Responses to cafeteria feeding in mice after the removal of interscapular brown adipose tissue

1982 ◽  
Vol 2 (11) ◽  
pp. 877-882 ◽  
Author(s):  
E. Connolly ◽  
J. A. Carnie

Feeding acafeteria diet to mice resulted in an increased energy intake of approximately 30% and this led to increases in the wet weight, total protein content, and total cytochrome oxidase activity of interscapular and dorso-cervical brown adipose tissue. Surgical removal of interscapular brown adipose tissue, followed by cafeteria feeding, gave rise to an elevation in dorso-cervical brown adipose tissue wet weight, total protein content, and total cytochrome oxidase activity, compared to intact cafeteria-fed mice. Cafeteria feeding with or without the removal of interscapular brown adipose tissue did not lead to significant increases in body weight compared to stock-fed control mice, but both cafeteria-fed groups of mice showed significant elevations in body fat content indicating that the induced hyperphagia led to a relative obesity in the cafeteria-fed groups. The results presented are consistent with an increased thermogenic activity in the brown adipose tissue of cafeteria-fed mice, and the effect of the removal of interscapular brown adipose tissue further indicates the quantitative importance of the tissue in the control of body weight.

1981 ◽  
Vol 241 (2) ◽  
pp. E116-E120 ◽  
Author(s):  
J. Himms-Hagen ◽  
J. Triandafillou ◽  
C. Gwilliam

Feeding a "cafeteria" diet for 2 wk to male Holtzman rats resulted in a weight gain that was, on average, only slightly more than that of control rats fed a regular chow diet. Wet weight, DNA, and total protein content of interscapular brown adipose tissue were more than doubled in the cafeteria-fed rats and proliferation of mitochondria paralleled tissue growth. After 2 wk of recovery from cafeteria feeding, the expanded size of the tissue had completely regressed to a normal level. Brown adipose tissue mitochondria of cafeteria-fed rats bound 3 times more purine nucleotides than mitochondria of chow-fed control rats, but no change in the proportion of polypeptides with molecular weight in the region of 32,000 could be detected. The changes in brown adipose tissue and its mitochondria in cafeteria-fed rats correspond to those seen previously in noradrenaline-treated rats, i.e., tissue growth accompanied by mitochondrial proliferation and an unmasking of proton conductance pathways. The increase in 32,000-mol-wt polypeptides seen in brown adipose tissue mitochondria of cold-acclimated rats does not occur in the cafeteria-fed rats. Control mechanisms are presumed to differ, either quantitatively or qualitatively, in the two situations, cold exposure and overeating, which both cause growth of brown adipose tissue.


1990 ◽  
Vol 258 (2) ◽  
pp. R418-R424 ◽  
Author(s):  
A. Geloen ◽  
P. Trayhurn

The role of insulin in the regulation of the thermogenic activity and capacity (uncoupling protein content) of brown adipose tissue (BAT) has been investigated using mice made diabetic with streptozotocin and then subsequently infused with different doses of insulin. After 12 days of diabetes, the animals received either 0, 8, 16, or 32 units of insulin.kg body wt-1.day-1 delivered by osmotic minipumps implanted subcutaneously for 12 days. After 12 days of diabetes, body weight, interscapular BAT, and epididymal white adipose tissue weights were each reduced. In BAT, significant decreases (P less than 0.05) in the mitochondrial protein content (63%), cytochrome oxidase activity (79%), mitochondrial GDP binding (51%), and the specific mitochondrial concentration and total tissue content of uncoupling protein (71 and 89%, respectively) were obtained, indicating that the thermogenic activity and capacity of the tissue were reduced in diabetes. The infusion of insulin at a dose of 8 units.kg-1.day-1 normalized mitochondrial GDP binding and doubled the concentration of uncoupling protein. Body weight, epididymal white adipose tissue weight, and the mitochondrial protein content of BAT were restored with 16 units of insulin.kg-1.day-1. Higher doses of insulin did not further increase the specific mitochondrial concentration of uncoupling protein, but the mitochondrial content (and thereby the total uncoupling protein content) of BAT was increased and blood glucose normalized. There was a significant correlation between the dose of insulin replacement and several of the parameters measured in BAT: mitochondrial protein content (r = 0.68, P less than 0.001), cytochrome oxidase activity (r = 0.54, P less than 0.001), and total uncoupling protein content (r = 0.68, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 259 (2) ◽  
pp. R324-R332 ◽  
Author(s):  
J. Cui ◽  
G. Zaror-Behrens ◽  
J. Himms-Hagen

