Adipose tissue is a critical regulator of osteoarthritis

Author:

Collins Kelsey H.ORCID,Lenz Kristin L.,Pollitt Eleanor N.,Ferguson DanielORCID,Hutson Irina,Springer Luke E.,Oestreich Arin K.ORCID,Tang RuhangORCID,Choi Yun-Rak,Meyer Gretchen A.,Teitelbaum Steven L.,Pham Christine T. N.ORCID,Harris Charles A.,Guilak FarshidORCID

Abstract

Osteoarthritis (OA), the leading cause of pain and disability worldwide, disproportionally affects individuals with obesity. The mechanisms by which obesity leads to the onset and progression of OA are unclear due to the complex interactions among the metabolic, biomechanical, and inflammatory factors that accompany increased adiposity. We used a murine preclinical model of lipodystrophy (LD) to examine the direct contribution of adipose tissue to OA. Knee joints of LD mice were protected from spontaneous or posttraumatic OA, on either a chow or high-fat diet, despite similar body weight and the presence of systemic inflammation. These findings indicate that adipose tissue itself plays a critical role in the pathophysiology of OA. Susceptibility to posttraumatic OA was reintroduced into LD mice using implantation of a small adipose tissue depot derived from wild-type animals or mouse embryonic fibroblasts that undergo spontaneous adipogenesis, implicating paracrine signaling from fat, rather than body weight, as a mediator of joint degeneration.

Funder

HHS | National Institutes of Health

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

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