Reduced norepinephrine turnover in interscapular brown adipose tissue of obese rats after ovariectomy

Metabolism ◽  
1987 ◽  
Vol 36 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Toshihide Yoshida ◽  
Hitoshi Nishioka ◽  
Keiji Yoshioka ◽  
Motoharu Kondo
1987 ◽  
Vol 252 (2) ◽  
pp. R402-R408 ◽  
Author(s):  
T. Yoshida ◽  
J. S. Fisler ◽  
M. Fukushima ◽  
G. A. Bray ◽  
R. A. Schemmel

The effects of dietary fat content, lighting cycle, and feeding time on norepinephrine turnover in interscapular brown adipose tissue, heart, and pancreas, and on blood 3-hydroxybutyrate, serum glucose, insulin, and corticosterone have been studied in two strains of rats that differ in their susceptibility to dietary obesity. S 5B/Pl rats, which are resistant to dietary obesity, have a more rapid turnover of norepinephrine in interscapular brown adipose tissue and heart and a greater increase in the concentration of norepinephrine in brown fat when eating a high-fat diet than do Osborne-Mendel rats, which are sensitive to fat-induced obesity. Light cycle and feeding schedule are important modulators of sympathetic activity in heart and pancreas but not in brown fat. Rats of the resistant strain also have higher blood 3-hydroxybutyrate concentrations and lower insulin and corticosterone levels than do rats of the susceptible strain. A high-fat diet increases 3-hydroxybutyrate concentrations and reduces insulin levels in both strains. These studies show, in rats eating a high-fat diet, that differences in norepinephrine turnover, particularly in brown adipose tissue, may play an important role in whether dietary obesity develops and in the manifestations of resistance to this phenomenon observed in the S 5B/Pl rat.


1984 ◽  
Vol 247 (2) ◽  
pp. R290-R295 ◽  
Author(s):  
J. S. Fisler ◽  
T. Yoshida ◽  
G. A. Bray

Catecholamine turnover in response to fasting, cold exposure, and a high-fat diet has been measured in the Osborne-Mendel rat, which readily develops obesity when fed a high-fat diet, and the S 5B/P1 rat, which does not. We have tested the hypothesis that this difference in response to diet might be associated with altered rates of norepinephrine or epinephrine turnover. The endogenous norepinephrine concentration in interscapular brown adipose tissue was significantly greater in fasted S 5B/P1 rats than in fasted Osborne-Mendel rats. The fractional norepinephrine turnover rate in interscapular brown adipose tissue of fasted animals was also greater in the S 5B/P1 rat than in the Osborne-Mendel rat. Cold exposure increased the fractional norepinephrine turnover rate in interscapular brown adipose tissue for both strains of rats but increased the fractional norepinephrine turnover rate in the pancreas in only the Osborne-Mendel rats. The turnover of epinephrine and the adrenal concentration of this hormone were not different between the two strains. Normal and high-fat diets were fed to both strains; the Osborne-Mendel rats were pair fed the high-fat diet to prevent excess weight gain. Endogenous concentrations of norepinephrine in interscapular brown adipose tissue was increased by the high-fat diet; the increase was greater in S 5B/P1 rats. The high-fat diet resulted in increased norepinephrine turnover in interscapular brown adipose tissue of the S 5B/P1 rat but not the Osborne-Mendel rat.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 248 (1) ◽  
pp. E20-E25 ◽  
Author(s):  
M. Saito ◽  
Y. Minokoshi ◽  
T. Shimazu

The interscapular brown adipose tissue (IBAT) from obese rats with lesions of the ventromedial hypothalamus (VMH) was approximately 5 times heavier than those from controls. This hypertrophy of IBAT was associated with a marked enlargement of constituent adipocytes and their apparent transformation from multiloculated structure of lipid droplets into the uniloculated structure. The rate of fatty acid synthesis in IBAT of the obese rats was less than one-tenth of that in control rats and approximated the value in white adipose tissue (WAT) when they were starved for 24 h. When rats were fed, the synthetic rate was increased, but the lipogenic response of IBAT in the obese rats was much greater than that in controls, the extent of the response being comparable to that of WAT. The IBAT temperature rose rapidly on electrical stimulation of the sympathetic nerves to the tissue in control rats, whereas the temperature response was reduced markedly in the obese rats. It was suggested that thermogenesis in BAT was impaired in obese rats with VMH lesions by decreasing triglyceride turnover in BAT, probably due to dysfunction of the sympathetic nervous system and a consequent transformation of BAT into WAT.


