Pingel Jessica, Petersen M Christine H, Fredberg Ulrich, Kjær Søren G, Quistorff Bjørn, Langberg Henning, Hansen Jacob B
Department of Exercise and Nutrition, University of Copenhagen, Copenhagen, Denmark.
Department of Biology, University of Copenhagen, Copenhagen, Denmark; Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
PLoS One. 2015 May 21;10(5):e0127811. doi: 10.1371/journal.pone.0127811. eCollection 2015.
Achilles tendinopathy is a painful inflammatory condition characterized by swelling, stiffness and reduced function of the Achilles tendon. Kager's fat pad is an adipose tissue located in the area anterior to the Achilles tendon. Observations reveal a close physical interplay between Kager's fat pad and its surrounding structures during movement of the ankle, suggesting that Kager's fat pad may stabilize and protect the mechanical function of the ankle joint.
The aim of this study was to characterize whether Achilles tendinopathy was accompanied by changes in expression of inflammatory markers and metabolic enzymes in Kager's fat pad.
A biopsy was taken from Kager's fat pad from 31 patients with chronic Achilles tendinopathy and from 13 healthy individuals. Gene expression was measured by reverse transcription-quantitative PCR. Focus was on genes related to inflammation and lipid metabolism.
Expression of the majority of analyzed inflammatory marker genes was increased in patients with Achilles tendinopathy compared to that in healthy controls. Expression patterns of the patient group were consistent with reduced lipolysis and increased fatty acid β-oxidation. In the fat pad, the pain-signaling neuropeptide substance P was found to be present in one third of the subjects in the Achilles tendinopathy group but in none of the healthy controls.
Gene expression changes in Achilles tendinopathy patient samples were consistent with Kager's fat pad being more inflamed than in the healthy control group. Additionally, the results indicate an altered lipid metabolism in Kager's fat pad of Achilles tendinopathy patients.
跟腱病是一种疼痛性炎症疾病，其特征为跟腱肿胀、僵硬和功能减退。卡格脂肪垫是位于跟腱前方区域的脂肪组织。观察结果显示，在踝关节运动过程中，卡格脂肪垫与其周围结构之间存在密切的物理相互作用，这表明卡格脂肪垫可能稳定并保护踝关节的机械功能。
本研究的目的是确定跟腱病是否伴有卡格脂肪垫中炎症标志物和代谢酶表达的变化。
从31例慢性跟腱病患者和13名健康个体的卡格脂肪垫中获取活检样本。通过逆转录定量PCR测量基因表达。重点关注与炎症和脂质代谢相关的基因。
与健康对照组相比，跟腱病患者中大多数分析的炎症标志物基因的表达增加。患者组的表达模式与脂解减少和脂肪酸β氧化增加一致。在脂肪垫中，发现疼痛信号神经肽P物质在跟腱病组三分之一的受试者中存在，但在健康对照组中均未发现。
跟腱病患者样本中的基因表达变化与卡格脂肪垫比健康对照组炎症更严重一致。此外，结果表明跟腱病患者的卡格脂肪垫中脂质代谢发生了改变。
