Elimination of fibrin polymer formation or crosslinking, but not fibrinogen deficiency, is protective against diet-induced obesity and associated pathologies

CONCLUSIONS: Consistent with prior studies, Fib𝛾390-396A mice were significantly protected from increased adiposity, NAFLD, hypercholesterolemia and diabetes while Fib- and siFga-treated mice gained as much weight and developed obesity-associated pathologies identical to wildtype mice. FibAEK and FXIII- mice displayed an intermediate phenotype with partial protection from some obesity-associated pathologies. Results here indicate that fibrin(ogen) lacking αM β2 binding function offers substantial protection from obesity and associated disease that is partially recapitulated by preventing fibrin polymer formation or crosslinking of the wildtype molecule, but not by reduction or complete elimination of fibrinogen. Finally, these findings support the concept that fibrin polymerization and crosslinking are required for the full implementation of fibrin-driven inflammation in obesity.PMID:36111375 | DOI:10.1111/jth.15877

Source: Thrombosis and Haemostasis - September 16, 2022 Category: Hematology Authors: Woosuk S Hur Katharine C King Yesha N Patel Y-Van Nguyen Zimu Wei Yi Yang Lih Jiin Juang Jerry Leung Christian J Kastrup Alisa S Wolberg James P Luyendyk Matthew J Flick Source Type: research