Interscapular brown adipose tissue (BAT) of capsaicin-desensitized (Cap-Des) rats is atrophied, having a lower wet weight, a reduced total protein content, and as little as 10% of the normal content of uncoupling protein (UCP). Because the mitochondrial concentration of UCP, relative to other mitochondrial proteins, is not altered in Cap-Des rats, it is concluded that most of the mitochondria of BAT of Cap-Des rats have been lost. Consistent with this interpretation is a reduction of almost 40% of the overall thermogenic response to infused norepinephrine by anesthetized Cap-Des rats. Feeding a palatable diet had a delayed thermogenic effect and no trophic effect on BAT of Cap-Des rats. Food selection and intake were normal in Cap-Des rats, and diet-induced weight gain was the same as in control rats. Exposure of Cap-Des rats to cold for 1 or 7 days exerted a normal thermogenic effect on BAT but a delayed trophic effect. The cold-induced increase in thyroxine 5'-deiodinase in BAT occurred normally. Cap-Des rats were hypothermic at 1 day but normothermic by 7 days of cold exposure. The concentration of thyroid hormones in their blood was normal. It is suggested that the depletion of sensory neuropeptides in BAT presumed to be brought about by Cap-Des results either in loss of a trophic influence on mitochondriogenesis in BAT or in lack of an inhibitory influence on mitochondrial breakdown in BAT and leads to atrophy of BAT in rats living at 26 degrees C and an impaired response to stimulation by diet.(ABSTRACT TRUNCATED AT 250 WORDS)


1980 ◽  
Vol 239 (1) ◽  
pp. C18-C22 ◽  
Author(s):  
J. Himms-Hagen ◽  
C. Gwilliam

The size (wet weight, total protein, total cytochrome oxidase) of interscapular brown adipose tissue is reduced to about one-half of normal in the cardiomyopathic hamster (BIO 14.6). The mitochondria are normal in binding of purine nucleotides [guanosine 5'-diphosphate (GDP)] and in proportion of polypeptides in the region of 32,000, both indices of the thermogenic proton conductance pathway, and in specific activity of cytochrome oxidase. Brown adipose tissue of the cardiomyopathic hamster can grow during acclimation to 4 degrees C, but its size remains smaller than in cold-acclimated normal hamsters. Mitochondrial polypeptide composition is not altered by acclimation to cold, but a large increase in mitochondrial GDP binding occurs in both normal and cardiomyopathic hamsters. The reduced calorigenic response of cardiomyopathic hamsters to catecholamines (Horwitz, B.A., and G.E. Hanes, Proc. Soc. Exp. Biol. Med. 147: 393-395, 1974) may, at least in part, be explained by a reduction in the amount of brown adipose tissue, the major site of this response. A defect in control of growth of this tissue in the cardiomyopathic hamster is suggested.


1982 ◽  
Vol 47 (3) ◽  
pp. 653-658 ◽  
Author(s):  
E. Connolly ◽  
R. D. Morrisey ◽  
J. A. Carnie

1. The removal of the interscapular brown adipose tissue (IBAT) led to an increase in body-weight of normal, lean mice as compared to anaesthetized controls.2. No significant difference in food consumption could be detected between the two groups of mice over the period of the experiment.3. Fat extraction of the whole carcasses with chloroform: methanol showed a statistically significant increase in fat content in the animals without IBAT.4. There was no apparent failure in the operated animals to sustain core temperature when exposed to a cold stress situation (4° for 24 h).5. There was no difference in the wet weight, protein content or cytochrorne oxidase content of the dorso-cervical brown adipose tissue (DCBAT) between operated and control mice. This is indicative of a lack of proliferation of other brown adipose tissue sites in the operated mice in response to the removal of the IBAT.6. It is suggested that brown adipose tissue is implicated in dietary themiogenesis in the mouse.


1985 ◽  
Vol 231 (3) ◽  
pp. 761-764 ◽  
Author(s):  
R Bazin ◽  
D Ricquier ◽  
F Dupuy ◽  
J Hoover-Plow ◽  
M Lavau

The thermogenic capacity of brown adipose tissue has been investigated in I-strain mice to determine whether this tissue could play a role in the lower efficiency of food utilization reported in this strain of mice. (1) As compared with C57BL mice (a control strain), interscapular-brown-adipose-tissue weight and lipid percentage were decreased by 40% and 13% respectively in I-strain mice. (2) Mitochondrial protein content and cytochrome c oxidase activity were similar in the two strains, but the number of mitochondrial GDP-binding sites and uncoupling-protein content were increased by 2-fold in I-strain mice. (3) Fatty acid synthetase and citrate-cleavage enzyme (units/mg of protein) were 3-fold higher in the brown adipose tissue of I-strain mice. These results indicate that I-strain mice possess a very active brown adipose tissue. This enhanced capacity of energy dissipation in brown adipose tissue could contribute to the decreased capacity of I-strain mice to store adipose tissue.


1969 ◽  
Vol 47 (12) ◽  
pp. 975-980 ◽  
Author(s):  
P. Hahn ◽  
Z. Drahota ◽  
J. Skala ◽  
S. Kazda ◽  
Molly E. Towell

Rats aged 7 to 9 days were injected for 1 to 3 days with 5 mg/100 g body weight cortisone acetate per day. This led to an increase in the weight of brown adipose tissue, an increase in its fat content, and a decrease in its protein content. The content of norepinephrine in brown adipose tissue was decreased by cortisone treatment. The in vitro increase in O2 consumption following the addition of 5 μg nore-pinephrine/ml in vitro to brown adipose tissue from control animals was abolished by cortisone administration. Lipolysis due to norepinephrine was, however, not affected and was even slightly increased in cortisone-treated rats. Mitochondrial succinate–tetrazolium reductase activity was decreased after treatment with cortisone. It is concluded that cortisone alters the mitochondria of brown adipose tissue but has little effect on lipolysis as such. The content of norepinephrine in brown adipose tissue was found to decrease immediately after birth and then to return rapidly to higher levels.


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