1984 ◽  
Vol 247 (2) ◽  
pp. E181-E189 ◽  
Author(s):  
L. Landsberg ◽  
M. E. Saville ◽  
J. B. Young

The sympathetic nervous system (SNS) plays a critical role in the regulation of mammalian thermogenic responses to cold exposure and dietary intake. Catecholamine-stimulated thermogenesis is mediated by the beta-adrenergic receptor. In the rat brown adipose tissue is the major site of metabolic heat production in response to both cold (nonshivering thermogenesis) and diet (diet-induced thermogenesis). Measurements of norepinephrine turnover rate in interscapular brown adipose tissue of the rat demonstrate increased sympathetic activity in response to both cold exposure and overfeeding. In adult humans, a physiologically significant role for brown adipose tissue has not been established but cannot be excluded. It appears likely that dietary changes in SNS activity are related, at least in part, to the changes in metabolic rate that occur in association with changes in dietary intake.


2008 ◽  
Vol 295 (2) ◽  
pp. R417-R428 ◽  
Author(s):  
C. Kay Song ◽  
Cheryl H. Vaughan ◽  
Erin Keen-Rhinehart ◽  
Ruth B. S. Harris ◽  
Denis Richard ◽  
...  

A precise understanding of neural circuits controlling lipid mobilization and thermogenesis remains to be determined. We have been studying the sympathetic nervous system (SNS) contributions to white adipose tissue (WAT) lipolysis largely in Siberian hamsters. Central melanocortins are implicated in the control of the sympathetic outflow to WAT, and, moreover, the melanocortin 4 receptors (MC4-R) appear to be principally involved. We previously found that acute third ventricular melanotan II (MTII; an MC3/4-R agonist) injections increase sympathetic drive (norepinephrine turnover) to interscapular brown adipose tissue (IBAT) and IBAT temperature. Here we tested whether MC4-R mRNA is expressed in IBAT SNS outflow neurons using in situ hybridization for the former and injections of the transneuronal viral retrograde tract tracer, pseudorabies virus (PRV) into IBAT, for the latter. Significant numbers of double-labeled cells for PRV and MC4-R mRNA were found across the neuroaxis (mean of all brain sites ∼60%), including the hypothalamic paraventricular nucleus (PVH; ∼80%). Acute parenchymal MTII microinjections into the PVH of awake, freely-moving hamsters, using doses below those able to increase IBAT temperature when injected into the third ventricle, increased IBAT temperature for as long as 4 h, as measured by temperature transponders implanted below the tissue. Collectively, these data add significant support to the view that central melanocortins are important in controlling IBAT thermogenesis via the SNS innervation of this tissue, likely through the MC4-Rs.


1994 ◽  
Vol 266 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
L. A. Cassis

Previous studies demonstrated that interscapular brown adipose tissue (ISBAT) produces angiotensin II (ANG II), which facilitates sympathetic neurotransmission (SN). ANG II content and regulation of SN were examined in young (17 days) and adult (16 wk) Zucker obese and lean rats. ANG II content in ISBAT from preobese rats was decreased compared with lean littermates. Evoked 3H overflow in ISBAT slices preloaded with [3H]NE was greater in preobese rats compared with control. ANG II increased evoked 3H overflow in ISBAT slices to a greater extent in preobese rats compared with control. [3H]NE uptake in ISBAT slices from preobese rats was decreased compared with control. In adult obese rats, plasma renin activity was decreased compared with control. ISBAT ANG II content was increased in adult obese rats compared with control. Evoked 3H overflow in ISBAT slices preloaded with [3H]NE was not different between obese and control. ANG II did not increase evoked 3H overflow in obese rats; however, ANG II increased evoked 3H overflow in lean rats. [3H]NE uptake in ISBAT slices from obese rats was decreased compared with control. These results suggest that ANG II modulation of SN activity is decreased in ISBAT from adult obese rats. In contrast, in young obese rats, increased SN activity and ANG II regulation of SN were evident in brown adipose tissue.


