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Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy

BACKGROUND: 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 Kag...

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Autores principales: Pingel, Jessica, Petersen, M. Christine H., Fredberg, Ulrich, Kjær, Søren G., Quistorff, Bjørn, Langberg, Henning, Hansen, Jacob B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440827/
https://www.ncbi.nlm.nih.gov/pubmed/25996876
http://dx.doi.org/10.1371/journal.pone.0127811
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author Pingel, Jessica
Petersen, M. Christine H.
Fredberg, Ulrich
Kjær, Søren G.
Quistorff, Bjørn
Langberg, Henning
Hansen, Jacob B.
author_facet Pingel, Jessica
Petersen, M. Christine H.
Fredberg, Ulrich
Kjær, Søren G.
Quistorff, Bjørn
Langberg, Henning
Hansen, Jacob B.
author_sort Pingel, Jessica
collection PubMed
description BACKGROUND: 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. AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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spelling pubmed-44408272015-05-29 Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy Pingel, Jessica Petersen, M. Christine H. Fredberg, Ulrich Kjær, Søren G. Quistorff, Bjørn Langberg, Henning Hansen, Jacob B. PLoS One Research Article BACKGROUND: 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. AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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. Public Library of Science 2015-05-21 /pmc/articles/PMC4440827/ /pubmed/25996876 http://dx.doi.org/10.1371/journal.pone.0127811 Text en © 2015 Pingel et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Pingel, Jessica
Petersen, M. Christine H.
Fredberg, Ulrich
Kjær, Søren G.
Quistorff, Bjørn
Langberg, Henning
Hansen, Jacob B.
Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy
title Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy
title_full Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy
title_fullStr Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy
title_full_unstemmed Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy
title_short Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy
title_sort inflammatory and metabolic alterations of kager's fat pad in chronic achilles tendinopathy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440827/
https://www.ncbi.nlm.nih.gov/pubmed/25996876
http://dx.doi.org/10.1371/journal.pone.0127811
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