GDP binding to hamster brown fat mitochondria is reduced during hibernation

1985 ◽  
Vol 249 (6) ◽  
pp. R689-R693 ◽  
Author(s):  
B. A. Horwitz ◽  
J. S. Hamilton ◽  
K. S. Kott

Preparation for hibernation is accompanied by increased thermogenic capacity of brown fat (BAT), an important site of thermogenesis during arousal from hibernation. This study examined whether that thermogenic capacity is reduced in hibernation and reactivated during arousal. In one set of experiments, Syrian hamsters were exposed to short photoperiod (10:14 light-dark) and cold (7 degrees C). Those not hibernating at death (n = 10) served as controls for those that were (n = 9). A third group (n = 10) was killed 80–90 min after arousal was initiated by manual perturbation. Mitochondrial GDP binding (nmol/mg mitochondrial protein) was used to estimate thermogenic capacity. In a second experimental series, BAT citrate (si)-synthase and 3-hydroxyacyl-CoA dehydrogenase activities were measured in hibernating and nonhibernating hamsters. Although there were no differences in the maximum activities of these enzymes, GDP binding was markedly lower in the hibernators relative to the nonhibernators (0.214 +/- 0.031 vs. 0.535 +/- 0.039). However, in the partially aroused hamsters, GDP binding had doubled (0.438 +/- 0.04). Thus hibernation is accompanied by a substantial reduction of BAT thermogenic capacity (as manifested by GDP binding), which is reversed during arousal. The rapidity of this reversal indicates that it does not involve the synthesis of new GDP binding sites.

1986 ◽  
Vol 251 (5) ◽  
pp. R963-R970 ◽  
Author(s):  
K. S. Kott ◽  
B. J. Moore ◽  
B. A. Horwitz

Previous studies showed that short photoperiod increased brown fat (BAT) mass and reduced gonadal size and gonadal hormone secretion in hamsters. The present study investigated the possibility that the effects on BAT were dependent on reduced levels of gonadal hormones. BAT from male Syrian hamsters exposed to short photoperiod for 10 wk was significantly greater in mass, protein content, and total maximal citrate synthase and beta-hydroxyacyl-CoA dehydrogenase activities than was BAT from long-photoperiod hamsters, These differences between short- and long-photoperiod exposure were observed in hamsters housed at 21 as well as at 8 degrees C. Short photoperiod also increased the total recovered mitochondrial GDP binding, a finding consistent with increased BAT thermogenic capacity. These short-photoperiod effects were neither mimicked by castration of long-photoperiod hamsters nor prevented by high levels of testosterone administered to short-photoperiod animals. Castration did attenuate the effects of short photoperiod on BAT growth if, after surgery and prior to short-photoperiod exposure, the animals were housed at a long photoperiod for 2-3 wk. In contrast, in hamsters immediately placed at short photoperiod after surgery, castration did not inhibit short-photoperiod effects. The present three experiments demonstrate that, in addition to increasing BAT mass, short photoperiod elevates the thermogenic capacity of BAT, and this elevation does not require the absence or a much reduced testosterone level.


1989 ◽  
Vol 256 (1) ◽  
pp. R174-R180
Author(s):  
K. S. Kott ◽  
B. J. Moore ◽  
L. Fournier ◽  
B. A. Horwitz

Previous studies demonstrated that short photoperiod exposure significantly decreases circulating prolactin levels. The present study investigated the possibility that concomitant changes in brown fat tissue mass, protein content, thermogenic capacity, and carcass composition are dependent on this change in prolactin levels. Male golden (Syrian) hamsters were sham operated and exposed to a short (10L:14D) or long (14L:10D) photoperiod. A third group was implanted with exogenous pituitaries under the right kidney capsule and exposed to a short photoperiod. In experiment I, 4 wk of short- vs. long-photoperiod exposure did not result in significant changes in circulating prolactin levels, nor was there an increase in brown fat mass, protein content, or thermogenic capacity. Four weeks of short-photoperiod exposure did significantly increase carcass lipid content. However, this increase did not occur in hamsters exposed to 4 wk of short photoperiod but made hyperprolactinemic (implanted with two exogenous pituitaries). Ten weeks of short photoperiod significantly reduced circulating prolactin levels. Concomitantly, brown fat mass, protein content, and thermogenic capacity, as well as carcass fat, were increased. These short-photoperiod-induced changes were not observed in similarly exposed hamsters that were made hyperprolactinemic via two implanted pituitaries. In experiment II, similar changes in brown fat and body composition occurred in sham-operated hamsters exposed to 10 wk of short photoperiod. These changes were prevented in hamsters exposed to 10 wk of short photoperiod but made hyperprolactinemic via only one implanted pituitary. These results suggest that decreased prolactin is a necessary condition for the increased brown fat mass, protein content, and thermogenic capacity that occurs when golden hamsters are exposed to short photoperiod.


