scholarly journals Effects of platelet-activating factor on lipid metabolism in rats in vivo. Origin of the hypertriglyceridaemia

1991 ◽  
Vol 280 (2) ◽  
pp. 541-543 ◽  
Author(s):  
R D Evans ◽  
V Ilic ◽  
D H Williamson

Administration of platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine; PAF) did not alter the rate of triacylglycerol entry into the plasma. The gastrointestinal absorption of [1-14C]triolein was, however, inhibited by PAF, yet there was increased accumulation of [14C]lipid in the plasma and hypertriglyceridaemia. The half-life of injected [9,10(n)-3H]triolein in the plasma increased by 47%, and there was decreased accumulation of [3H]lipid in brown adipose tissue. This was accompanied by a decrease in lipoprotein lipase activity. The hypertriglyceridaemia induced by PAF appears to be mainly due to decreased peripheral removal, one important site affected being brown adipose tissue.

1988 ◽  
Vol 254 (2) ◽  
pp. E155-E161 ◽  
Author(s):  
C. Carneheim ◽  
J. Nedergaard ◽  
B. Cannon

The cellular basis for the cold-induced increase in lipoprotein lipase activity in rat brown adipose tissue was investigated. Rats were treated with inhibitory agents and either exposed to cold for 4 h or injected with isoprenaline. Lipoprotein lipase activity was followed in acetone-ether extracts of the tissue. Besides cold, both the beta-adrenergic agonist isoprenaline and the adenylate cyclase activator cholera toxin were able to increase lipoprotein lipase activity in the tissue. The protein synthesis inhibitor cycloheximide fully abolished this response; the half-life of lipoprotein lipase activity was both in control and in the cold-exposed state approximately 2 h. Also the mRNA synthesis inhibitor actinomycin D fully abolished the cold-, the isoprenaline-, and the cholera toxin-induced increases in lipoprotein lipase activity; the half-life of lipoprotein lipase mRNA was estimated to be 20-30 h. However, in animals returned to control conditions after a 4-h cold stress, the decline in activity corresponded to a half-life of only 4 h. It was concluded that the increase in lipoprotein lipase activity in the brown adipose tissue of cold-exposed rats is not due to an activation of preexisting enzyme nor due to an increased half-life of functional enzyme. Rather it is suggested that in brown adipose tissue the rate of lipoprotein lipase gene transcription is positively regulated by the cellular level of cAMP and that this increase in lipoprotein lipase mRNA leads directly to an increased rate of enzyme synthesis and hence to the increase in activity.


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.


Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3577-3588 ◽  
Author(s):  
Yuri Fujimoto ◽  
Yoshimi Nakagawa ◽  
Aoi Satoh ◽  
Kanako Okuda ◽  
Akiko Shingyouchi ◽  
...  

Transcription factor E3 (TFE3) is a transcription factor that binds to E-box motifs and promotes energy metabolism-related genes. We previously reported that TFE3 directly binds to the insulin receptor substrate-2 promoter in the liver, resulting in increased insulin response. However, the role of TFE3 in other tissues remains unclear. In this study, we generated adipose-specific TFE3 transgenic (aP2-TFE3 Tg) mice. These mice had a higher weight of white adipose tissue (WAT) and brown adipose tissue than wild-type (WT) mice under fasting conditions. Lipase activity in the WAT in these mice was lower than that in the WT mice. The mRNA level of adipose triglyceride lipase (ATGL), the rate-limiting enzyme for adipocyte lipolysis, was significantly decreased in aP2-TFE3 Tg mice. The expression of Foxo1, which directly activates ATGL expression, was also suppressed in transgenic mice. Promoter analysis confirmed that TFE3 suppressed promoter activities of the ATGL gene. In contrast, G0S2 and Perilipin1, which attenuate ATGL activity, were higher in transgenic mice than in WT mice. These results indicated that the decrease in lipase activity in adipose tissues was due to a decrease in ATGL expression and suppression of ATGL activity. We also showed that thermogenesis was suppressed in aP2-TFE3 Tg mice. The decrease in lipolysis in WAT of aP2-TFE3 Tg mice inhibited the supply of fatty acids to brown adipose tissue, resulting in the inhibition of the expression of thermogenesis-related genes such as UCP1. Our data provide new evidence that TFE3 regulates lipid metabolism by controlling the gene expression related to lipolysis and thermogenesis in adipose tissue.


1989 ◽  
Vol 259 (3) ◽  
pp. 673-678 ◽  
Author(s):  
J M Argilés ◽  
F J Lopez-Soriano ◽  
R D Evans ◽  
D H Williamson

Intravenous administration of a single dose (20 micrograms) of recombinant interleukin-1-beta to virgin, lactating and litter-removed rats rapidly decreased intestinal lipid absorption in all groups. In vivo, oxidation of [14C]triolein to 14CO2 was also significantly decreased by interleukin-1. In addition, the cytokine decreased [14C]lipid accumulation in the mammary gland of lactating rats and in the adipose tissue of virgin and litter-removed rats. The decrease in lipid uptake in the interleukin-treated rats was accompanied by hypertriglyceridaemia; however, there was no significant decrease in tissue lipoprotein lipase activity, except in heart from lactating rats. In contrast, interleukin-1 administration had no effect on lipogenesis in liver, white or brown adipose tissue of virgin rats fed on glucose. These results suggest that interleukin-1 profoundly affects lipid metabolism by delaying intestinal absorption and decreasing tissue uptake.


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

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