Nonshivering thermogenesis in the rat. II. Measurements of blood flow with microspheres point to brown adipose tissue as the dominant site of the calorigenesis induced by noradrenaline

1978 ◽  
Vol 56 (1) ◽  
pp. 110-122 ◽  
Author(s):  
David O. Foster ◽  
M. Lorraine Frydman
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Anatomical Site ◽  
Nonshivering Thermogenesis ◽  
White Rats ◽  
Brown Adipose ◽  
Respiratory Movements ◽  
Fractional Distribution

Cardiac output (CO) and the fractional distribution (FD) of γ-labeled plastic microspheres (15 ± 5 μm) injected into the left ventricle were used to calculate blood flow to organs and tissues of barbital-sedated warm-acclimated (WA) or cold-acclimated (CA) white rats at rest and then during their maximal calorigenic response to infused noradrenaline (NA). Flow to the major masses of brown adipose tissue (BAT) increased in WA rats from a mean of 0.81 ml/min (0.92% of CO) at rest to 13.5 ml/min (11.4% of CO) during calorigenesis; it increased in CA rats from 2.3 ml/min (2.6% of CO) to 57.2 ml/min (33.5% of CO). Flow to skeletal muscle increased in WA rats from 12.0 ml/min at rest to 15.1 ml/min during calorigenesis; it increased in CA rats from 9.9 ml/min to 14.5 ml/min. Flow to heart and to muscles involved in respiratory movements was two to five times greater during calorigenesis. Flow to most other tissues and organs increased or decreased by less than 40%.Arteriovenous differences in blood oxygen [Formula: see text] across interscapular BAT (IBAT) during rest and during calorigenesis together with measurements of blood flow established that IBAT alone accounted for 14% of the extra O2 used by CA rats during NA-induced calorigenesis. If during calorigenesis other masses of BAT have an [Formula: see text] as great as that for IBAT, the major masses of BAT together would account for 60% of the calorigenic response of the CA rat. In contrast, even if the skeletal muscle of the CA rat used all the O2 in the blood flowing through it during calorigenesis, it could not have been responsible for more than 12% of the calorigenic response.The rat, long considered to exemplify major participation of skeletal muscle in nonshivering thermogenesis (NST), now becomes just one of a growing list of species for which there is explicit or circumstantial evidence that NST occurs principally in BAT. It thus becomes reasonable to propose as a general principle that BAT is the primary anatomical site of the NST that is characteristic of many small mammals: CA adults, newborns, and hibernators alike.

Tissue distribution of cold-induced thermogenesis in conscious warm- or cold-acclimated rats reevaluated from changes in tissue blood flow: The dominant role of brown adipose tissue in the replacement of shivering by nonshivering thermogenesis

1979 ◽  
Vol 57 (3) ◽  
pp. 257-270 ◽  
Author(s):  
David O. Foster ◽  
M. Lorraine Frydman
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Tissue Distribution ◽  
Cold Exposure ◽  
Tissue Blood Flow ◽  
Anatomical Site ◽  
Nonshivering Thermogenesis ◽  
White Rats ◽  
Brown Adipose

Radioactive microspheres (12–16 μm) were used to measure cardiac output (CO), its fractional distribution, and hence tissue blood flow in conscious, warm-acclimated (WA) or cold-acclimated (CA) white rats exposed to temperatures of 25, 21, 6, −6, and −19 °C, the objective being to assess the tissue distribution of cold-induced thermogenesis. Total oxygen consumption was also measured. CA rats at 25 °C (CA25) had elevated arteriovenous shunting and other signs of heat stress. CA21 proved more suitable controls for the CA group. The cold-induced changes in blood flow to total skeletal muscle not involved in respiratory movements (M) and to the major masses of brown adipose tissue (BAT) were quantitatively very different in the two acclimation groups: in WA25 and CA21 flows to M were 31 (0.24 CO) and 27 (0.17 CO) mL/min, respectively, while flows to BAT were 2.1 and 9.7 mL/min; in WA−19 and CA−19 flows to M were 62 (0.32 CO) and 35 (0.16 CO) mL/min, respectively, while flows to BAT were 25 and 56 mL/min. In contrast, the effects of cold exposure on flows to other tissues and organs were remarkably alike in the two acclimation groups: e.g., flows to heart, ribcage, and diaphragm increased about three times between 25 and −19 °C, flow to the skin fell about 50%, and flows to the hepatosplanchnic region and kidneys were little or not at all affected by cold exposure. Estimates of the contributions of different tissues and organs to cold-induced thermogenesis were made on the basis of the relative changes in blood flow. It is concluded that BAT is by far the dominant anatomical site of the increased heat production of cold-exposed CA rats, and that nonshivering thermogenesis in BAT supplements considerably the shivering thermogenesis of cold-exposed WA rats.

