Active-dimeric form of lipoprotein lipase increases in the adipose tissue of patients with rheumatoid arthritis treated with prednisolone.

The synthesis, activity and mass of LPL in adipose tissue were studied in patients with rheumatoid arthritis (RA) treated with prednisolone (PSL) (PSL-treated group) and untreated patients with osteoarthritis (untreated group). LPL activity and mass in the extracts of acetone/ether powder of adipose tissue were 2.4 and 1.6 times, respectively, higher in the PSL-treated group than in the untreated group. There were no differences in the amount of 35S incorporated into LPL during the 2-h incubation of adipose tissue with [35S]methionine between PSL-treated and untreated groups. These results indicate that degradation of LPL was inhibited in the adipose tissue of the PSL-treated group. In the adipose tissue of the untreated group, 72% of the LPL was the inactive-monomeric form, which was eluted with 0.4-0.75 M NaCl from the heparin-Sepharose column, and 28% was the active-dimeric form, which was eluted with 0.8-1.2 M NaCl. In the adipose tissue of the PSL-treated group, 40% was inactive-monomeric, and 60% was active-dimeric. Thus, the relative amount of the active-dimeric form of LPL was increased in the adipose tissue of the PSL-treated group. Taken together, our present results indicate that the higher level of LPL activity in the PSL-treated group was a result of the inhibition of the degradation of the active-dimeric form.