Purpose. Complement plays an important role in the pathogenesis of @entity1020 ( @entity1020 ) and trials are currently being conducted to investigate the effect of complement inhibition on @entity1020 progression. We previously found that the plasma level of @entity47528 ( @entity47528 ), which is the rate limiting enzyme of the complement alternative pathway, was significantly decreased following @entity8665 supplementation. @entity47528 is synthesized by adipose tissue, which is also the main storage site of @entity8665 . In view of these findings we tested the hypothesis whether @entity8665 could affect @entity47528 synthesis by adipocytes. Methods. A cell line of mature @entity1 adipocytes was incubated with 50    g/mL @entity8665 for 24 and 48   h, whereafter @entity47528 mRNA and protein expression were measured. Results. @entity8665 significantly inhibited adipocyte @entity47528 mRNA expression and @entity47528 protein release into adipocyte culture supernatants. Conclusions. Our earlier observations showing that a daily @entity8665 supplement in individuals with early signs of @entity1020 lowered the level of circulating @entity47528 might be caused by blocking adipocyte @entity47528 production.

XXXX Leads to a Decrease of Factor D Secretion by Cultured Mature @entity1 Adipocytes.

@entity1 :: ('9606', 'Species') :: ['human'] @entity1020 :: ('MESH:D008268', 'Disease') :: ['age related macular degeneration', 'AMD'] @entity47528 :: ('MESH:C565027', 'Disease') :: ['FD', 'factor D'] @entity8665 :: ('MESH:D014975', 'Chemical') :: ['lutein', 'Lutein']
@entity8665 :: (MESH:D014975,Chemical) :: ['Lutein']
