Effect of Temperature on Lipoprotein Lipase and Lipogenic Enzyme Activities in Brown Adipose Tissue of Hypophysectomized Rats

1985 ◽  
Vol 17 (04) ◽  
pp. 176-180 ◽  
Author(s):  
M. Goubern ◽  
M. Laury ◽  
L. Zizine ◽  
R. Portet
1989 ◽  
Vol 256 (5) ◽  
pp. E645-E650 ◽  
Author(s):  
C. M. Carneheim ◽  
S. E. Alexson

Induction of lipoprotein lipase activity in brown adipose tissue (BAT) in response to cold stress has earlier been shown to be regulated by a beta-adrenergic mechanism and to be dependent on mRNA synthesis. In the present study, we have investigated the acute effects of refeeding after a short starvation period and the hormonal mechanism underlying the observed effects. Refeeding was found to rapidly increase tissue wet weight and lipoprotein lipase activity. The increase in enzyme activity could be blocked by the RNA synthesis inhibitor actinomycin D, indicating a gene activation. beta-Adrenergic blockade had no effect on this elevation of enzyme activity, but the increase could be mimicked by insulin injection. The results suggest that BAT contains two different pathways for regulation of lipoprotein lipase activity, both involving mRNA synthesis.


1996 ◽  
Vol 314 (1) ◽  
pp. 261-267 ◽  
Author(s):  
María-Jesus OBREGÓN ◽  
Barbara CANNON ◽  
Jan NEDERGAARD

The levels of mRNA coding for the uncoupling protein (UCP) and for lipoprotein lipase (LPL) were monitored in the brown adipose tissue of newborn rat pups. At 5 h after birth, the mRNA levels of UCP and LPL were high in pups exposed singly to 28 °C and low in pups kept singly at thermoneutrality (36 °C); in pups staying with the dam, the UCP mRNA levels were intermediate. However, the LPL mRNA levels were lower in pups staying with the dam than in pups at 36 °C, implying that factors additional to environmental temperature influenced LPL gene expression. Injection of noradrenaline into pups at thermoneutrality (36 °C) led to increases in UCP and LPL gene expression, but noradrenaline injections had no further effect in cold-exposed pups. The adrenergic effects were mediated via β-adrenergic receptors. The cold-induced increases in both UCP and LPL gene expression were abolished by the β-adrenergic antagonist propranolol. Thus differences in adrenergic responsiveness could not explain the differential expression of the UCP and LPL genes observed in pups staying with the dam. The presence of a physiological suppressor was examined by feeding single pups at 28 °C with different foods: nothing, water, Intralipid, cow's milk, rat milk and rat colostrum. None of these agents led to suppression of UCP gene expression, but colostrum led to a selective suppression of LPL gene expression. It was concluded that the genes for UCP and LPL were responsive to adrenergic stimuli immediately after birth, and it is suggested that a component of rat colostrum can selectively suppress LPL gene expression.


1987 ◽  
Vol 252 (1) ◽  
pp. R160-R165 ◽  
Author(s):  
C. J. Billington ◽  
T. J. Bartness ◽  
J. Briggs ◽  
A. S. Levine ◽  
J. E. Morley

Despite long-standing observations of a whole-body thermogenic effect of glucagon, the role of glucagon in activating thermogenesis in brown adipose tissue has not often been studied. We investigated the ability of administered glucagon to produce alterations in brown adipose tissue similar to changes produced by accepted stimuli of brown fat activity: cold, norepinephrine, and overfeeding. Eighteen days of glucagon injections (1 mg/kg) to male Sprague-Dawley rats produced, relative to saline-injected controls, decreases in feed efficiency and increases in brown adipose tissue weight, protein content, DNA content, and mitochondrial mass as reflected in cytochrome oxidase activity. The observed changes were similar, though of lesser magnitude, to changes produced in these same parameters induced by administration of norepinephrine (250 micrograms/kg) for a positive control group. Four days of glucagon administration (1 mg/kg) produced increases in specific activity of cytochrome oxidase and lipoprotein lipase. After 8 days of glucagon administration, changes in whole-pad activity similar to those seen with 18 days of administration were present. Glucagon also increased whole-pad lipoprotein lipase activity after 4 and 8 days. Surgically denervated interscapular brown adipose tissue retained its ability to respond to exogenous glucagon, though the magnitude of the response was diminished. Guanosine 5'-diphosphate (GDP) binding to brown adipose tissue mitochondria was measured as an assessment of functional state after 5 days of glucagon (1 mg/kg). There was an increase in GDP binding relative to controls whether expressed as picomoles per milligram mitochondrial protein or nanomoles per pad.(ABSTRACT TRUNCATED AT 250 WORDS)


1967 ◽  
Vol 45 (11) ◽  
pp. 1763-1771 ◽  
Author(s):  
Jane C. Roberts ◽  
Robert E. Smith

The effects of temperature in vitro upon metabolic rates of homogenates of brown fat and liver from control and cold-acclimated rats have been examined over the range 10–37 °C. At all temperatures, brown adipose tissue exhibits a higher rate of oxygen consumption [Formula: see text] than does liver, α-ketoglutarate being used as substrate. At 10 °C, brown adipose tissue retains a larger percentage (36–38%) of its 37 °C metabolic rate than does liver (22–24%).Q10 values and energies of activation (Ea) have been determined and compared with other data reported for these tissues. At 20 °C, breaks appear in the Arrhenius plots for liver from both control and cold-acclimated rats and also for brown fat from control rats, but not for the brown fat from cold-acclimated rats. Thus brown adipose tissue from cold-acclimated rats retains relatively higher levels of respiration at temperatures below the 20 °C breaking point than does brown fat from control rats.In view of previously reported cold-induced increases in mass, vascularity, and [Formula: see text] of brown fat, this decreased temperature sensitivity in the cold-acclimated rats appears wholly consonant with the adaptive behavior of brown fat in its role as a thermogenic effector.


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