1988 ◽  
Vol 8 (3) ◽  
pp. 327-332 ◽  
Author(s):  
Edward Preston ◽  
Joan Triandafillou ◽  
Nicholas Haas

1991 ◽  
Vol 261 (2) ◽  
pp. R501-R507 ◽  
Author(s):  
C. J. Billington ◽  
J. E. Briggs ◽  
J. G. Link ◽  
A. S. Levine

Our aims were to further characterize the stimulatory effect of glucagon on brown fat and to test the hypothesis that physiological levels of hyperglucagonemia would stimulate brown fat thermogenesis. In the first set of experiments, glucagon (1 mg/kg sc twice daily) or vehicle control was administered three times in 26 h. This large dose of glucagon produced increases in GDP binding to brown fat mitochondria. In addition, Scatchard analysis indicated a glucagon-induced increase in number of GDP binding sites without evidence for alteration in binding site affinity. No consistent increase in brown fat mitochondrial GDP binding was produced 2 h after a single injection of glucagon (1 mg/kg). In the second set of experiments, glucagon was administered intraperitoneally by constant osmotic minipump infusion. Glucagon in a dose of 150 micrograms.kg-1.day-1 for 5 days produced significant increases in GDP binding to brown fat mitochondria, whereas glucagon serum levels were increased but stayed within the usual physiological range. A larger dose of glucagon administered by constant infusion virtually eliminated body weight gain over 7 days while significantly increasing nucleotide binding (GDP) to brown fat mitochondria. An important role for glucagon in thermogenic regulation is suggested.


1971 ◽  
Vol 49 (6) ◽  
pp. 501-507 ◽  
Author(s):  
Josef Skala ◽  
Peter Hahn

An injection of a single dose of cortisone acetate (5 mg/100 g body weight) to 9-day-old rats resulted in the following changes in brown adipose tissue 24 h later: (1) the fresh weight was increased due to fat accumulation; (2) the DNA content of whole interscapular brown fat stayed unaltered, while the RNA content was increased; (3) specific activities of cytoplasmic alpha-glycerophosphate dehydrogenase and malic enzyme were increased; (4) the percentage of mitochondrial protein in the whole tissue protein was not changed, but mitochondria seemed to be more fragile, fewer were recovered by a standard isolation procedure, and more cytochrome c oxidase contaminated the microsomal fraction; (5) mitochondrial alpha-glycero-phosphate dehydrogenase and succinate dehydrogenase activities were decreased per milligram homogenate protein and (in isolated mitochondrial fraction) per milligram mitochondrial protein; (6) the endogenous respiration of brown fat mitochondria was activated much less by carnitine and CoA; and (7) CO2 formation from palmitate-14C by isolated mitochondria was considerably lower.A similar injection to 30-day-old rats had no significant effect.It is suggested that a single injection of cortisone affects the mitochondrial structure of brown adipose tissue and the ability to oxidize fatty acids and that it is effective on day 10 but not on day 30.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 274-OR ◽  
Author(s):  
GUOXIAO WANG ◽  
JESSE G. MEYER ◽  
WEIKANG CAI ◽  
MENGYAO E. LI ◽  
SAMIR SOFTIC ◽  
...  

1984 ◽  
Vol 9 (11) ◽  
pp. 489-491 ◽  
Author(s):  
David G. Nicholls ◽  
Eduardo Rial

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