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Leptin-deficient mice have altered three-dimensional growth plate histomorphometry

BACKGROUND: Leptin is an adipokine that regulates energy homeostasis and is also needed for normal bone growth and maintenance. Mutation in the lep gene, which characterizes the ob/ob mouse model, results in the development of obesity and type 2 diabetes mellitus, as well as reduced limb bone length...

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Autores principales: Hung, Jun, Al-Nakkash, Layla, Broderick, Tom L., Castro, Monica, Plochocki, Jeffrey H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6346570/
https://www.ncbi.nlm.nih.gov/pubmed/30697359
http://dx.doi.org/10.1186/s13098-019-0402-5
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author Hung, Jun
Al-Nakkash, Layla
Broderick, Tom L.
Castro, Monica
Plochocki, Jeffrey H.
author_facet Hung, Jun
Al-Nakkash, Layla
Broderick, Tom L.
Castro, Monica
Plochocki, Jeffrey H.
author_sort Hung, Jun
collection PubMed
description BACKGROUND: Leptin is an adipokine that regulates energy homeostasis and is also needed for normal bone growth and maintenance. Mutation in the lep gene, which characterizes the ob/ob mouse model, results in the development of obesity and type 2 diabetes mellitus, as well as reduced limb bone length and increased fracture risk. However, the relationship between limb bone length and growth plate cartilage structure in obese diabetic adolescents is incompletely understood. Here, we tested the hypothesis that leptin deficiency affects the microstructure of growth plate cartilage in juvenile ob/ob mice. METHODS: Tibial growth plate cartilage structure was compared between lean and obese, leptin-deficient (ob/ob) female mice aged 10 weeks. We used confocal laser scanning microscopy to assess 3D histological differences in Z stacks of growth plate cartilage at 0.2 µm intervals, 80–100 µm in depth. Histomorphometric comparisons were made between juvenile lean and ob/ob mice. RESULTS: We found obese mice have significantly reduced tibial length and growth plate height in comparison with lean mice (P < 0.05). Obese mice also have fewer chondrocyte columns in growth plate cartilage with reduced chondrocyte cell volumes relative to lean mice (P < 0.05). CONCLUSIONS: These data help explicate the relationship between growth plate cartilage structure and bone health in obese diabetic juvenile mice. Our findings suggest obesity and diabetes may adversely affect growth plate cartilage structure. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13098-019-0402-5) contains supplementary material, which is available to authorized users.
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spelling pubmed-63465702019-01-29 Leptin-deficient mice have altered three-dimensional growth plate histomorphometry Hung, Jun Al-Nakkash, Layla Broderick, Tom L. Castro, Monica Plochocki, Jeffrey H. Diabetol Metab Syndr Short Report BACKGROUND: Leptin is an adipokine that regulates energy homeostasis and is also needed for normal bone growth and maintenance. Mutation in the lep gene, which characterizes the ob/ob mouse model, results in the development of obesity and type 2 diabetes mellitus, as well as reduced limb bone length and increased fracture risk. However, the relationship between limb bone length and growth plate cartilage structure in obese diabetic adolescents is incompletely understood. Here, we tested the hypothesis that leptin deficiency affects the microstructure of growth plate cartilage in juvenile ob/ob mice. METHODS: Tibial growth plate cartilage structure was compared between lean and obese, leptin-deficient (ob/ob) female mice aged 10 weeks. We used confocal laser scanning microscopy to assess 3D histological differences in Z stacks of growth plate cartilage at 0.2 µm intervals, 80–100 µm in depth. Histomorphometric comparisons were made between juvenile lean and ob/ob mice. RESULTS: We found obese mice have significantly reduced tibial length and growth plate height in comparison with lean mice (P < 0.05). Obese mice also have fewer chondrocyte columns in growth plate cartilage with reduced chondrocyte cell volumes relative to lean mice (P < 0.05). CONCLUSIONS: These data help explicate the relationship between growth plate cartilage structure and bone health in obese diabetic juvenile mice. Our findings suggest obesity and diabetes may adversely affect growth plate cartilage structure. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13098-019-0402-5) contains supplementary material, which is available to authorized users. BioMed Central 2019-01-24 /pmc/articles/PMC6346570/ /pubmed/30697359 http://dx.doi.org/10.1186/s13098-019-0402-5 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Short Report
Hung, Jun
Al-Nakkash, Layla
Broderick, Tom L.
Castro, Monica
Plochocki, Jeffrey H.
Leptin-deficient mice have altered three-dimensional growth plate histomorphometry
title Leptin-deficient mice have altered three-dimensional growth plate histomorphometry
title_full Leptin-deficient mice have altered three-dimensional growth plate histomorphometry
title_fullStr Leptin-deficient mice have altered three-dimensional growth plate histomorphometry
title_full_unstemmed Leptin-deficient mice have altered three-dimensional growth plate histomorphometry
title_short Leptin-deficient mice have altered three-dimensional growth plate histomorphometry
title_sort leptin-deficient mice have altered three-dimensional growth plate histomorphometry
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6346570/
https://www.ncbi.nlm.nih.gov/pubmed/30697359
http://dx.doi.org/10.1186/s13098-019-0402-5
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