Effects of different dietary saturated fatty acid consumption on cartilage health: evidence from preclinical rat models

Effects of different dietary saturated fatty acid consumption on cartilage health: evidence from preclinical rat models

Purpose: The source, type and level of saturation of dietary fats may be critical factors underlying an inflammatory condition in articular joints and contribute to the development of osteoarthritis (OA). Saturated fats are characterized as triglycerides with fatty acids that have no double bonds between carbon atoms. Western diet predominantly consist of fats rich in stearic acid, palmitic acid, myristic acid and lauric acid, all saturated fats. To date there are no studies that have investigated if any of these fatty acids can lead to articular cartilage damage in the joints. The goal of the present study is to evaluate the effects of different types of saturated diets on joint cartilage in a rat model.

Methods: To evaluate the chronic impact of a diet high in saturated fats on joint cartilage health,male wistar rats, weighing 330-340 g, were fed either a corn starch diet or a diet rich in simple sugars including fructose together with either lauric acid (C12), myristic acid (C14), palmitic acid (C16), stearic acid (C18) or beef tallow (mainly stearic and trans fatty acids). After 16 weeks, the knee joints were assessed by micro-CT, histology, and immunohistochemistry for changes to articular cartilage,
synovial membrane, and bone morphology. Serum cytokine concentrations were assessed with multiplex cytokine assays to determine levels of the inflammatory cytokines IL-1, IL-6 and TNF. The lipid profile, glucose levels, body weight and food consumption of the animals were recorded throughout the study period.

Results: This study showed that rats on high carbohydrate-, stearic acid-, or plamitic acid-rich diets had degenerative cartilage changes similar to that seen in OA cartilage. Suprisingly, animals that were fed lauric acid and myristic acid saturated fats had cartilage structures that were indistinguishable from corn starch fed controls, suggesting that the type of dietary fatty acids play a significant role in OA risk. As cartilage changes progressed, it was observed that diets supplemented with stearic acid and palmitic acid coincided with significantly increased glucose intolerance, abdominal obesity, hypertension and fatty liver, whereas rats fed lauric and myristic acid fats these effects lessened.

Conclusions: This study indicates that effect of saturated fats on OA risk depends on the type of fatty acids present in the food. Thus, reducing or modulating certain types of saturated fatty acids in the diet may contribute to prevent or slow the progression of OA.

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