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

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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Effects of thyroid hormones on mitochondrial oxygen consumption in brown adipose tissue and heart from cold-exposed hypothyroid rats

Acta Endocrinologica ◽

10.1530/acta.0.1270072 ◽

1992 ◽

Vol 127 (1) ◽

pp. 72-75 ◽

Cited By ~ 8

Author(s):

LF Cageao ◽

IR Mignone ◽

CR Ricci ◽

CC Brignone ◽

JA Brignone ◽

...

Keyword(s):

Adipose Tissue ◽

Oxygen Consumption ◽

Brown Adipose Tissue ◽

Cold Exposure ◽

Room Temperature ◽

Treated Group ◽

Maximal Response ◽

Mitochondrial Oxygen Consumption ◽

Iopanoic Acid ◽

Brown Adipose

The present work measured brown adipose tissue and heart mitochondrial oxygen consumption in hypothyroid rats treated with replacement doses of T3, T4 or T4 plus iopanoic acid and kept at 4°C for 24 h. Heart oxygen consumption in normal, untreated hypothyroid and T4-treated hypothyroid rats was unaffected by cold exposure. In rats treated with T4 plus iopanoic acid, rates of oxygen consumption were normal in those maintained at 4°C as well as in those kept at room temperature, despite serum T3 concentration being significantly decreased. The cold-exposed T3-treated hypothyroid rats showed a marked decrease in oxygen consumption (p<0.02) and α-glycerophosphate dehydrogenase activity, a T3-dependent enzyme. Mitochondrial oxygen consumption in brown fat from normal (p<0.01), T4-(p<0.02) and T4 plus iopanoic acid-treated (p<0.01) rats rose more than twofold in response to cold. In the T3-treated group, oxygen consumption at room temperature was higher (p<0.02) than in any other group at similar temperatures. However, the T3-treated group showed no changes in oxygen consumption in response to cold, perhaps because this group reached the maximal response at room temperature. The untreated and the T3-treated hypothyroid rats (both groups devoid of T4) did not survive at 4°C unless T4 or several-fold replacement amounts of T3 were administered. The data demonstrate the crucial role of T4 in thermogenesis during cold exposure.

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Alterations of Insulin Content and Insulin Binding to Plasma Membranes in Rat Brown Adipose Tissue during Cold Exposure and Cold Acclimation.

The Japanese Journal of Physiology ◽

10.2170/jjphysiol.43.51 ◽

1993 ◽

Vol 43 (1) ◽

pp. 51-65 ◽

Cited By ~ 5

Author(s):

Shigeyuki OKANO ◽

Kazue KIKUCHI ◽

Akihiro KUROSHIMA

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Cold Exposure ◽

Plasma Membranes ◽

Insulin Binding ◽

Insulin Content ◽

Brown Adipose

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Type 2 iodothyronine deiodinase is upregulated in rat slow- and fast-twitch skeletal muscle during cold exposure

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00637.2013 ◽

2014 ◽

Vol 307 (11) ◽

pp. E1020-E1029 ◽

Cited By ~ 15

Author(s):

Ruy A. Louzada ◽

Maria C. S. Santos ◽

João Paulo A. Cavalcanti-de-Albuquerque ◽

Igor F. Rangel ◽

Andrea C. F. Ferreira ◽

...

Keyword(s):

Skeletal Muscle ◽

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Soleus Muscle ◽

Cold Exposure ◽

Skeletal Muscles ◽

Nonshivering Thermogenesis ◽

Brown Adipose

During cold acclimation, shivering is progressively replaced by nonshivering thermogenesis. Brown adipose tissue (BAT) and skeletal muscle are relevant for nonshivering thermogenesis, which depends largely on thyroid hormone. Since the skeletal muscle fibers progressively adapt to cold exposure through poorly defined mechanisms, our intent was to determine whether skeletal muscle type 2 deiodinase (D2) induction could be implicated in the long-term skeletal muscle cold acclimation. We demonstrate that in the red oxidative soleus muscle, D2 activity increased 2.3-fold after 3 days at 4°C together with the brown adipose tissue D2 activity, which increased 10-fold. Soleus muscle and BAT D2 activities returned to the control levels after 10 days of cold exposure, when an increase of 2.8-fold in D2 activity was detected in white glycolytic gastrocnemius but not in red oxidative gastrocnemius fibers. Propranolol did not prevent muscle D2 induction, but it impaired the decrease of D2 in BAT and soleus after 10 days at 4°C. Cold exposure is accompanied by increased oxygen consumption, UCP3, and PGC-1α genes expression in skeletal muscles, which were partialy prevented by propranolol in soleus and gastrocnemius. Serum total and free T3 is increased during cold exposure in rats, even after 10 days, when BAT D2 is already normalized, suggesting that skeletal muscle D2 activity contributes significantly to circulating T3 under this adaptive condition. In conclusion, cold exposure is accompanied by concerted changes in the metabolism of BAT and oxidative and glycolytic skeletal muscles that are paralleled by type 2 deiodinase activation.

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Glycerokinase activity in brown adipose tissue: a sympathetic regulation?

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00419.2001 ◽

2002 ◽

Vol 282 (4) ◽

pp. R1185-R1190 ◽

Cited By ~ 21

Author(s):

N. H. Kawashita ◽

W. T. L. Festuccia ◽

M. N. Brito ◽

M. A. F. Moura ◽

S. R. C. Brito ◽

...

