Profibrotic Infrapatellar Fat Pad Remodeling Without M1 Macrophage Polarization Precedes Knee Osteoarthritis in Mice With Diet‐Induced Obesity

Objective To test the hypothesis that high‐fat (HF) diet–induced obesity increases proinflammatory cytokine expression, macrophage infiltration, and M1 polarization in the infrapatellar fat pad (IFP) prior to knee cartilage degeneration. Methods We characterized the effect of HF feeding on knee OA p...

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Veröffentlicht in:Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2017-06, Vol.69 (6), p.1221-1232
Hauptverfasser: Barboza, Erika, Hudson, Joanna, Chang, Wan‐Pin, Kovats, Susan, Towner, Rheal A., Silasi‐Mansat, Robert, Lupu, Florea, Kent, Collin, Griffin, Timothy M.
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container_issue 6
container_start_page 1221
container_title Arthritis & rheumatology (Hoboken, N.J.)
container_volume 69
creator Barboza, Erika
Hudson, Joanna
Chang, Wan‐Pin
Kovats, Susan
Towner, Rheal A.
Silasi‐Mansat, Robert
Lupu, Florea
Kent, Collin
Griffin, Timothy M.
description Objective To test the hypothesis that high‐fat (HF) diet–induced obesity increases proinflammatory cytokine expression, macrophage infiltration, and M1 polarization in the infrapatellar fat pad (IFP) prior to knee cartilage degeneration. Methods We characterized the effect of HF feeding on knee OA pathology, body adiposity, and glucose intolerance in male C57BL/6J mice and identified a diet duration that induces metabolic dysfunction prior to cartilage degeneration. Magnetic resonance imaging and histomorphology were used to quantify changes in the epididymal, subcutaneous, and infrapatellar fat pads and in adipocyte sizes. Finally, we used targeted gene expression and protein arrays, immunohistochemistry, and flow cytometry to quantify differences in fat pad markers of inflammation and immune cell populations. Results Twenty weeks of feeding with an HF diet induced marked obesity, glucose intolerance, and early osteoarthritis (OA), including osteophytes and cartilage tidemark duplication. This duration of HF feeding increased the IFP volume. However, it did not increase IFP inflammation, macrophage infiltration, or M1 macrophage polarization as observed in epididymal fat. Furthermore, leptin protein levels were reduced. This protection from obesity‐induced inflammation corresponded to increased IFP fibrosis and the absence of adipocyte hypertrophy. Conclusion The IFP does not recapitulate classic abdominal adipose tissue inflammation during the early stages of knee OA in an HF diet–induced model of obesity. Consequently, these findings do not support the hypothesis that IFP inflammation is an initiating factor of obesity‐induced knee OA. Furthermore, the profibrotic and antihypertrophic responses of IFP adipocytes to HF feeding suggest that intraarticular adipocytes are subject to distinct spatiotemporal structural and metabolic regulation among fat pads.
