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

2014 ◽  
Vol 307 (11) ◽  
pp. E1020-E1029 ◽  
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.

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

2003 ◽  
Vol 95 (4) ◽  
pp. 1584-1590 ◽  
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.

Cold exposure potentiates the effect of insulin on in vivo glucose uptake

1987 ◽  
Vol 253 (2) ◽  
pp. E179-E186 ◽  
Author(s):  
A. L. Vallerand ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
White Adipose Tissue ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Insulin Injection ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Insulin Responses

The effects of cold exposure (48 h at 4 degrees C) and insulin injection (0.5 U/kg iv) on the rates of net 2-[3H]deoxyglucose uptake (Ki) in peripheral tissues were investigated in warm-acclimated rats (25 degrees C). Cold exposure and insulin treatment independently increased Ki values in skeletal muscles (soleus, extensor digitorum longus, and vastus lateralis), heart, white adipose tissue (subcutaneous, gonadal, and retroperitoneal), and brown adipose tissue (P less than 0.01). The effects of cold exposure were particularly evident in brown adipose tissue where the Ki increased greater than 100 times. When the two treatments were combined (insulin injection in cold-exposed rats), it was found that cold exposure synergistically enhanced the maximal insulin responses for glucose uptake in brown adipose tissue, all white adipose tissue depots, and skeletal muscles investigated. The results indicate that cold exposure induces an "insulin-like" effect on Ki that does not appear to be specifically associated with shivering thermogenesis in skeletal muscles, because that effect was observed in all insulin-sensitive tissues. The data also demonstrate that cold exposure significantly potentiates the maximal insulin responses for glucose uptake in the same tissues. This potentialization may result from an enhanced responsiveness of peripheral tissues to insulin, possibly occurring at metabolic steps lying beyond the insulin receptor and an increased tissue blood flow augmenting glucose and insulin availability and thereby amplifying glucose uptake.

scholarly journals Quantification in vivo of the effects of insulin on glucose utilization in individual tissues of warm- and cold-acclimated rats

1986 ◽  
Vol 237 (3) ◽  
pp. 789-795 ◽  
Author(s):  
S A Smith ◽  
P Young ◽  
M A Cawthorne
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Glucose Utilization ◽  
Insulin Treatment ◽  
Glucose Production ◽  
Whole Body ◽  
Metabolic Index ◽  
Brown Adipose

Cold-acclimation of rats (3 weeks, 4 degrees C) had no effect on basal rates of glucose production or utilization. Under euglycaemic-clamp conditions, in which the circulating insulin concentration was increased by approx. 50 microunits/ml, cold-acclimated rats showed a greater increase in glucose utilization and a greater suppression of endogenous glucose production. Tissue sites of glucose utilization were investigated by using a tracer dose of 2-deoxy-D-[14C]glucose and a glucose metabolic index determined for each tissue. In 5 h-starved warm-acclimated rats, heart had the highest glucose metabolic index. This was increased further by both cold-acclimation and insulin treatment. The glucose metabolic index of skeletal muscle was 3.5-14-fold lower than that of heart, but, as a result of the large muscle mass, skeletal muscle made the largest contribution to whole-body glucose utilization. White and brown adipose tissue had low glucose metabolic indices in warm-acclimated rats under basal conditions, and the indices were not increased by the insulin treatment. However, cold-acclimation produced a significant increase in the glucose metabolic index of brown adipose tissue, but not of white adipose tissue. In contrast with the warm-acclimated rats, insulin treatment of cold-acclimated rats resulted in a marked increase in the glucose metabolic index of brown adipose tissue. The results provide evidence that cold-acclimation produces a selective alteration in the insulin-sensitivity of brown adipose tissue.

scholarly journals Deiodinase Activities in Thyroids and Tissues of Iodine-Deficient Female Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 529-536 ◽  
Author(s):  
Rosalia Lavado-Autric ◽  
Rosa Maria Calvo ◽  
Raquel Martinez de Mena ◽  
Gabriella Morreale de Escobar ◽  
Maria-Jesus Obregon
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Cerebral Cortex ◽  
Brown Adipose Tissue ◽  
Female Rats ◽  
Iodothyronine Deiodinase ◽  
Brown Adipose ◽  
Type 3

