scholarly journals Lipid metabolism in the obese Zucker rat. Disposal of an oral [14C]triolein load and lipoprotein lipase activity

1991 ◽  
Vol 274 (3) ◽  
pp. 651-656 ◽  
Author(s):  
E J López-Soriano ◽  
N Carbó ◽  
J M Argilés

Oxidation in vivo of [14C]triolein to 14CO2 was significantly lower in obese (fa/fa) Zucker rats as compared with their lean (+/?) controls. In response to a 24 h starvation period, both lean and obese rats showed an enhanced rate of [14C]triolein oxidation. There were, however, no changes in the rate of intestinal absorption of [14C]triolein between the lean and obese animals. Conversely, the total tissular [14C]lipid accumulation was significantly higher in white adipose tissue, carcass and plasma in the obese animals, whereas that of brown adipose tissue was lower. This was associated with a marked hyperinsulinaemia and hypertriglyceridaemia in the fa/fa animals. Starvation dramatically decreased [14C]lipid accumulation in white adipose tissue of the lean Zucker rats, but had no effect in the obese rats. The lipogenic rate of the obese rats was significantly higher than that of lean rats in liver, white adipose tissue, skeletal muscle and carcass. Lipoprotein lipase activity (per g of tissue) was significantly lower in both white and brown adipose tissue of obese versus lean rats; however, total activity was higher in both tissues. Starvation significantly lowered perigenital-adipose-tissue lipoprotein lipase activity in the lean groups, and had no effect in the obese ones. These results demonstrate that the tissue capacity of exogenous lipid uptake is involved, but cannot be the only factor influencing the maintenance of obesity in these animals. Thus, in the adult fa/fa rat, the large increase in obesity is not solely dependent on a deviation of energy-producing substrate metabolism towards the storage of lipids in white fat. Other factors, such as a low rate of oxidation, a high lipogenic rate and decreased brown-adipose-tissue activity are involved in the perseverance of the obesity syndrome.

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.


1988 ◽  
Vol 254 (2) ◽  
pp. 539-546 ◽  
Author(s):  
C M Oller do Nascimento ◽  
D H Williamson

1. The effects of starvation and refeeding on the disposal of oral [14C]triolein between 14CO2 production and 14C-lipid accumulation in tissues of virgin rats, lactating rats and lactating rats with pups removed were studied. 2. Starvation (24 h) increased 14CO2 production in lactating rats and lactating rats with pups removed to values found in virgin rats. This increase was accompanied by decreases in 14C-lipid accumulation in mammary gland and pups of lactating rats and in white and brown adipose tissue of lactating rats with pups removed. 3. Short-term (2 h) refeeding ad libitum decreased 14CO2 production in lactating rats and lactating rats with pups removed, and restored the 14C-lipid accumulation in mammary glands plus pups and in white and brown adipose tissue respectively 4. Insulin deficiency induced with mannoheptulose inhibited the restoration of 14C-lipid accumulation in white adipose tissue on refeeding of lactating rats with pups removed, but did not prevent the restoration of 14C-lipid accumulation in mammary gland. 5. Changes in the activity of lipoprotein lipase in mammary gland and white adipose tissue paralleled the changes in 14C-lipid accumulation in these tissues. 6. It is concluded that 14C-lipid accumulation in mammary gland may not be affected by changes in plasma insulin concentration and that it is less sensitive to starvation than is lipogenesis or lactose synthesis. This has the advantage that the milk lipid content can still be maintained from hepatic very-low-density lipoprotein for a period after withdrawal of food. The major determinant of the disposal of oral 14C-triolein appears to be the total tissue activity of lipoprotein lipase. When this is high in mammary gland (fed lactating rats) or white adipose tissue (fed lactating rats with pups removed), less triacylglycerol is available for the muscle mass and consequently less is oxidized.


1996 ◽  
Vol 37 (8) ◽  
pp. 1685-1695
Author(s):  
M Klingenspor ◽  
C Ebbinghaus ◽  
G Hülshorst ◽  
S Stöhr ◽  
F Spiegelhalter ◽  
...  

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.


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