Comparison of microspheres and 86Rb+ as tracers of the distribution of cardiac output in rats indicates invalidity of 86Rb+-based measurements

1978 ◽  
Vol 56 (1) ◽  
pp. 97-109 ◽  
Author(s):  
David O. Foster ◽  
M. Lorraine Frydman
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Valid Measure ◽  
White Rats ◽  
Direct Measurements ◽  
Brown Adipose ◽  
Valid Data ◽  
Distribution Of Cardiac Output ◽  
Fractional Distribution

The technique of using γ-labeled plastic microspheres (15 ± 5 μm) to measure cardiac output (CO) and its fractional distribution (FD) to individual tissues and organs was judged by various criteria to give valid data when applied to barbital-sedated warm-acclimated or cold-acclimated (CA) white rats, which were either resting or responding calorigenically to infused noradrenaline (NA). The FD of CO to each of 16 tissues or organs of CA rats at rest or responding to NA was then estimated both with 86Rb+ and with microspheres, the two tracers being injected simultaneously. For only seven of the tissues examined in resting rats and only one in NA-infused rats was the FD of CO estimated with 86Rb+ not significantly different from that estimated with microspheres. 86Rb+ to microsphere ratios of the FD of CO to individual tissues ranged from 3.5 and 3.0 for liver and skeletal muscle, respectively, down to 0.09 and 0.07 for brown adipose tissue (BAT) and brain. Since microsphere-based estimates of blood flow to the interscapular BAT of CA rats responding to NA were corroborated by direct measurements of venous efflux from the tissue, it is unequivocal that the 86Rb+-based estimate of the fraction of CO directed to interscapular BAT was highly erroneous. When considered along with data from the literature, the present findings support a conclusion that the uptake of 86Rb+ by a tissue frequently does not provide a valid measure of the FD of CO to the tissue. Some of the factors that are likely responsible for this situation are discussed, and it is suggested that only by a fortuitous combination of circumstances does the uptake of 86Rb+ by a tissue sometimes match the FD of CO to the tissue.

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.

Decreased Half-Life of Some Mitochondrial Proteins in Skeletal Muscle and Brown Adipose Tissue of Cold-Acclimated Rats

1971 ◽  
Vol 49 (12) ◽  
pp. 1015-1018 ◽  
Author(s):  
L. Bukowiecki ◽  
Jean Himms-Hagen
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Half Life ◽  
Mitochondrial Proteins ◽  
Nonshivering Thermogenesis ◽  
Brown Adipose

Evidence is presented for a decreased half-life of certain mitochondrial proteins in skeletal muscle and brown adipose tissue of cold-acclimated rats living in the cold; nonshivering thermo-genesis is known to occur in both these tissues. No such decrease occurs in liver or kidney, tissues in which nonshivering thermogenesis does not occur. It is concluded that acclimation to cold causes a change in the rate of synthesis and/or in the amount of certain mitochondrial proteins and that this change may be associated with the development of the capacity for nonshivering thermogenesis.