Severe iodine deficiency is characterized by goiter, preferential synthesis, and secretion of T3 in thyroids, hypothyroxinemia in plasma and tissues, normal or low plasma T3, and slightly increased plasma TSH. We studied changes in deiodinase activities and mRNA in several tissues of rats maintained on low-iodine diets (LIDs) or LIDs supplemented with iodine (LID+I). T4 and T3 concentrations decreased in plasma, tissues, and thyroids of LID rats, and T4 decreased more than T3 (50%). The highest type 1 iodothyronine deiodinase (D1) activities were found in the thyroid, kidney, and the liver; pituitary, lung, and ovary had lower D1 activities; but the lowest levels were found in the heart and skeletal muscle. D1 activity decreased in all tissues of LID rats (10–40% of LID+I rats), except for ovary and thyroids, which D1 activity increased 2.5-fold. Maximal type 2 iodothyronine deiodinase (D2) activities were found in thyroid, brown adipose tissue, and pituitary, increasing 6.5-fold in thyroids of LID rats and about 20-fold in the whole gland. D2 always increased in response to LID, and maximal increases were found in the cerebral cortex (19-fold), thyroid, brown adipose tissue, and pituitary (6-fold). Lower D2 activities were found in the ovary, heart, and adrenal gland, which increased in LID. Type 3 iodothyronine deiodinase activity was undetectable. Thyroidal Dio1 and Dio2 mRNA increased in the LID rats, and Dio1 decreased in the lung, with no changes in mRNA expression in other tissues. Our data indicate that LID induces changes in deiodinase activities, especially in the thyroid, to counteract the low T4 synthesis and secretion, contributing to maintain the local T3 concentrations in the tissues with D2 activity.

Glycerokinase activity in brown adipose tissue: a sympathetic regulation?

2002 ◽  
Vol 282 (4) ◽  
pp. R1185-R1190 ◽  
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.

scholarly journals Cold and Exercise: Therapeutic Tools to Activate Brown Adipose Tissue and Combat Obesity

Biology ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 9 ◽  
Author(s):  
Carmem Peres Valgas da Silva ◽  
Diego Hernández-Saavedra ◽  
Joseph White ◽  
Kristin Stanford
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Lipid Uptake ◽  
Mitochondrial Uncoupling ◽  
Bat Activity ◽  
Brown Adipose

The rise in obesity over the last several decades has reached pandemic proportions. Brown adipose tissue (BAT) is a thermogenic organ that is involved in energy expenditure and represents an attractive target to combat both obesity and type 2 diabetes. Cold exposure and exercise training are two stimuli that have been investigated with respect to BAT activation, metabolism, and the contribution of BAT to metabolic health. These two stimuli are of great interest because they have both disparate and converging effects on BAT activation and metabolism. Cold exposure is an effective mechanism to stimulate BAT activity and increase glucose and lipid uptake through mitochondrial uncoupling, resulting in metabolic benefits including elevated energy expenditure and increased insulin sensitivity. Exercise is a therapeutic tool that has marked benefits on systemic metabolism and affects several tissues, including BAT. Compared to cold exposure, studies focused on BAT metabolism and exercise display conflicting results; the majority of studies in rodents and humans demonstrate a reduction in BAT activity and reduced glucose and lipid uptake and storage. In addition to investigations of energy uptake and utilization, recent studies have focused on the effects of cold exposure and exercise on the structural lipids in BAT and secreted factors released from BAT, termed batokines. Cold exposure and exercise induce opposite responses in terms of structural lipids, but an important overlap exists between the effects of cold and exercise on batokines. In this review, we will discuss the similarities and differences of cold exposure and exercise in relation to their effects on BAT activity and metabolism and its relevance for the prevention of obesity and the development of type 2 diabetes.

Stimulatory effects of cold exposure and cold acclimation on glucose uptake in rat peripheral tissues

1990 ◽  
Vol 259 (5) ◽  
pp. R1043-R1049 ◽  
Author(s):  
A. L. Vallerand ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Shivering Thermogenesis ◽  
Stimulation Of

The effects of cold exposure on the net rates of 2-[3H]deoxy-D-glucose uptake (Ki) in rat peripheral tissues were investigated comparatively in warm- and cold-acclimated animals to determine whether cold acclimation induces regulatory alterations in glucose metabolism. Acute exposure of warm-acclimated (25 degrees C) rats to cold (48 h at 5 degrees C) markedly increased the Ki values in red and white skeletal muscles (2-5 times), in the heart (8 times), in several white adipose tissue (WAT) depots (4-20 times), and in brown adipose tissue (BAT) (110 times). After cold acclimation (3 wk at 5 degrees C), the Ki values further increased in the heart (15 times) and WAT (up to 29 times) but decreased in BAT (36 times). Remarkably, glucose uptake was still increased in muscles of cold-exposed/cold-acclimated animals (that do not shiver), demonstrating that enhanced glucose uptake may occur in muscles in the absence of shivering thermogenesis (or contractile activity). When cold-acclimated rats were returned to the warm for 18 h, the Ki values of all tissues, except WAT, returned to control levels. Cold exposure synergistically potentiated the stimulation of tissue glucose uptake induced by a maximal effective dose of insulin (0.5 U/kg iv) in warm- as well as in cold-acclimated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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