doi_str_mv 10.1002/art.40056
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Methods We characterized the effect of HF feeding on knee OA pathology, body adiposity, and glucose intolerance in male C57BL/6J mice and identified a diet duration that induces metabolic dysfunction prior to cartilage degeneration. Magnetic resonance imaging and histomorphology were used to quantify changes in the epididymal, subcutaneous, and infrapatellar fat pads and in adipocyte sizes. Finally, we used targeted gene expression and protein arrays, immunohistochemistry, and flow cytometry to quantify differences in fat pad markers of inflammation and immune cell populations. Results Twenty weeks of feeding with an HF diet induced marked obesity, glucose intolerance, and early osteoarthritis (OA), including osteophytes and cartilage tidemark duplication. This duration of HF feeding increased the IFP volume. However, it did not increase IFP inflammation, macrophage infiltration, or M1 macrophage polarization as observed in epididymal fat. Furthermore, leptin protein levels were reduced. This protection from obesity‐induced inflammation corresponded to increased IFP fibrosis and the absence of adipocyte hypertrophy. Conclusion The IFP does not recapitulate classic abdominal adipose tissue inflammation during the early stages of knee OA in an HF diet–induced model of obesity. Consequently, these findings do not support the hypothesis that IFP inflammation is an initiating factor of obesity‐induced knee OA. Furthermore, the profibrotic and antihypertrophic responses of IFP adipocytes to HF feeding suggest that intraarticular adipocytes are subject to distinct spatiotemporal structural and metabolic regulation among fat pads.</description><identifier>ISSN: 2326-5191</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.40056</identifier><identifier>PMID: 28141918</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Abdominal Fat ; Adipocytes ; Adipocytes - metabolism ; Adipocytes - pathology ; Adipose tissue ; Adipose Tissue - diagnostic imaging ; Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Animals ; Arthritis ; Cartilage ; Cartilage diseases ; Degeneration ; Diet ; Diet, High-Fat ; Feeding ; Fibrosis ; Flow cytometry ; Gene expression ; Glucose ; Glucose Intolerance - etiology ; Glucose Intolerance - metabolism ; Glucose tolerance ; Hypertrophy ; Hypotheses ; Immune system ; Immunohistochemistry ; Infiltration ; Inflammation ; Inflammation Mediators - metabolism ; Intolerance ; Knee ; Knee Joint - metabolism ; Knee Joint - pathology ; Leptin ; Leptin - metabolism ; Macrophages ; Macrophages - metabolism ; Magnetic resonance imaging ; Magnetic Resonance Imaging - methods ; Male ; Metabolism ; Mice ; Mice, Inbred C57BL ; Obesity ; Obesity - etiology ; Obesity - metabolism ; Osteoarthritis ; Osteoarthritis, Knee - etiology ; Osteoarthritis, Knee - metabolism ; Osteophytes ; Polarization ; Protein arrays ; Proteins ; Rodents ; Time Factors</subject><ispartof>Arthritis &amp; rheumatology (Hoboken, N.J.), 2017-06, Vol.69 (6), p.1221-1232</ispartof><rights>2017, American College of Rheumatology</rights><rights>2017, American College of Rheumatology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3886-3a92fbd7efca34a0ea97cec420ee515a64990e4496b25c9d455b2af22bec321f3</citedby><cites>FETCH-LOGICAL-c3886-3a92fbd7efca34a0ea97cec420ee515a64990e4496b25c9d455b2af22bec321f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fart.40056$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.40056$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28141918$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Barboza, Erika</creatorcontrib><creatorcontrib>Hudson, Joanna</creatorcontrib><creatorcontrib>Chang, Wan‐Pin</creatorcontrib><creatorcontrib>Kovats, Susan</creatorcontrib><creatorcontrib>Towner, Rheal A.</creatorcontrib><creatorcontrib>Silasi‐Mansat, Robert</creatorcontrib><creatorcontrib>Lupu, Florea</creatorcontrib><creatorcontrib>Kent, Collin</creatorcontrib><creatorcontrib>Griffin, Timothy M.</creatorcontrib><title>Profibrotic Infrapatellar Fat Pad Remodeling Without M1 Macrophage Polarization Precedes Knee Osteoarthritis in Mice With Diet‐Induced Obesity</title><title>Arthritis &amp; rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheumatol</addtitle><description>Objective To test the hypothesis that high‐fat (HF) diet–induced obesity increases proinflammatory cytokine expression, macrophage infiltration, and M1 polarization in the infrapatellar fat pad (IFP) prior to knee cartilage degeneration. Methods We characterized the effect of HF feeding on knee OA pathology, body adiposity, and glucose intolerance in male C57BL/6J mice and identified a diet duration that induces metabolic dysfunction prior to