Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats

ABSTRACT Leptin is a proinflammatory adipokine that contributes to obesity‐associated osteoarthritis (OA), especially in women. However, the extent to which leptin causes knee OA separate from the effect of increased body weight is not clear. We hypothesized that leptin is necessary to induce knee O...

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Main Authors: Yao Fu, Albert Batushansky, Michael Kinter, Janet L. Huebner, Virginia B. Kraus, Timothy M. Griffin
Format: Article
Language:English
Published: Oxford University Press 2023-07-01
Series:JBMR Plus
Subjects:
Online Access:https://doi.org/10.1002/jbm4.10754
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author Yao Fu
Albert Batushansky
Michael Kinter
Janet L. Huebner
Virginia B. Kraus
Timothy M. Griffin
author_facet Yao Fu
Albert Batushansky
Michael Kinter
Janet L. Huebner
Virginia B. Kraus
Timothy M. Griffin
author_sort Yao Fu
collection DOAJ
description ABSTRACT Leptin is a proinflammatory adipokine that contributes to obesity‐associated osteoarthritis (OA), especially in women. However, the extent to which leptin causes knee OA separate from the effect of increased body weight is not clear. We hypothesized that leptin is necessary to induce knee OA in obese female rats but not sufficient to induce knee OA in lean rats lacking systemic metabolic inflammation. The effect of obesity without leptin signaling was modeled by comparing female lean Zucker rats to pair fed obese Zucker rats, which possess mutant fa alleles of the leptin receptor gene. The effect of leptin without obesity was modeled in female F344BN F1 hybrid rats by systemically administering recombinant rat leptin versus saline for 23 weeks via osmotic pumps. Primary OA outcomes included cartilage histopathology and subchondral bone micro‐computed tomography. Secondary outcomes included targeted cartilage proteomics, serum inflammation, and synovial fluid inflammation following an acute intra‐articular challenge with interleukin‐1β (IL‐1β). Compared to lean Zucker rats, obese Zucker rats developed more severe tibial osteophytes and focal cartilage lesions in the medial tibial plateau, with modest changes in proximal tibial epiphysis trabecular bone structure. In contrast, exogenous leptin treatment, which increased plasma leptin sixfold without altering body weight, caused mild generalized cartilage fibrillation and reduced Safranin O staining compared to vehicle‐treated animals. Leptin also significantly increased subchondral and trabecular bone volume and bone mineral density in the proximal tibia. Cartilage metabolic and antioxidant enzyme protein levels were substantially elevated with leptin deficiency and minimally suppressed with leptin treatment. In contrast, leptin treatment induced greater changes in systemic and local inflammatory mediators compared to leptin receptor deficiency, including reduced serum IL‐6 and increased synovial fluid IL‐1β. In conclusion, rat models that separately elevate leptin or body weight develop distinct OA‐associated phenotypes, revealing how obesity increases OA pathology through both leptin‐dependent and independent pathways. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.
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spelling doaj.art-aa1cc937840a407a886dca46ed9028482024-07-02T22:08:09ZengOxford University PressJBMR Plus2473-40392023-07-0177n/an/a10.1002/jbm4.10754Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female RatsYao Fu0Albert Batushansky1Michael Kinter2Janet L. Huebner3Virginia B. Kraus4Timothy M. Griffin5Aging and Metabolism Research Program Oklahoma Medical Research Foundation Oklahoma City Oklahoma USAAging and Metabolism Research Program Oklahoma Medical Research Foundation Oklahoma City Oklahoma USAAging and Metabolism Research Program Oklahoma Medical Research Foundation Oklahoma City Oklahoma USADuke Molecular Physiology Institute Duke University, School of Medicine, Duke University Durham North Carolina USADuke Molecular Physiology Institute Duke University, School of Medicine, Duke University Durham North Carolina USAAging and Metabolism Research Program Oklahoma Medical Research Foundation Oklahoma City Oklahoma USAABSTRACT Leptin is a proinflammatory adipokine that contributes to obesity‐associated osteoarthritis (OA), especially in women. However, the extent to which leptin causes knee OA separate from the effect of increased body weight is not clear. We hypothesized that leptin is necessary to induce knee OA in obese female rats but not sufficient to induce knee OA in lean rats lacking systemic metabolic inflammation. The effect of obesity without leptin signaling was modeled by comparing female lean Zucker rats to pair fed obese Zucker rats, which possess mutant fa alleles of the leptin receptor gene. The effect of leptin without obesity was modeled in female F344BN F1 hybrid rats by systemically administering recombinant rat leptin versus saline for 23 weeks via osmotic pumps. Primary OA outcomes included cartilage histopathology and subchondral bone micro‐computed tomography. Secondary outcomes included targeted cartilage proteomics, serum inflammation, and synovial fluid inflammation following an acute intra‐articular challenge with interleukin‐1β (IL‐1β). Compared to lean Zucker rats, obese Zucker rats developed more severe tibial osteophytes and focal cartilage lesions in the medial tibial plateau, with modest changes in proximal tibial epiphysis trabecular bone structure. In contrast, exogenous leptin treatment, which increased plasma leptin sixfold without altering body weight, caused mild generalized cartilage fibrillation and reduced Safranin O staining compared to vehicle‐treated animals. Leptin also significantly increased subchondral and trabecular bone volume and bone mineral density in the proximal tibia. Cartilage metabolic and antioxidant enzyme protein levels were substantially elevated with leptin deficiency and minimally suppressed with leptin treatment. In contrast, leptin treatment induced greater changes in systemic and local inflammatory mediators compared to leptin receptor deficiency, including reduced serum IL‐6 and increased synovial fluid IL‐1β. In conclusion, rat models that separately elevate leptin or body weight develop distinct OA‐associated phenotypes, revealing how obesity increases OA pathology through both leptin‐dependent and independent pathways. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.https://doi.org/10.1002/jbm4.10754ADIPOKINESKNEEMETABOLIC SYNDROMEMETABOLISMOBESITYOSTEOARTHRITIS
spellingShingle Yao Fu
Albert Batushansky
Michael Kinter
Janet L. Huebner
Virginia B. Kraus
Timothy M. Griffin
Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats
JBMR Plus
ADIPOKINES
KNEE
METABOLIC SYNDROME
METABOLISM
OBESITY
OSTEOARTHRITIS
title Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats
title_full Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats
title_fullStr Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats
title_full_unstemmed Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats
title_short Effects of Leptin and Body Weight on Inflammation and Knee Osteoarthritis Phenotypes in Female Rats
title_sort effects of leptin and body weight on inflammation and knee osteoarthritis phenotypes in female rats
topic ADIPOKINES
KNEE
METABOLIC SYNDROME
METABOLISM
OBESITY
OSTEOARTHRITIS
url https://doi.org/10.1002/jbm4.10754
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