Restoration of lipoprotein lipase activity in insulin-deficient rats by insulin infusion is tissue-specific

1991 ◽  
Vol 69 (6) ◽  
pp. 746-751 ◽  
Author(s):  
Yves Deshaies ◽  
Alain Géloën ◽  
Anne Paulin ◽  
Ludwik J. Bukowiecki

The activity of lipoprotein lipase was measured in white and brown adipose tissues, red vastus lateralis muscle, and heart of rats that have been insulin deficient (streptozotocin, 75 mg∙kg−1) for 2 weeks, and that have then received implants of insulin-delivering minipumps (17 U∙kg−1∙day−1) for 1 or 4 days. Normal glycemia was restored in insulin-deficient animals after 4 days of insulin treatment. Hypertriglyceridemia, but not hypercholesterolemia, was reversed after 4 days of insulin infusion. After 2 weeks of insulin deficiency, fasting lipoprotein lipase activity was lowered in all tissues studied. In white adipose tissue, lipoprotein lipase decreased to 50% of control values. After a single day of insulin infusion, even if tissue weight has not yet been greatly affected, total activity was completely restored to control levels. Enzyme activity in brown adipose tissue was also depressed in deficient animals, and insulin infusion was followed by a slow recovery of activity, to a level intermediate between those of control and insulin-deficient groups. Insulin status had milder effects on lipoprotein lipase activity in vastus lateralis muscle than in the adipose tissues. Deficient rats displayed 60% less activity than controls, and 4 days of hormone infusion only partially restored enzyme activity. There was a large loss of lipoprotein lipase in the heart following 2 weeks of insulin depletion, which was not counteracted by hormone infusion. Thus the speed and extent of recovery of lipoprotein lipase activity following hormone replacement in insulin-deficient animals varied widely among tissues. These findings suggest that insulin is part of the factors that determine the tissue specificity of lipoprotein lipase regulation.Key words: insulin, lipoprotein lipase, white adipose tissue, brown adipose tissue, skeletal muscle, heart.

1992 ◽  
Vol 70 (12) ◽  
pp. 1555-1562 ◽  
Author(s):  
Rekia Belahsen ◽  
Yves Deshaies

This study evaluated the effects of β2-adrenoceptor stimulation on some determinants of triglyceride metabolism. Male Sprague–Dawley rats were injected twice daily with clenbuterol (30 μg∙kg−1) for 7 days, or with an equivalent volume of vehicle. Serum triglycerides, hepatic triglyceride secretion rate, and lipoprotein lipase activity in white and brown adipose tissues as well as in red vastus lateralis muscle and heart were evaluated in the fasting state and following a fat-free, high-sucrose meal, 3 h after the last agonist injection. In rats killed in the fasting and postprandial states, clenbuterol reduced the mass of white adipose tissue (−25 and −12%, respectively; p < 0.02), whereas it increased the mass of vastus lateralis muscle (+11 and +7%; p < 0.002) and heart (+13 and +10%; p < 0.0001). In vehicle-injected animals, the fasting state was associated with lower lipoprotein lipase activity in white and brown adipose tissues, and higher enzyme activity in vastus lateralis and heart, compared with the postprandial state. Postprandially, treatment with clenbuterol reduced lipoprotein lipase activity in white adipose (−24%), whereas it increased enzyme activity in brown adipose (+107%) as well as in vastus lateralis (+35%). In fasted animals, no significant variation of enzyme activity in these tissues was observed following clenbuterol treatment, whereas in the heart, a decrease of lipoprotein lipase activity was observed (−22%). Clenbuterol lowered serum triglycerides significantly (−23%), but not their rate of secretion, whereas the agonist decreased the insulin to glucagon ratio only in the postprandial state. These results suggest that modulation of triglyceride-rich lipoprotein metabolism, particularly tissue-specific alterations in lipoprotein lipase activity, may be one of the pathways through which clenbuterol affects partitioning of lipid substrates.Key words: triglyceride, lipoprotein lipase, tissue specificity, meal intake, β2 agonist.


1988 ◽  
Vol 255 (2) ◽  
pp. R226-R231
Author(s):  
Y. Deshaies ◽  
J. Arnold ◽  
J. Lalonde ◽  
D. Richard

The combined effects of a high-fat-supplemented diet and exercise training on serum lipids as well as on lipoprotein lipase activity in white and brown adipose tissues of the rat were evaluated. Male Wistar rats were fed ad libitum either a stock diet or the stock diet supplemented with food items rich in fat. Half of each dietary group was submitted to daily treadmill running for 35 days. Food intake and final body weight were raised by the high-fat-supplemented diet and lowered by exercise training. Postprandial serum triglycerides were not affected by diet or exercise, whereas the latter decreased total cholesterol in the high-fat group only (14%, P less than 0.01). Total lipoprotein lipase activity in white adipose tissue was elevated (120%, P less than 0.01) by high-fat feeding, and this increase was greatly reduced by concomitant exercise training. In brown adipose tissue, however, the large elevation (104%, P less than 0.01) in enzyme activity brought by the high-fat diet was unaltered by concomitant training. Thus a high-fat-supplemented diet increased lipoprotein lipase activity in both an energy-storing and a heat-producing tissue, and exercise training was able to counteract this effect in white, but not in brown, adipose tissue. These findings support the notion that the regulation of lipoprotein lipase is tissue specific.


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 37 (8) ◽  
pp. 1685-1695
Author(s):  
M Klingenspor ◽  
C Ebbinghaus ◽  
G Hülshorst ◽  
S Stöhr ◽  
F Spiegelhalter ◽  
...  

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