cartilage degeneration. Magnetic resonance imaging and histomorphology were used to quantify changes in the epididymal, subcutaneous, and infrapatellar fat pads and in adipocyte sizes. Finally, we used targeted gene expression and protein arrays, immunohistochemistry, and flow cytometry to quantify differences in fat pad markers of inflammation and immune cell populations. Results Twenty weeks of feeding with an HF diet induced marked obesity, glucose intolerance, and early osteoarthritis (OA), including osteophytes and cartilage tidemark duplication. This duration of HF feeding increased the IFP volume. However, it did not increase IFP inflammation, macrophage infiltration, or M1 macrophage polarization as observed in epididymal fat. Furthermore, leptin protein levels were reduced. This protection from obesity‐induced inflammation corresponded to increased IFP fibrosis and the absence of adipocyte hypertrophy. Conclusion The IFP does not recapitulate classic abdominal adipose tissue inflammation during the early stages of knee OA in an HF diet–induced model of obesity. Consequently, these findings do not support the hypothesis that IFP inflammation is an initiating factor of obesity‐induced knee OA. 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rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis Rheumatol</addtitle><date>2017-06</date><risdate>2017</risdate><volume>69</volume><issue>6</issue><spage>1221</spage><epage>1232</epage><pages>1221-1232</pages><issn>2326-5191</issn><eissn>2326-5205</eissn><abstract>Objective To test the hypothesis that high‐fat (HF) diet–induced obesity increases proinflammatory cytokine expression, macrophage infiltration, and M1 polarization in the infrapatellar fat pad (IFP) prior to knee cartilage degeneration. Methods We characterized the effect of HF feeding on knee OA pathology, body adiposity, and glucose intolerance in male C57BL/6J mice and identified a diet duration that induces metabolic dysfunction prior to cartilage degeneration. Magnetic resonance imaging and histomorphology were used to quantify changes in the epididymal, subcutaneous, and infrapatellar fat pads and in adipocyte sizes. Finally, we used targeted gene expression and protein arrays, immunohistochemistry, and flow cytometry to quantify differences in fat pad markers of inflammation and immune cell populations. Results Twenty weeks of feeding with an HF diet induced marked obesity, glucose intolerance, and early osteoarthritis (OA), including osteophytes and cartilage tidemark duplication. This duration of HF feeding increased the IFP volume. However, it did not increase IFP inflammation, macrophage infiltration, or M1 macrophage polarization as observed in epididymal fat. Furthermore, leptin protein levels were reduced. This protection from obesity‐induced inflammation corresponded to increased IFP fibrosis and the absence of adipocyte hypertrophy. Conclusion The IFP does not recapitulate classic abdominal adipose tissue inflammation during the early stages of knee OA in an HF diet–induced model of obesity. Consequently, these findings do not support the hypothesis that IFP inflammation is an initiating factor of obesity‐induced knee OA. Furthermore, the profibrotic and antihypertrophic responses of IFP adipocytes to HF feeding suggest that intraarticular adipocytes are subject to distinct spatiotemporal structural and metabolic regulation among fat pads.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28141918</pmid><doi>10.1002/art.40056</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Alma/SFX Local Collection; Wiley Blackwell Journals
subjects Abdominal Fat
Adipocytes
Adipocytes - metabolism
Adipocytes - pathology
Adipose tissue
Adipose Tissue - diagnostic imaging
Adipose Tissue - metabolism
Adipose Tissue - pathology
Animals
Arthritis
Cartilage
Cartilage diseases
Degeneration
Diet
Diet, High-Fat
Feeding
Fibrosis
Flow cytometry
Gene expression
Glucose
Glucose Intolerance - etiology
Glucose Intolerance - metabolism
Glucose tolerance
Hypertrophy
Hypotheses
Immune system
Immunohistochemistry
Infiltration
Inflammation
Inflammation Mediators - metabolism
Intolerance
Knee
Knee Joint - metabolism
Knee Joint - pathology
Leptin
Leptin - metabolism
Macrophages
Macrophages - metabolism
Magnetic resonance imaging
Magnetic Resonance Imaging - methods
Male
Metabolism
Mice
Mice, Inbred C57BL
Obesity
Obesity - etiology
Obesity - metabolism
Osteoarthritis
Osteoarthritis, Knee - etiology
Osteoarthritis, Knee - metabolism
Osteophytes
Polarization
Protein arrays
Proteins
Rodents
Time Factors
title Profibrotic Infrapatellar Fat Pad Remodeling Without M1 Macrophage Polarization Precedes Knee Osteoarthritis in Mice With Diet‐Induced Obesity
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