Adenosine and the regional differences in adipose tissue metabolism in women

1988 ◽  
Vol 118 (3) ◽  
pp. 327-331 ◽  
Author(s):  
Susanna Stoneham ◽  
Tuula Kiviluoto ◽  
Leila Keso ◽  
Jorma J. Ohisalo

Abstract. Adenosine content in abdominal and femoral adipose tissue in menstruating women was 0.38 ± 0.10 and 0.59 ± 0.14 nmol/g of wet weight, respectively (mean ± sem; N = 17). No difference in adenosine sensitivity was found between abdominal and femoral adipocytes. In lactating women, the adenosine content was lower in femoral than in abdominal adipose tissue (0.40 ± 0.08 and 0.57 ± 0.08 nmol/g of wet weight, respectively; N = 10). Adenosine sensitivity in femoral adipocytes was not increased during lactation. As adenosine is a locally acting insulin-like effector, these results suggest that the higher adenosine content in femoral adipose tissue in menstruating women could explain its higher lipoprotein lipase activity and tendency to accumulate fat. During lactation, the lower extracellular adenosine concentration would allow lipid mobilization preferentially from the femoral site.

1984 ◽  
Vol 246 (4) ◽  
pp. E327-E333 ◽  
Author(s):  
C. Carneheim ◽  
J. Nedergaard ◽  
B. Cannon

Lipoprotein lipase activity in adult rats was investigated in animals subjected to cold and to different hormonal treatments. In contrast to changes in tissue wet weight and total protein content, which showed a lag time of about 1 day, lipoprotein lipase activity was markedly (fourfold) increased after only 4 h in the cold. Total lipoprotein lipase activity reached a plateau already after 1-3 days, whereas wet weight and protein content did not plateau until 3 wk. Neither insulin nor glucose injections could mimic the cold-induced increase in lipoprotein lipase activity seen after 4 h. However, the effect of norepinephrine injections was identical to the effect of cold. The beta-agonist isoprenaline was as effective as norepinephrine, whereas the alpha-agonist phenylephrine had no effect. The beta-antagonist propranolol inhibited the cold-induced increase in lipoprotein lipase activity. It is concluded that, in contrast to white adipose tissue, brown adipose tissue lipoprotein lipase is stimulated in vivo by a beta-adrenergic mechanism and that it is this beta-adrenergic mechanism that is responsible for the rapid recruitment of lipoprotein lipase during cold exposure.


1993 ◽  
Vol 34 (2) ◽  
pp. 219-228
Author(s):  
MH Maslowska ◽  
AD Sniderman ◽  
LD MacLean ◽  
K Cianflone

1978 ◽  
Vol 176 (3) ◽  
pp. 865-872 ◽  
Author(s):  
P Ashby ◽  
D P Bennett ◽  
I M Spencer ◽  
D S Robinson

Changes in adipose-tissue lipoprotein lipase activity that are independent of protein synthesis were investigated in an incubation system in vitro. Under appropriate conditions at 25 degrees C a progressive increase in the enzyme activity occurs that is energy-dependent. Part of the enzyme is rapidly inactivated when the tissue is incubated with adrenaline or adrenaline plus theophylline. The mechanism of this inactivation appears to be distinct from, and to follow, the activation of the enzyme. A hypothesis is presented to account for the results in terms of an activation of the enzyme during obligatory post-translational processing and a catecholamine-regulated inactivation of the enzyme as an alternative to secretion from the adipocyte.


1993 ◽  
Vol 16 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Hiroshi UEKI ◽  
Yusuke OHKURA ◽  
Toshio MOTOYASHIKI ◽  
Nobuaki TOMINAGA ◽  
Tetsuo MORITA

1997 ◽  
Vol 200 (22) ◽  
pp. 2913-2917 ◽  
Author(s):  
P L Lutz ◽  
R Reiners

This study investigated the relationship between energy failure and neurotransmitter release in the frog (Rana pipiens) brain during 1-3 h of anoxia. Unlike truly anoxia-tolerant species, the frog does not defend its brain energy charge. When exposed to anoxia at 25 degrees C, there is an immediate fall in brain ATP levels, which reach approximately 20% of normoxic levels in approximately 60 min. The frog, nevertheless, survives another 1-2 h of anoxia. At 100 min of anoxia, there is an increase in extracellular adenosine concentration, probably originating from the increased intracellular adenosine concentration caused by the breakdown of intracellular ATP. Increases in the levels of extracellular glutamate and GABA do not occur until 1-2 h after ATP depletion. This response is quite unlike that recorded for other vertebrates, anoxia-tolerant or anoxia-intolerant, where energy failure quickly results in an uncontrolled and neurotoxic release of excitatory neurotransmitters. In the frog, the delay in excitotoxic neurotransmitter release may be one of the factors that allow a period of survival after energy failure. Clearly, energy failure by itself is not a fatal event in the frog brain.


Sign in / Sign up

Export Citation Format

Share Document