Abstract

Purpose: Experimental studies show that administering diets rich in lipids (high fat diets) leads to osteoarthritis (OA). Thus, it appears from the available literature that the source, or type of dietary fat and its level of saturation may be a critical factor in the development of an underlying inflammatory condition in the body that may lead to OA development. There are different types of saturated fatty acids. Western diet predominantly consist of fats rich in stearic acid, palmitic acid, myristic acid and lauric acid. However, so far no studies have investigated what type of saturated fatty acid in particular lead to cartilage damage. Therefore the goal of this present study is to evaluate the effects of administering different types of saturated diets on the morphology of the cartilage, subchondral bone and pain related behavior. Methods: The current study evaluates the chronic impact of high saturated fat feeding on joint cartilage health using a rat model. Male wistar rats weighing 330–340g received either 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, knee OA was assessed by cartilage and synovium histology in addition to bone morphology. Serum cytokine concentrations were determined with multiplex assay. We further monitored lipid profile, glucose levels, and body weight and food consumption throughout the study period. Furthermore, the influence of different saturated fatty acid (SFA) types on the progression of OA was evaluated in menisectomy OA model by monitoring pain-related behavior, the changes in glial activity in the spinal cord (SC) and the dorsal root ganglions (DRG) of rats fed with the different saturated fat diets. Results: Our results indicate that the rats on a high-carbohydrate diet, stearic acid rich and plamitic acid diet showed cartilage degenerative changes that are similar to OA cartilage. Surprisingly, the rats that were fed with lauric acid and myristic acid saturated fats showed similar cartilage structure to control rats that were fed with corn starch diet, indicating marked differences in OA risk depending on the type of dietary fatty acids. As cartilage changes progress, we found that supplementation with stearic acid and palmitic acid markedly increased glucose intolerance, abdominal obesity, hypertension and fatty liver. However such effects were decreased in the rats that are fed with lauric and myristic acid fats. Furthermore, the rats on palmitic (PA) and stearic acid (SA) diets increased the progression of OA in menisectomy rats, which was characterized by increased knee cartilage degeneration and decreased bone volume density (BMD). In addition, these diet groups also exhibited decreased hind paw withdrawal thresholds, grip strength, and increased joint hypersensitivity compared to the other saturated fat groups. Furthermore, significant spinal astrogliosis and microgliosis were also observed in these diet groups. On the contrary, lauric acid (LA) diet group rats exhibited decreased degeneration of the cartilage, increased hind paw withdrawal thresholds, grip strength and decreased joint hypersensitivity. In addition, lower number of spinal GFAP and IBA-1 positive cells were observed signifying decreased astrogliosis and microgliosis respectively. Conclusions: In conclusion, our study indicates that effect of saturated fats on OA risk and pain depends on the kind of fatty acids present in the blood. Thus, reducing or modulating certain types of saturated fatty acids in the diet may help in preventing or slowing the progression of OA.

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