Glutathion content, rate of apoptosis, and brown adipose tissue mass in rats exposed to different ambient temperatures

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.

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

Molecular Metabolism ◽

10.1016/j.molmet.2017.05.004 ◽

2017 ◽

Vol 6 (7) ◽

pp. 715-724 ◽

Cited By ~ 13

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

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

Journal of Pineal Research ◽

10.1111/jpi.12472 ◽

2018 ◽

Vol 64 (4) ◽

pp. e12472 ◽

Cited By ~ 48

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

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y86-166 ◽

1986 ◽

Vol 64 (7) ◽

pp. 970-975 ◽

Cited By ~ 4

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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Characterization and regulation of cold-induced heat shock protein expression in mouse brown adipose tissue

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.269.1.r38 ◽

1995 ◽

Vol 269 (1) ◽

pp. R38-R47 ◽

Cited By ~ 15

Author(s):

J. M. Matz ◽

M. J. Blake ◽

H. M. Tatelman ◽

K. P. Lavoi ◽

N. J. Holbrook

Keyword(s):

Adipose Tissue ◽

Heat Shock ◽

Brown Adipose Tissue ◽

Cold Exposure ◽

Elevated Temperatures ◽

Uncoupling Protein ◽

Hsp70 Expression ◽

Mitochondrial Uncoupling ◽

Ambient Temperatures ◽

Brown Adipose

The accumulation of heat shock proteins (HSPs) after the exposure of cells or organisms to elevated temperatures is well established. It is also known that a variety of other environmental and cellular metabolic stressors can induce HSP synthesis. However, few studies have investigated the effect of cold temperature on HSP expression. Here we report that exposure of Institute of Cancer Research (ICR) mice to cold ambient temperatures results in a tissue-selective induction of HSPs in brown adipose tissue (BAT) coincident with the induction of mitochondrial uncoupling protein synthesis. Cold-induced HSP expression is associated with enhanced binding of heat shock transcription factors to DNA, similar to that which occurs after exposure of cells or tissues to heat and other metabolic stresses. Adrenergic receptor antagonists were found to block cold-induced HSP70 expression in BAT, whereas adrenergic agonists induced BAT HSP expression in the absence of cold exposure. These findings suggest that norepinephrine, released in response to cold exposure, induces HSP expression in BAT. Norepinephrine appears to initiate transcription of HSP genes after binding to BAT adrenergic receptors through, as yet, undetermined signal transduction pathways. Thermogenesis results from an increase in activity and synthesis of several metabolic enzymes in BAT of animals exposed to cold challenge. The concomitant increase in HSPs may function to facilitate the translocation and activity of the enzymes involved in this process.

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Caloric Restriction Paradoxically Increases Adiposity in Mice With Genetically Reduced Insulin

Endocrinology ◽

10.1210/en.2016-1102 ◽

2016 ◽

Vol 157 (7) ◽

pp. 2724-2734 ◽

Cited By ~ 11

Author(s):

Derek A. Dionne ◽

Søs Skovsø ◽

Nicole M. Templeman ◽

Susanne M. Clee ◽

James D. Johnson

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Caloric Restriction ◽

Gene Dosage ◽

Tissue Growth ◽

Tissue Mass ◽

Brown Adipose ◽

Paradoxical Effects ◽

Plasma Insulin Levels ◽

Ad Libitum

Antiadiposity effects of caloric restriction (CR) are associated with reduced insulin/IGF-1 signaling, but it is unclear whether the effects of CR would be additive to genetically reducing circulating insulin. To address this question, we examined female Ins1+/−:Ins2−/− mice and Ins1+/+:Ins2−/− littermate controls on either an ad libitum or 60% CR diet. Although Igf1 levels declined as expected, CR was unable to reduce plasma insulin levels in either genotype below their ad libitum-fed littermate controls. In fact, 53-week-old Ins1+/−:Ins2−/− mice exhibited a paradoxical increase in circulating insulin in the CR group compared with the ad libitum-fed Ins1+/−:Ins2−/− mice. Regardless of insulin gene dosage, CR mice had lower fasting glucose and improved glucose tolerance. Although body mass and lean mass predictably fell after CR initiation, we observed a significant and unexpected increase in fat mass in the CR Ins1+/−:Ins2−/− mice. Specifically, inguinal fat was significantly increased by CR at 66 weeks and 106 weeks. By 106 weeks, brown adipose tissue mass was also significantly increased by CR in both Ins1+/−:Ins2−/− and Ins1+/+:Ins2−/− mice. Interestingly, we observed a clear whitening of brown adipose tissue in the CR groups. Mice in the CR group had altered daily energy expenditure and respiratory exchange ratio circadian rhythms in both genotypes. Multiplexed analysis of circulating hormones revealed that CR was associated with increased fasting and fed levels of the obesogenic hormone, glucose-dependent insulinotropic polypeptide. Collectively these data demonstrate CR has paradoxical effects on adipose tissue growth in the context of genetically reduced insulin.

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Cold-defense function of brown adipose tissue during sleep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.5.r1060 ◽

1993 ◽

Vol 265 (5) ◽

pp. R1060-R1064 ◽

Cited By ~ 2

Author(s):

M. Calasso ◽

E. Zantedeschi ◽

P. L. Parmeggiani

Keyword(s):

Adipose Tissue ◽

Ambient Temperature ◽

Brown Adipose Tissue ◽

Nasal Mucosa ◽

Interscapular Brown Adipose Tissue ◽

Ambient Temperatures ◽

Brown Adipose ◽

Before And After ◽

Defense Function

Rats with chronically implanted electroencephalograph scalp electrodes and thermistors were exposed to 24 and 4 degrees C ambient temperatures during the light hours before and after acclimation to 4 degrees C ambient temperature for 9 days. During synchronized sleep, deep interscapular temperature was higher at 4 degrees C than at 24 degrees C both before and after acclimation to cold. After ablation of brown adipose tissue, deep interscapular temperature was lower at 4 degrees C than at 24 degrees C during synchronized sleep. In the presence of brown adipose tissue, deep interscapular temperature decreased sharply during desynchronized sleep at 4 degrees C both before and after acclimation to cold. This decrease was subsequent to and correlated with an increase in the temperature of the nasal mucosa. The decrease in deep interscapular temperature during desynchronized sleep at 4 degrees C ambient temperature was markedly reduced by ablation of the interscapular brown adipose tissue.

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