Effect Of Exercise Training On Adipose Tissue Lipoprotein Lipase Gene Expression In Obese Women Undergoing Weight Loss

2009 ◽  
Vol 41 ◽  
pp. 38-39
Author(s):  
Tongjian You ◽  
Xuewen Wang ◽  
Rongze Yang ◽  
Wan Shen ◽  
Dawei Gong ◽  
...  
Metabolism ◽  
1995 ◽  
Vol 44 (12) ◽  
pp. 1596-1605 ◽  
Author(s):  
John M. Ong ◽  
Rosa B. Simsolo ◽  
Mehrnoosh Saghizadeh ◽  
John W.F. Goers ◽  
Philip A. Kern

1987 ◽  
Vol 58 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Lori A. Smolin ◽  
Mary B. Grosvenor ◽  
David J. Handelsman ◽  
Jo Anne Brasel

1. Adipose tissue lipoprotein lipase (EC 3.1.1.34; AT-LPL), a rate-limiting enzyme in triglyceride storage in adipose tissue, is hormonally regulated and may be important in the maintenance of obesity.2. In twelve obese women, AT-LPL activity was measured before weight loss, during weight loss and after 1 and 2 weeks of weight maintenance on either a high-carbohydrate or a high-protein diet.3. When related to tissue weight, AT-LPL activity during the 2 weeks of weight maintenance was higher than the initial AT-LPL activity; there was no difference when activity was expressed per cell.4. Changes in AT-LPL activity were not affected by diet composition. AT-LPL activity correlated with insulin levels and a change in the insulin sensitivity of AT-LPL was observed after weight loss.


1992 ◽  
Vol 263 (3) ◽  
pp. E500-E506 ◽  
Author(s):  
J. R. Mitchell ◽  
A. Jacobsson ◽  
T. G. Kirchgessner ◽  
M. C. Schotz ◽  
B. Cannon ◽  
...  

The regulation of lipoprotein lipase gene expression in brown adipose tissue was studied. Rats were preacclimated to 21 degrees C. Exposure to cold (4 degrees C) resulted in a rapid increase in the level of lipoprotein lipase mRNA in the tissue. The level peaked (expressed per microgram total RNA) after approximately 8 h and then slowly declined. The increased lipoprotein lipase mRNA level was not due to an increased stability of the mRNA, but, in a transition event from a high to a low expression of the lipoprotein lipase gene, a transcription-dependent process was recruited that accelerated the breakdown of lipoprotein lipase mRNA. Norepinephrine injections increased lipoprotein lipase mRNA levels in the tissue; this effect was mediated via a beta-adrenergic receptor. The effect of cold could be mimicked by norepinephrine injections, and these two effects were not additive, indicating that the cold effect was mediated by norepinephrine. The lipoprotein lipase mRNA level was also increased by insulin injections (into fasted animals); thus an increase in lipoprotein lipase gene expression in brown adipose tissue may be induced via two different stimuli, which, intracellularly, would be mediated via different signaling systems. In all investigated conditions, the changes in lipoprotein lipase mRNA levels observed here were parallelled by alterations in lipoprotein lipase activity reported earlier from this laboratory. It was therefore concluded that, under the conditions studied, lipoprotein lipase activity in brown adipose tissue was primarily regulated at the transcriptional level.


1994 ◽  
Vol 77 (6) ◽  
pp. 2564-2571 ◽  
Author(s):  
E. V. Lambert ◽  
G. Wooding ◽  
M. I. Lambert ◽  
J. H. Koeslag ◽  
T. D. Noakes

Short-term detraining has been characterized by increased body mass and rapid body fat accretion. However, detraining has also been associated with increased food intake, especially in rats genetically predisposed to obesity. Thus, it has been difficult to separate refeeding effects from alterations resulting from the cessation of exercise training. In the present study, the in vitro activity of adipose tissue lipoprotein lipase (ATLPL) was measured in freely running wheel-trained rats and rats that had stopped training for 1, 2, or 3 days or 1 or 2 wk, respectively. Heparin-releasable ATLPL activity was measured at rest and after acute exhaustive exercise. Feeding efficiency (change in body mass/kJ ingested energy), fat pad mass, and adipocyte size were also measured. The rate of weight gain in 1- and 2-wk detrained rats was significantly higher than that of sedentary control or trained rats (P < 0.05). Feeding efficiency was also higher in 1-wk detrained rats than in all other groups (P < 0.005). However, food energy intake was not different between trained rats, 1- and 2-wk detrained rats, or sedentary control rats. ATLPL activity in all groups was highest after acute exhaustive exercise. ATLPL activity in 1-wk detrained rats was nearly threefold higher compared with that in trained rats (P < 0.005) and was not different from that of sedentary control rats. These results suggest that the cessation of exercise training causes an enhanced capacity for lipogenesis independent of changes in food energy intake or the acute effects of the last bout of exercise.


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