1987 ◽  
Vol 253 (5) ◽  
pp. E515-E520 ◽  
Author(s):  
P. Trayhurn ◽  
M. C. Wusteman

Sympathetic activity has been assessed, by measurements of norepinephrine turnover, in interscapular brown adipose tissue of mice during lactation. Norepinephrine turnover was reduced in brown adipose tissue from early lactation until weaning. The reduction in turnover occurred in dams suckling either large-or small-sized litters. Norepinephrine turnover returned to the control level after natural weaning and increased rapidly after abrupt weaning at peak lactation. Acute exposure to cold resulted in a large increase in norepinephrine turnover in brown adipose tissue of lactating mice, as in control animals. These results indicate that sympathetic activity is suppressed in brown adipose tissue during lactation, but sympathetic responsiveness is retained. The reduction in sympathetic activity is likely to be responsible for the decrease in brown adipose tissue thermogenesis in lactation. Norepinephrine turnover in the heart tended to be reduced at peak lactation, suggesting that there may be a general decrease in sympathetic activity in the lactating animal. In contrast to the normal animal, the hyperphagia of lactation does not lead to an activation of the sympathetic nervous system.


1991 ◽  
Vol 260 (2) ◽  
pp. R278-R283 ◽  
Author(s):  
F. Assimacopoulos-Jeannet ◽  
M. Moinat ◽  
P. Muzzin ◽  
C. Colomb ◽  
B. Jeanrenaud ◽  
...  

The aim of the study was to examine in the obese Zucker (fa/fa) rats the effect of a peroxisome proliferator nafenopin on liver and brown adipose tissue peroxisomal and mitochondrial beta-oxidation enzyme activities and on the overall energy dissipation. A 17-day nafenopin treatment increased liver wet weight 2.1-fold and liver total acyl-CoA oxidase and mitochondria beta-oxidative activities 32- and 4.6-fold, respectively. It increased the interscapular brown adipose tissue (IBAT) acyl-CoA oxidase activity 2.1-fold but had no effect on the mitochondria beta-oxidative activity. Because nafenopin was found to decrease food intake by 22%, obese nafenopin-treated rats were compared with a group of obese pair-fed rats. Both food restriction and nafenopin treatment decreased body weight gain, but a decrease (14%) in fat content was only observed in nafenopin-treated rats. Food restriction of obese rats decreased the mean metabolic rate by 13%, and nafenopin treatment prevented this decrease. Both food restriction and nafenopin treatment decreased the mean daily respiratory quotient (RQ). However, the RQ of nafenopin-treated rats was steadily lower than that of control, whereas that of food-restricted rats was the same as that of control animals during the feeding period and decreased when food supply was exhausted. The increase in liver and IBAT fatty acid beta-oxidative activities may be the cause of the decreased lipid accretion measured in obese rats.


1992 ◽  
Vol 282 (1) ◽  
pp. 231-235 ◽  
Author(s):  
D M Smith ◽  
S R Bloom ◽  
M C Sugden ◽  
M J Holness

Starvation (48 h) decreased the concentration of mRNA of the insulin-responsive glucose transporter isoform (GLUT 4) in interscapular brown adipose tissue (IBAT) (56%) and tibialis anterior (10%). Despite dramatic [7-fold (tibialis anterior) and 40-fold (IBAT)] increases in glucose utilization after 2 and 4 h of chow re-feeding, no significant changes in GLUT 4 mRNA concentration were observed in these tissues over this re-feeding period. The results exclude changes in GLUT 4 mRNA concentration in mediating the responses of glucose transport in these tissues to acute re-feeding after prolonged starvation.


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