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Cold Exposure ◽

Turnover Rates ◽

Physiological Conditions ◽

Balanced Diet ◽

Norepinephrine Turnover ◽

Brown Adipose ◽

Sympathetic Regulation

The effect of brown adipose tissue (BAT) sympathetic hemidenervation on the activity of glycerokinase (GyK) was investigated in different physiological conditions. In rats fed a balanced diet, the activity of the enzyme was ∼50% lower in BAT-denervated pads than in intact, innervated pads. In rats adapted to a high-protein, carbohydrate-free diet, norepinephrine turnover rates and BAT GyK activity were already reduced, and BAT denervation resulted in a further decrease in the activity of the enzyme. Cold acclimation of normally fed rats at 4°C for 10 days markedly increased the activity of the enzyme. Cold exposure (4°C) for 6 h was insufficient to stimulate BAT GyK, but the activity of the enzyme was already increased after 12 h of cold exposure. The cold-induced BAT GyK stimulation was completely blocked in BAT-denervated pads. The data indicate that an adequate sympathetic flow to BAT is required for the maintenance of normal levels of GyK activity and for the enzyme response to situations, such as cold exposure, which markedly increase BAT sympathetic flow.

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Amino acid and glucose uptake by rat brown adipose tissue. Effect of cold-exposure and acclimation

Biochemical Journal ◽

10.1042/bj2520843 ◽

1988 ◽

Vol 252 (3) ◽

pp. 843-849 ◽

Cited By ~ 32

Author(s):

F J López-Soriano ◽

J A Fernández-López ◽

T Mampel ◽

F Villarroya ◽

R Iglesias ◽

...

Keyword(s):

Amino Acids ◽

Adipose Tissue ◽

Amino Acid ◽

Brown Adipose Tissue ◽

Glucose Uptake ◽

Cold Acclimation ◽

Cold Exposure ◽

Acid Oxidation ◽

Interscapular Brown Adipose Tissue ◽

Brown Adipose

The net uptake/release of glucose, lactate and amino acids from the bloodstream by the interscapular brown adipose tissue of control, cold-exposed and cold-acclimated rats was estimated by measurement of arteriovenous differences in their concentrations. In the control animals amino acids contributed little to the overall energetic needs of the tissue; glucose uptake was more than compensated by lactate efflux. Cold-exposure resulted in an enhancement of amino acid utilization and of glucose uptake, with high lactate efflux. There was a net glycine and proline efflux that partly compensated the positive nitrogen balance of the tissue; amino acids accounted for about one-third of the energy supplied by glucose to the tissue. Cold-acclimation resulted in a very high increase in glucose uptake, with a parallel decrease in lactate efflux and amino acid consumption. Branched-chain amino acids, however, were more actively utilized. This was related with a much higher alanine efflux, in addition to that of glycine and proline. It is suggested that most of the glucose used during cold-exposure is returned to the bloodstream as lactate under conditions of active lipid utilization, amino acids contributing their skeletons largely in anaplerotic pathways. On the other hand, cold-acclimation resulted in an important enhancement of glucose utilization, with lowered amino acid oxidation. Amino acids are thus used as metabolic substrates by the brown adipose tissue of rats under conditions of relatively scarce substrate availability, but mainly as anaplerotic substrates, in parallel to glucose. Cold-acclimation results in a shift of the main substrates used in thermogenesis from lipid to glucose, with a much lower need for amino acids.

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Brown adipose tissue hyperplasia: a fundamental mechanism of adaptation to cold and hyperphagia

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1982.242.6.e353 ◽

1982 ◽

Vol 242 (6) ◽

pp. E353-E359 ◽

Cited By ~ 17

Author(s):

L. Bukowiecki ◽

A. J. Collet ◽

N. Follea ◽

G. Guay ◽

L. Jahjah

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Acclimation ◽

Cold Exposure ◽

Interstitial Cells ◽

Brown Adipocyte ◽

Brown Adipocytes ◽

Interscapular Brown Adipose Tissue ◽

Blood Capillaries ◽

Brown Adipose

Cold acclimation (4 degrees C) and "cafeteria diets" increased the thermic response of rats to catecholamines. This phenomenon was accompanied by six- to eightfold increases of interscapular brown adipose tissue (IBAT) weight, total tissue cytochrome oxidase activity, and total number of brown adipocytes. Quantitative radioautographic experiments using [3H]thymidine disclosed that cold exposure markedly enhanced the mitotic activity in blood capillaries and small-venule endothelial cells, adipose tissue interstitial cells, and preadipocytes rather than in fully differentiated brown adipocytes. IBAT mitotic index increased 70 times over control values after only 2 days of cold exposure. Thereafter, the proliferative activity progressively decreased. IBAT cell composition was modified during cold acclimation as the percentage of interstitial cells and preadipocytes increased over the other cellular types. Because brown adipose tissue is the principal site of norepinephrine-induced thermogenesis in homeothermal animals, it is suggested that brown adipocyte proliferation from precursor cells represents the fundamental phenomenon explaining the increased capacity of cold-acclimated animals to respond calorigenically to catecholamines.

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