A high-fat diet has negative effects on tendon resident cells in an in vivo rat model.


Journal

International orthopaedics
ISSN: 1432-5195
Titre abrégé: Int Orthop
Pays: Germany
ID NLM: 7705431

Informations de publication

Date de publication:
05 2022
Historique:
received: 02 10 2021
accepted: 04 02 2022
pubmed: 25 2 2022
medline: 14 4 2022
entrez: 24 2 2022
Statut: ppublish

Résumé

Tendinopathy is a major complication of diet-induced obesity. However, the effects of a high-fat diet (HFD) on tendon have not been well characterised. We aimed to determine: [1] the impact of a HFD on tendon properties and gene expression; and [2] whether dietary transition to a control diet (CD) could restore normal tendon health. Sprague-Dawley rats were randomised into three groups from weaning and fed either a: CD, HFD or HFD for 12 weeks and then CD thereafter (HF-CD). Biomechanical, histological and structural evaluation of the Achilles tendon was performed at 17 and 27 weeks of age. Tail tenocytes were isolated with growth rate and collagen production determined. Tenocytes and activated THP-1 cells were exposed to conditioned media (CM) of visceral adipose tissue explants, and gene expression was analysed. There were no differences in the biomechanical, histological or structural tendon properties between groups. However, tenocyte growth and collagen production were increased in the HFD group at 27 weeks. There was lower SOX-9 expression in the HFD and HF-CD groups at 17 weeks and higher expression of collagen-Iα1 and matrix metalloproteinase-13 in the HFD group at 27 weeks. THP-1 cells exposed to adipose tissue CM from animals fed a HFD or HF-CD had lower expression of Il-10 and higher expression of Il-1β. In this rodent model, a HFD negatively altered tendon cell characteristics. Dietary intervention restored some gene expression changes; however, adipose tissue secretions from the HF-CD group promoted an increased inflammatory state in macrophages. These changes may predispose tendon to injury and adverse events later in life.

Sections du résumé

BACKGROUND
Tendinopathy is a major complication of diet-induced obesity. However, the effects of a high-fat diet (HFD) on tendon have not been well characterised. We aimed to determine: [1] the impact of a HFD on tendon properties and gene expression; and [2] whether dietary transition to a control diet (CD) could restore normal tendon health.
METHODS
Sprague-Dawley rats were randomised into three groups from weaning and fed either a: CD, HFD or HFD for 12 weeks and then CD thereafter (HF-CD). Biomechanical, histological and structural evaluation of the Achilles tendon was performed at 17 and 27 weeks of age. Tail tenocytes were isolated with growth rate and collagen production determined. Tenocytes and activated THP-1 cells were exposed to conditioned media (CM) of visceral adipose tissue explants, and gene expression was analysed.
RESULTS
There were no differences in the biomechanical, histological or structural tendon properties between groups. However, tenocyte growth and collagen production were increased in the HFD group at 27 weeks. There was lower SOX-9 expression in the HFD and HF-CD groups at 17 weeks and higher expression of collagen-Iα1 and matrix metalloproteinase-13 in the HFD group at 27 weeks. THP-1 cells exposed to adipose tissue CM from animals fed a HFD or HF-CD had lower expression of Il-10 and higher expression of Il-1β.
CONCLUSIONS
In this rodent model, a HFD negatively altered tendon cell characteristics. Dietary intervention restored some gene expression changes; however, adipose tissue secretions from the HF-CD group promoted an increased inflammatory state in macrophages. These changes may predispose tendon to injury and adverse events later in life.

Identifiants

pubmed: 35201374
doi: 10.1007/s00264-022-05340-1
pii: 10.1007/s00264-022-05340-1
pmc: PMC9001221
doi:

Substances chimiques

Collagen 9007-34-5

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1181-1190

Informations de copyright

© 2022. The Author(s).

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Auteurs

Scott M Bolam (SM)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.
Department of Orthopedic Surgery, Auckland City Hospital, 2 Park Road, Grafton, Auckland, New Zealand.

Subhajit Konar (S)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.

Young-Eun Park (YE)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.

Karen E Callon (KE)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.

Josh Workman (J)

Chemical and Materials Engineering, University of Auckland, 5 Grafton Rd, Auckland, New Zealand.

A Paul Monk (AP)

Department of Orthopedic Surgery, Auckland City Hospital, 2 Park Road, Grafton, Auckland, New Zealand.
Auckland Bioengineering Institute, University of Auckland, 70 Symonds St, Grafton, Auckland, New Zealand.

Brendan Coleman (B)

Department of Orthopedic Surgery, Middlemore Hospital, 100 Hospital Road, Otahuhu, Auckland, New Zealand.

Jillian Cornish (J)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.

Mark H Vickers (MH)

Liggins Institute, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.

Jacob T Munro (JT)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand.
Department of Orthopedic Surgery, Auckland City Hospital, 2 Park Road, Grafton, Auckland, New Zealand.

David S Musson (DS)

Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand. d.musson@auckland.ac.nz.
Department of Nutrition & Dietetics, University of Auckland, 85 Park Road, Grafton, 1023, Auckland, New Zealand. d.musson@auckland.ac.nz.

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