scholarly journals The effects of corticosterone, cold exposure and overfeeding with sucrose on brown adipose tissue of obese Zucker rats (fa/fa)

1983 ◽  
Vol 214 (1) ◽  
pp. 215-223 ◽  
Author(s):  
S Holt ◽  
D A York ◽  
J T R Fitzsimons
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Zucker Rats ◽  
Brown Adipose ◽  
Obese Rats ◽  
Brown Adipose Tissue Thermogenesis ◽  
Obese Zucker Rats ◽  
Normal Increase

GDP binding to brown-adipose-tissue mitochondria was decreased in obese Zucker rats. Adrenalectomy restored both GDP binding and serum tri-iodothyronine of obese rats to values observed in lean rats. The effects of adrenalectomy on GDP binding and serum tri-iodothyronine were reversed by corticosterone. Decreasing food intake had no effect on brown-adipose-tissue GDP binding in obese rats. Young (5-week-old) obese rats showed a normal increase in brown-adipose-tissue mitochondrial GDP binding after housing at 4 degrees C for 7 days, but this response was attenuated in 10-week-old obese rats. Overfeeding with sucrose increased brown-adipose-tissue thermogenesis in lean, but not in obese, rats. After adrenalectomy, overfeeding with sucrose enhanced brown-adipose-tissue mitochondrial GDP binding in obese rats.

scholarly journals The effect of adrenalectomy on GDP binding to brown-adipose-tissue mitochondria of obese rats

1982 ◽  
Vol 208 (3) ◽  
pp. 819-822 ◽  
Author(s):  
Susan Holt ◽  
David A. York
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Binding Sites ◽  
Zucker Rats ◽  
Lean Control ◽  
Brown Adipose ◽  
Obese Rats ◽  
Number Of Binding Sites ◽  
Obese Zucker Rats

GDP binding to brown-adipose-tissue mitochondria of young obese Zucker rats (fa/fa) was significantly lower than in lean control rats, as a result of a decrease in the number of binding sites. Adrenalectomy of fa/fa rats restored GDP binding to control values. Corticosterone replacement suppressed GDP binding in adrenalectomized obese rats.

scholarly journals Effects of Exercise Training on Brown Adipose Tissue Thermogenesis in Ovariectomized Obese Rats.

1989 ◽  
Vol 36 (3) ◽  
pp. 403-408 ◽  
Author(s):  
KEIJI YOSHIOKA ◽  
TOSHIHIDE YOSHIDA ◽  
YASUO WAKABAYASHI ◽  
HITOSHI NISHIOKA ◽  
MOTOHARU KONDO
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Obese Rats ◽  
Brown Adipose Tissue Thermogenesis

Enhanced acute response to corticosterone in genetically obese (ob/ob) mice

1989 ◽  
Vol 257 (2) ◽  
pp. E133-E138 ◽  
Author(s):  
K. Tokuyama ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Single Injection ◽  
Neural Activation ◽  
Normal Body Temperature ◽  
Acute Response ◽  
Rapid Action ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

Our previous work showed that ob/ob mice responded to physiological concentrations of blood corticosterone (maintained by implanted pellets of corticosterone in adrenalectomized mice) by increasing food intake and blood insulin concentration to a much greater extent than did lean mice. The present study sought to determine whether the chronic presence of corticosterone was necessary or whether a single injection would also have these effects. Lean and ob/ob mice were adrenalectomized at 4.5 wk of age, injected with corticosterone at 10.5 wk of age, and killed 6 or 15 h after injection. A markedly exaggerated hyperinsulinemia was seen in ob/ob mice at 15 h. Food intake increased in both lean and obese mice, and brown adipose tissue thermogenesis (as reflected by mitochondrial guanosine 5'-diphosphate binding) was suppressed in both. We conclude that the ob/ob mouse has an excessive central sensitivity and responsiveness to a rapid action of corticosterone that results in neural activation of insulin secretion and suppression of brown adipose tissue thermogenesis. The persistence of some degree of obesity in the adrenalectomized ob/ob mouse is attributed to the remaining slight hyperinsulinemia coupled with reduced energy expenditure due to persistent thermoregulation at a lower than normal body temperature.

Restricted food intake limits brown adipose tissue hypertrophy in cold exposure

Life Sciences ◽  
1982 ◽  
Vol 30 (17) ◽  
pp. 1423-1426 ◽  
Author(s):  
T. Scott Johnson ◽  
Shawne Murray ◽  
James B. Young ◽  
Lewis Landsberg
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Adipose ◽  
Restricted Food Intake

Effect of adrenalectomy and glucocorticoid replacement on development of obesity

1986 ◽  
Vol 250 (4) ◽  
pp. R595-R607 ◽  
Author(s):  
M. R. Freedman ◽  
B. A. Horwitz ◽  
J. S. Stern
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Protein Content ◽  
Body Fat ◽  
Plasma Insulin ◽  
Tissue Protein ◽  
Steroid Dose ◽  
Brown Adipose ◽  
Obese Rats

