for 6 weeks) caused brown adipose tissue (BAT) atrophy in hamsters. Fasting-induced atrophy was characterized by reductions in tissue mass, DNA, protein, and thermogenin. By contrast, food restriction had no effect on tissue cellularity (DNA) but markedly reduced the tissue protein and thermogenin contents. The concentration of thermogenin in isolated mitochondria was unchanged by fasting or food restriction. Dystrophic hamsters had a reduced BAT mass when compared with weight-matched control hamsters. This resulted from a reduction in tissue cellularity since BAT DNA, protein and thermogenin contents were all reduced. The extent of binding of [3H]guanosine diphosphate to isolated mitochondria and their content of thermogenin were similar in normal and dystrophic hamsters. In response to cold exposure, as in normal hamsters, BAT of dystrophic hamsters grew and the tissue thermogenin increased, but the mitochondrial concentration of thermogenin did not change. In response to fasting, in contrast with normal hamsters, there was no significant reduction in BAT DNA in dystrophic animals and the loss of tissue protein was reduced. However, the relative changes in BAT composition during chronic food restriction were similar in normal and dystrophic animals. Thus, reduction in hamster BAT thermogenic capacity during food deprivation may occur by loss of cells and (or) reduction in the tissue protein and thermogenin contents. The extent of protein and (or) DNA loss may be dependent upon the original tissue mass and the severity of food deprivation.

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