High Fat Diet Induced Longitudinal Metabolic Changes Contribute to Acceleration of Osteoarthritis in Mice

Poulami Datta¹, Yue Zhang^2,3, Alexa Parousis¹, Anirudh Sharma¹, Evgeny Rossomacha¹, Rajiv Gandhi¹, Jason Rockel¹ and Mohit Kapoor¹, ¹Toronto Western Research Institute, University Health Network, Toronto, ON, Canada, ²Toronto Western Hospital, Arthritis Program, University Health Network, Toronto, ON, Canada, ³The first clinical college, Harbin Medical University, Harbin, China

Meeting: 2016 ACR/ARHP Annual Meeting

Date of first publication: September 28, 2016

Keywords: dietary supplements, Mouse model, obesity, osteoarthritis and surgery

Session Information

Date: Tuesday, November 15, 2016

Title: Biology and Pathology of Bone and Joint - Poster I

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: The contribution of metabolic changes induced by high fat diet (HFD) to OA is poorly understood. We sought to determine if diet regulates longitudinal changes to metabolic factors that contribute to OA.

Methods: Mice were fed normal chow diet until 9 weeks of age and then placed onto HFD or lean diet (LD) for 18 weeks, followed by resumption of normal chow, and evaluated longitudinally up to 12 months of age. Some mice were subjected to surgically-induced OA at the end of special diet. Plasma and knee joints were collected at each time points.

Results: We determined that HFD significantly increased fasting blood glucose levels, body weight, BMI and leptin levels as compared to LD fed mice. Histopathological analysis using OARSI scoring clearly showed that HFD fed mice exhibited accelerated spontaneous OA at 9 months of age as well as acceleration in the surgically induced OA at 10 and 20 wks post surgery in comparison to LD fed mice. Of the 170 metabolites analysed in blood plasma at each time point, lysophosphatidyl choline analogues (lysoPCaC20:4, lysoPCaC17:0, lysoPCaC18:0) and one phosphatidyl choline analogue (PCaaC36:2) were increased longitudinally in the HFD fed mice. Our ongoing studies are now evaluating if these LysoPC metabolomics signatures are responsible for initiating and accelerating cartilage degradative process observed in HFD fed mice and if we may predict the osteoarthritis severity by using some biomarkers as well as the involvement of the leptin-driven pathway.

Conclusion: We identified that high fat diet induces and maintains selective metabolic changes and increases OA progression in both spontaneous and surgically induced OA. We anticipate that these identified metabolomics signatures are involved in OA pathogenesis during obesity and therapeutic modulation of leptin pathway may help to attenuate or reverse OA pathologies.

*PD & YZ has equal first author contribution

Disclosure: P. Datta, None; Y. Zhang, None; A. Parousis, None; A. Sharma, None; E. Rossomacha, None; R. Gandhi, None; J. Rockel, None; M. Kapoor, None.

To cite this abstract in AMA style:

Datta P, Zhang Y, Parousis A, Sharma A, Rossomacha E, Gandhi R, Rockel J, Kapoor M. High Fat Diet Induced Longitudinal Metabolic Changes Contribute to Acceleration of Osteoarthritis in Mice [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/high-fat-diet-induced-longitudinal-metabolic-changes-contribute-to-acceleration-of-osteoarthritis-in-mice/. Accessed .

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