Oleate Prevents Palmitate-Induced Mitochondrial Dysfunction in Chondrocytes

Abstract

The association between obesity and osteoarthritis (OA) in joints not subjected to mechanical overload, together with the relationship between OA and metabolic syndrome, suggests that there are systemic factors related to metabolic disorders that are involved in the metabolic phenotype of OA. The aim of this work is study the effects of palmitate and oleate on cellular metabolism in an “in vitro” model of human chondrocytes. The TC28a2 chondrocyte cell line was used to analyze the effect of palmitate and oleate on mitochondrial and glycolytic function, Adenosine triphosphate (ATP) production and lipid droplets accumulation. Palmitate, but not oleate, produces mitochondrial dysfunction observed with a lower coupling efficiency, maximal respiration and spare respiratory capacity. Glycolytic function showed lower rates both glycolytic capacity and glycolytic reserve when cells were incubated with fatty acids (FAs). The production rate of total and mitochondrial ATP showed lower values in chondrocytes incubated with palmitic acid (PA). The formation of lipid droplets increased in FA conditions, being significantly higher when the cells were incubated with oleic acid (OL). These results may help explain, at least in part, the close relationship of metabolic pathologies with OA, as well as help to elucidate some of the factors that can define a metabolic phenotype in OA.

Differential Effects of Oleic and Palmitic Acids on Lipid Droplet-Mitochondria Interaction in the Hepatic Cell Line HepG2

“…The effect of OA promoting bigger and more abundant LDs compared to PA (Figure 1) (5) has also been observed in other cell types, such as pancreatic β-cells (38), chondrocytes (39), and H9C2 cardiomyoblasts (40). This greater capacity of OA to be esterified to TG and accumulated into LDs likely explains its reduced lipotoxicity compared to PA.…”

Adiponectin, May Be a Potential Protective Factor for Obesity-Related Osteoarthritis

“… 63 In a recent study, it was found that PA causes chondrocyte mitochondrial dysfunction and changes in glycolytic metabolism, and these effects can be partially reversed by MUFAs (such as OL). 64 In a study of the relation between diet and OA progression in 2092 OA patients, with increasing levels of SFA, joint space width decreases were 0.25 mm, 0.26 mm, 0.33 mm, and 0.37 mm at 12, 24, 36, 48 months, respectively. 65 …”

“… 62 Causes chondrocyte mitochondrial dysfunction and changes in glycolytic metabolism. 64 SA Induces the expression of IL-1β, IL-6 and TNF-α. 63 SFA Decreases joint space width.…”