Short-term Cold Acclimation Recruits Brown Adipose Tissue in Obese Humans

The effects of immunosympathectomy and acclimation to cold on the incorporation of glucose-U-14C into lipids of the interscapular brown adipose tissue, epididymal fat pad, and liver of rats have been investigated. Acclimation to cold was associated with an increase in glucose recovered in the total lipids of brown adipose tissue. These changes in glucose recovery were the same in immunosympathectomized as in intact rats. The brown adipose tissue of the two groups of cold-acclimated rats differed, however, in that this tissue in the immunosympathectomized animals was larger and had more lipid. Suggestions are raised to explain these findings. Neither immunosympathectomy nor cold acclimation produced any changes in white adipose tissue. Immunosympathectomy did not alter the liver's handling of glucose. However, cold-acclimation was associated with an increase in the relative weight of the liver and a decrease in glucose recovery in liver lipids.

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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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Effects of cold acclimation in dystrophic hamsters: reduction of heart necrosis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1986.250.2.r167 ◽

1986 ◽

Vol 250 (2) ◽

pp. R167-R174

Author(s):

M. Desautels ◽

R. A. Dulos

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Ventricular Hypertrophy ◽

Body Weight Gain ◽

Calcium Content ◽

Co2 Production ◽

Interscapular Brown Adipose Tissue ◽

Brown Adipose ◽

Plasma Creatine Kinase

The effects of cold acclimation on brown adipose tissue, heart, and skeletal muscles were evaluated to assess if the increase in metabolic activity associated with chronic exposure to 4 degrees C had any influence on the progression of the syndrome in dystrophic hamsters. Body weight gain was much slower in dystrophic animals kept at 22 degrees C and was unaffected by cold acclimation. Rates of O2 consumption and CO2 production were similar in normal and dystrophic hamsters kept at 22 degrees C, and both were increased in cold-acclimated normal and dystrophic animals. The amount of interscapular brown adipose tissue was about one-half of normal in dystrophic hamsters kept at 22 degrees C. In response to cold acclimation, as in normal hamsters, brown adipose tissue of dystrophic hamsters grew and increased its thermogenin content by more than fourfold. However, the concentration of thermogenin in isolated mitochondria remained unchanged. Heart ventricular hypertrophy was also observed in both normal and dystrophic hamsters after cold acclimation. The number and extent of cardiac necrotic lesions were significantly reduced in cold-acclimated dystrophic animals when compared with age-matched dystrophic hamsters kept at 22 degrees C. Heart calcium content and plasma creatine kinase levels were also reduced in dystrophic hamsters after cold acclimation. However, in soleus muscles the prevalence of centronucleated fibers, an indirect cumulative index of necrosis, as well as the extent of tissue necrosis were not significantly reduced in cold-acclimated dystrophic animals. Thus cold acclimation of dystrophic hamsters appeared to reduce necrosis predominantly in the heart.

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Neural influences on trophic changes in brown adipose tissue during cold acclimation

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.255.6.r874 ◽

1988 ◽

Vol 255 (6) ◽

pp. R874-R881 ◽

Cited By ~ 5

Author(s):

I. R. Park ◽

J. Himms-Hagen

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Elevated Level ◽

Uncoupling Protein ◽

Sympathetic Innervation ◽

Intact Tissue ◽

Brown Adipose ◽

Neural Influences

We studied the role of the sympathetic innervation in development and maintenance of increased levels of uncoupling protein (UCP) and of thyroxine 5'-deiodinase (TD) during cold-induced growth of brown adipose tissue (BAT). Interscapular BAT was unilaterally (and in some experiments, bilaterally) denervated either before acclimation to cold (4 degrees C) for 12 days or after 14 days of a total 28-day period of acclimation to cold. BAT norepinephrine was reduced to 3-7% of the normal level in denervated BAT for up to 26 days. Denervation slowed, but did not prevent, cold-induced increases in total protein, in mitochondrial GDP binding, and in mitochondrial UCP concentration, which all reached 50% or more of the elevated level in intact tissue. In contrast, TD activity did not exceed 10% of the elevated level in intact tissue at any time. Denervation after cold acclimation resulted in a very rapid loss of TD activity, a slower and selective loss (after a lag of 1 day) of UCP, and a much slower loss of tissue protein. We conclude that the sympathetic innervation is required for an optimal trophic response of BAT to cold acclimation and for maintenance in the hypertrophied state but that other factors are also involved. Induction and maintenance of TD in BAT does need the sympathetic innervation.

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Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00363.2003 ◽

2003 ◽

Vol 95 (4) ◽

pp. 1584-1590 ◽

Cited By ~ 18

Author(s):

Angel A. Zaninovich ◽

Inés Rebagliati ◽

Marcela Raíces ◽

Conrado Ricci ◽

Karl Hagmüller

Keyword(s):

Adipose Tissue ◽

Oxygen Consumption ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Cold Exposure ◽

Mitochondrial Respiration ◽

Mitochondrial Oxygen Consumption ◽

Normal Body ◽

Thyroid Ablation ◽

Brown Adipose

The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4°C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24°C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of β- and α1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3′-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.

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Cold acclimation increases the contribution of brown adipose tissue‐derived thermogenesis in adult humans

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.1204.1 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Denis P. Blondin ◽

Sébastien M. Labbé ◽

Éric E. Turcotte ◽

Denis Richard ◽

André C. Carpentier ◽

...

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Brown Adipose ◽

Adult Humans

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