scholarly journals Direct assessment of brown adipose tissue as a site of systemic tri-iodothyronine production in the rat

1987 ◽  
Vol 243 (1) ◽  
pp. 281-284 ◽  
Author(s):  
J A Fernandez ◽  
T Mampel ◽  
F Villarroya ◽  
R Iglesias

Tri-iodothyronine (T3)production by interscapular brown fat was studied by measurements of arterio-venous differences and blood flow across the tissue in rats exposed to the following situations: controls, acute cold, chronic cold and starvation. Results demonstrate that brown adipose tissue is a source of systemic T3 in the rat and that the T3 release is modulated according to the physiological situation of the animal: increased in cold exposure and inhibited in starvation.

1988 ◽  
Vol 8 (5) ◽  
pp. 465-469 ◽  
Author(s):  
Gérard Mory ◽  
Myriam Gawer ◽  
Jean-Claude Kader

Chronic cold exposure of rats (9 days at 5°C) induces an alteration of the fatty acid composition of phospholipids in brown adipose tissue. The alteration is due to an increase of the unsaturation degree of these lipids. The phenomenon can be reproduced by 10−7 mole. h−1 administration of noradrenaline for 9 days in rats kept at 25°C. Thus, phospholipid alteration in brown fat of cold exposed rats is most probably a consequence of the increase of sympathetic tone which occurs in this tissue during exposure to cold.


1984 ◽  
Vol 4 (11) ◽  
pp. 933-940 ◽  
Author(s):  
Stewart W. Mercer ◽  
Paul Trayhurn

Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, oh/oh mice show a substantial increase in GDP binding to brownadipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.


1959 ◽  
Vol 110 (3) ◽  
pp. 369-388 ◽  
Author(s):  
S. Edward Sulkin ◽  
Philip H. Krutzsch ◽  
Rae Allen ◽  
Craig Wallis

Studies on the pathogenesis of rabies in two species of experimentally infected insectivorous Chiroptera, the Mexican free-tailed bat (Tadarida mexicana), a quasi hibernator, and the little brown bat (Myotis lucifugus), a deep hibernator, provided evidence that brown adipose tissue may serve as an extraneural site for storage and multiplication of rabies virus. Although the Mexican free-tailed bat proved to be relatively insusceptible to experimental rabies infection, virus was demonstrated in the brown fat of 22 per cent of those animals shown to be infected by viral assay in white Swiss mice. Rabies infection in this species was most evident 20 to 40 days after intramuscular inoculation of virus. Rabies virus was found to be widely distributed in the little brown myotis 9 to 26 days following inoculation and virus concentrations in some of the tissues approached the level of the stock mouse brain virus suspension used in inoculating these bats. The shorter incubation period and higher virus titers in the tissues assayed reflect the increased susceptibility of Myotis lucifugus as compared with the Mexican free-tailed bat. Virus was demonstrated in the brown fat of 30 per cent of the experimentally infected Myotis. In the experimentally infected Myotis lucifugus and in the Syrian hamster which is highly susceptible to rabies infection, rabies virus was isolated more frequently from the brown fat than from the salivary gland indicating that in a susceptible host brown adipose tissue may be as frequent a site of viral proliferation as salivary gland. Since rabies virus was found to persist for long periods of time in the brown fat of experimentally infected bats and was occasionally demonstrated in this tissue alone, it is suggested that brown adipose tissue provides a mechanism by which these animals may serve as reservoirs for this agent in nature. The possibility that similar mechanisms may be involved in the maintenance of other viral agents during interepidemic periods is discussed.


1979 ◽  
Vol 57 (3) ◽  
pp. 257-270 ◽  
Author(s):  
David O. Foster ◽  
M. Lorraine Frydman

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.


1985 ◽  
Vol 63 (6) ◽  
pp. 595-598 ◽  
Author(s):  
W. H. Harris ◽  
D. O. Foster ◽  
B. E. Nadeau

This study was undertaken to determine if brown adipose tissue was involved in heat production during fever produced by S. abortus equi (1 μg) in unanesthetized rabbits aged 19–26 days. The fever (0.9–1.6 °C) occurred after a delay of 20–30 min and was frequently biphasic. Radiolabelled microspheres for measuring tissue blood flow were injected intraventricularly into three groups of animals: rabbits not given pyrogen, rabbits in which the febrile response to pyrogen was developing, and rabbits in which the febrile response had peaked. Blood flow to brown fat deposits and other organs was calculated from the fractional distribution of the microspheres and the recovery of microspheres in a reference arterial blood sample. At the fever peak, blood flow to brown fat was not significantly different (p > 0.05) from the control value (0.9 ± 0.2), but during the rising phase of the fever the flow increased significantly (p < 0.01) to 2.6 ± 0.4 mL min−1 g−1. The blood flow to muscles of the forelimbs and hind limbs was also increased significantly (p < 0.05) during the rising phase of the fever. No significant change in blood flow to other organs or tissues was found during the rising phase of the fever. These results indicate that both nonshivering as well as shivering thermogenesis contribute to heat production during development of fever in the young rabbit. However, nonshivering thermogenesis was not involved in the maintenance of the elevated body temperature after the fever had peaked.


1982 ◽  
Vol 60 (2) ◽  
pp. 107-113 ◽  
Author(s):  
David O. Foster ◽  
Florent Depocas ◽  
Gloria Zaror Behrens

The effects of sham, unilateral, and bilateral surgical denervation of rat interscapular brown adipose tissue (IBAT) on blood flow to the two IBAT pads of cold-acclimated (CA) rats during exposure of the animals to 22 or −6 °C and on the noradrenaline (NA) content and total dopamine-β-hydroxylase (DBH) (EC 1.14.17.1) activity of the pads in both warm-acclimated (WA) rats and CA rats were examined. Increase in IBAT blood flow upon cold exposure was taken as an index of sympathetically mediated calorigenesis in the tissue, and decreases in tissue levels of NA and DBH served as indices of the extent of destruction of the sympathetic innervation. At 24 h postsurgery, denervated pads of CA rats, whether from unilaterally or bilaterally denervated IBAT, had less than 3% of the NA, 40-44% of the DBH, and 0% of the 10-fold, cold-induced increase in blood flow measured in intact pads of CA rats with sham-operated or unilaterally denervated IBAT. IBAT bilaterally denervated for 24 h was as responsive in terms of its maximum increase in blood flow during infusion of CA rats with NA as intact IBAT. DBH in denervated pads of both WA rats and CA rats fell to 5% or less of control levels at 2 days postdenervation and remained at these low levels, as did NA, for at least 8 weeks. These results strongly support the longstanding but recently challenged hypothesis that each pad of rat IBAT is independently innervated by sympathetic fibers.


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Author(s):  
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