Biosynthetic capacity and regulatory aspects of prostaglandin E2 formation in adipocytes.

In contrast to previous studies, Parker et al. (Diabetes (1989) 38, 1123) have recently found that isolated rat adipocytes alone were unable to synthesize prostaglandins (PG) and that the PG measured in adipocyte suspensions were due to contaminating non-adipocyte cells. In the present study the capacity of adipocytes to produce PGE2 has further been explored. Preparations of isolated rat adipocytes were extensively washed in order to get rid of contaminating cells. The released PGE2 was measured by radioimmunoassay (RIA) after high-performance liquid chromatography (HPLC) separation. We found that after repetitive washing (up to 20 times) the isolated adipocytes were still able to synthesize PGE2 and this process was fully activatable by epinephrine, which indicates that pure adipocytes, themselves, are able to produce PGE2. However, addition of non-adipocyte material (from the adipose tissue) to 'pure' adipocytes (washed 10 times) enhanced the PGE2 synthesis significantly (P less than 0.001) as compared to 'pure' adipocytes alone. Thus, some kind of synergy exists between adipocytes and non-adipocyte cells in the adipose tissue in respect to PG formation. Some regulatory aspects of PG synthesis in 'pure' adipocytes were also investigated. Phospholipase A2 (2 U/ml) enhanced PGE2 synthesis significantly (119 +/- 21 to 658 +/- 85 pg/10(6) cells, P less than 0.001) without affecting lipolysis (glycerol release). The combined effect of epinephrine (5 microM) and phospholipase A2 (2 U/ml) on PGE2 formation was almost additive. Insulin inhibited the epinephrine-induced PG formation (P less than 0.01) but had no effects on the action induced by phospholipase A2.(ABSTRACT TRUNCATED AT 250 WORDS)