Corticosterone decreases nonshivering thermogenesis and increases lipid storage in brown adipose tissue

1995 ◽  
Vol 268 (1) ◽  
pp. R183-R191 ◽  
Author(s):  
A. M. Strack ◽  
M. J. Bradbury ◽  
M. F. Dallman
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucocorticoid Receptors ◽  
Uncoupling Protein ◽  
Lipid Storage ◽  
Scatchard Analysis ◽  
Nonshivering Thermogenesis ◽  
Diurnal Range ◽  
Brown Adipose ◽  
Intact Rats

Brown adipose tissue (BAT) contains glucocorticoid receptors; glucocorticoids are required for maintaining differentiated BAT in culture. These studies were performed to determine the effects of corticosterone on BAT thermogenic function and lipid storage. Rats were adrenalectomized and given subcutaneous corticosterone pellets in concentrations that maintained plasma corticosterone constant across the range of 0-20 micrograms/dl or were sham adrenalectomized. All variables were examined 5 days after surgery and corticosterone replacement. Measures of BAT function-thermogenic capacity [guanosine 5'-diphosphate (GDP) binding and uncoupling protein (UCP; a BAT-specific thermogenic protein)] and storage (BAT wet wt, protein, and DNA levels) were made. Plasma hormones (corticosterone, adrenocorticotropic hormone, insulin, 3,3',5-triiodothyronine, and thyroxine were measured. Corticosterone significantly affected BAT thermogenic measures: UCP content and binding of GDP to BAT mitochondria decreased with increasing corticosterone; GDP binding characteristics in BAT from similarly prepared rats examined by Scatchard analysis showed that maximum binding (Bmax) and dissociation constant (Kd) decreased with increasing corticosterone dose. BAT DNA was increased by adrenalectomy and maintained at intact levels with all doses of corticosterone; BAT lipid storage increased dramatically at corticosterone values higher than the daily mean level in intact rats. Histologically, the number and size of lipid droplets within BAT adipocytes increased markedly with increased corticosterone. White adipose depots were more sensitive to circulating corticosterone concentrations than were BAT depots and increased in weight at levels of corticosterone that were at or below the daily mean level of intact rats. We conclude that, within its diurnal range of concentration corticosterone acts to inhibit nonshivering thermogenesis and increase lipid storage.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition by Oxytetracycline of the Development of the Enhanced Response to Noradrenaline in Cold-Acclimated Rats: A New Approach to the Study of Nonshivering Thermogenesis

1971 ◽  
Vol 49 (6) ◽  
pp. 545-553 ◽  
Author(s):  
Jean Himms–Hagen
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Metabolic Response ◽  
Inner Membrane ◽  
Cytochrome Oxidase Activity ◽  
Mitochondrial Inner Membrane ◽  
Brown Adipose

The aim of these experiments was to depress the increased metabolic activity of the brown adipose tissue in the intact rat during acclimation to cold in order to elucidate further the possible thermogenic and endocrine functions of this tissue. The antibiotic oxytetracycline was administered twice daily for 2 weeks to rats living at 4 °C in an attempt to inhibit the proliferation of mitochondria and of mitochondrial inner membrane known to occur in the brown adipose tissue in response to cold; control rats received saline during the same period. Total cytochrome oxidase activity served as an index of the amount of mitochondrial inner membrane in brown adipose tissue, liver, and skeletal muscle. The development of an enhanced calorigenic response to intravenously infused noradrenaline served as an index of the extent of acclimation to cold.Treatment with oxytetracycline inhibited both the cold-induced increase in cytochrome oxidase activity in brown adipose tissue and the cold-induced development of an enhanced calorigenic response to noradrenaline in the intact rats; a direct correlation was noted between the amount of cytochrome oxidase in brown adipose tissue and the size of the metabolic response to noradrenaline of the intact animals. However, the amount of oxygen that could be consumed by the total cytochrome oxidase in the brown adipose tissue was itself too small to account for the increase in oxygen consumption by the rat. Treatment of the rats with oxytetracycline did not alter the cold-induced growth of brown adipose tissue (as judged by the increase in wet weight and the increase in total protein); it also did not alter the cytochrome oxidase activities of liver or skeletal muscle. The effect of oxytetracycline seems, therefore, to be fairly specific for the mitochondria of the most rapidly dividing tissue, the brown adipose tissue. The conclusion is drawn that a protein synthesized in the mitochondria of the brown adipose tissue in response to cold is essential for adaptation to cold.

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