Interpretive Summary: Evaluation of conjugated linoleic acid supplementation on markers of joint inflammation and cartilage metabolism in young horses challenged with lipopolysaccharide.
By: Surely Wallace
In an article published in the 2018 February issue of the Journal of Animal Science, researchers studied the effect of dietary conjugated linoleic acid (CLA) on bacterial lipopolysaccharide (LPS)-induced joint inflammation in horses. The goal was to determine if serum and synovial fluid concentration of CLA increased with supplementation, and whether this provided any protective anti-inflammatory effect that could be useful to treat osteoarthritis (OA) in horses.
Equine OA is a chronic degenerative process resulting from an injury or inflammation. It is a significant cause of equine lameness and affects both young and old horses. There is no cure for OA and long-term use of steroidal or non-steroidal anti-inflammatories have unwanted adverse effects. So, alternative treatments are needed. Glucosamine and omega 3 fatty acids were reported to have poor bioavailability or palpability in horses. The authors therefore investigated CLA, which was previously successful in reducing inflammation in pigs challenged with LPS.
The study period lasted 56 days and included 34 animals (17 yearling Quarter Horses, 9 fillies, 8 geldings). Animals were randomly separated into isocaloric control (“CON” 1% soybean oil) and treatment groups (“LOW” with 0.5% soybean oil and 0.5% CLA, and “HIGH” with 1% CLA). Phase I (days 1– 41) measured fatty acid concentration in serum and synovial fluid. At the start of Phase II (days 42–56), LPS from Escherichia coli 055:B5 was injected into the radial carpal joints of treatment animals; controls received Lactated Ringer solution (LRS). Synovial fluid was collected at 6, 12, 24 hours, and 7 and 14 days for analysis of cartilage metabolism biomarkers (C2C and CPII) and pro-inflammatory mediator PGE2.
During Phase I, serum CLA increased in LOW horses with peak concentration at 28 days. In HIGH horses, serum CLA peaked at 42 days then decreased from day 42 to 56 (concurrent with LPS challenge). No CLA was detected in CON horses. Additionally, arachidonic acid (PGE2 precursor) concentration was lower in the serum and synovial fluid of HIGH, compared with LOW and CON horses. During Phase II, there was no significant effect of diet on synovial PGE2 concentrations in LPS-challenged horses. However, cartilage degradation biomarker C2C was lower with dietary CLA treatment, with a greater decrease noted in the HIGH group. There was no significant difference in CPII (cartilage repair biomarker) with CLA, however the authors noted that CPII remained elevated over baseline even at the end of the study period.
This study suggests that dietary CLA may possibly play a role in mitigation of acute joint inflammation in horses by affecting inflammatory precursors and cartilage degradation biomolecules. With further study into better understanding these potential effects, there may be possible use of CLA as an OA nutraceutical in horses. The authors suggest that more in-depth studies into the effects of CLA on cartilage metabolism with specific focus on type II collagen (CPII), and with a larger study group size are needed.
To view the full article, “Evaluation of conjugated linoleic acid supplementation on markers of joint inflammation and cartilage metabolism in young horses challenged with lipopolysaccharide,” visit the Journal of Animal Science.