Mice lacking C1q are protected from high fat diet-induced hepatic insulin resistance and impaired glucose homeostasis

Abstract

Background: Complement is implicated in obesity and insulin resistance; however, the specific complement activation pathway involved is not known. Results: C1q in the classical pathway is required for activation of complement in response to high fat diets. Conclusion: C1q is an important contributor to high fat diet-induced insulin resistance. Significance: C1q may be an important therapeutic target for treating the derangements in metabolism associated with obesity. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.