Female obese and lean Zucker rats were adrenalectomized (ADX) or sham-operated at 4 wk of age. ADX animals were given daily injections of 0.01, 0.05, 0.50, 1.0, or 2.0 mg hydrocortisone/100 g body wt for 30 days. ADX rats gained less weight than sham-operated controls. Obese ADX rats at the lowest dose (0.01) had a net positive energy gain but lost body fat. As steroid dose increased, obese rats deposited more fat and less protein. Doses of 0.01 and 0.05 mg produced rats that were less fat than sham-operated controls, whereas doses of 0.50, 1.0, and 2.0 mg produced rats of comparable body fat composition. Obese rats were consistently fatter and had a significantly smaller percentage body protein than lean rats at each dose. Body fat elevation was reflected by heavier parametrial and retroperitoneal fat depots and larger fat cells at all doses except the lowest. Compared with sham-operated controls, lean and obese rats at the two lowest replacement doses (0.01, 0.05) exhibited significantly decreased plasma insulin and triglyceride levels and significantly elevated brown adipose tissue protein content and citrate synthase (CS) activity. Obese rats at these doses had significantly reduced adipose tissue lipoprotein lipase (LPL) activity in the retroperitoneal depot and lower food intake. Furthermore, these obese rats had adipose depot weights, cell sizes, LPL activity, and plasma insulin, glucose, and triglyceride comparable to that of lean sham-operated controls. As steroid dose increased (0.5, 1.0, 2.0), plasma insulin and triglyceride and food intake markedly increased only in obese rats. Adipose tissue LPL activity appeared unaffected by dose. Brown adipose tissue protein content and CS activity significantly decreased as dose increased in both lean and obese rats. At all doses of replacement obese rats were more responsive to steroid than were lean rats. Obese rats receiving 0.01 mg had comparable fat depot weights, cell sizes, and plasma insulin and triglyceride as lean rats receiving 50 times as much steroid per day (0.50 mg). These results suggest glucocorticoids play an important role in the early development of obesity in the Zucker rat and support the hypothesis that obese rats are more responsive to glucocorticoids than are lean rats.

Brown adipose tissue thermogenesis in testosterone-treated rats

1992 ◽  
Vol 126 (5) ◽  
pp. 434-437 ◽  
Author(s):  
María Abelenda ◽  
Maria Paz Nava ◽  
Alberto Fernández ◽  
María Luisa Puerta
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Sexual Hormones ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

The participation of sexual hormones in body weight regulation is partly accomplished by altering food intake. Nonetheless, female sexual hormones also alter brown adipose tissue thermogenesis in females. This study was aimed to find out if male hormones could alter brown adipose tissue thermogenesis in male rats. Testosterone was administered by means of Silastic capsules in adult male rats acclimated either at 28°C (thermoneutrality) or at 6°C (cold), treatment lasting 15 days. Food intake and body weight gain were reduced by hormonal treatment. However, brown adipose tissue mass, protein content, mitochondrial mass and GDP-binding were unchanged at both environmental temperatures. Accordingly, testosterone participation in body weight regulation is thought to be carried out without altering brown adipose tissue thermogenesis. A reduction in the weight of the sex accessory glands was also observed after cold acclimation.

scholarly journals Median preoptic area neurons are required for the cooling and febrile activations of brown adipose tissue thermogenesis in rat

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ellen Paula Santos da Conceição ◽  
Shaun F. Morrison ◽  
Georgina Cano ◽  
Pierfrancesco Chiavetta ◽  
Domenico Tupone
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Preoptic Area ◽  
Therapeutic Approaches ◽  
Dorsomedial Hypothalamus ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

Abstract Within the central neural circuitry for thermoregulation, the balance between excitatory and inhibitory inputs to the dorsomedial hypothalamus (DMH) determines the level of activation of brown adipose tissue (BAT) thermogenesis. We employed neuroanatomical and in vivo electrophysiological techniques to identify a source of excitation to thermogenesis-promoting neurons in the DMH that is required for cold defense and fever. Inhibition of median preoptic area (MnPO) neurons blocked the BAT thermogenic responses during both PGE2-induced fever and cold exposure. Disinhibition or direct activation of MnPO neurons induced a BAT thermogenic response in warm rats. Blockade of ionotropic glutamate receptors in the DMH, or brain transection rostral to DMH, blocked cold-evoked or NMDA in MnPO-evoked BAT thermogenesis. RNAscope technique identified a glutamatergic population of MnPO neurons that projects to the DMH and expresses c-Fos following cold exposure. These discoveries relative to the glutamatergic drive to BAT sympathoexcitatory neurons in DMH augment our understanding of the central thermoregulatory circuitry in non-torpid mammals. Our data will contribute to the development of novel therapeutic approaches to induce therapeutic hypothermia for treating drug-resistant fever, and for improving glucose and energy homeostasis.

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