Abstract
BackgroundLeptin 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.MethodsTibial 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.ResultsWe 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).ConclusionsThese 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.
Highlights
Obesity and type 2 diabetes mellitus (T2DM) are on the rise worldwide in children and adolescents [1, 2]
Our data are in agreement with the mounting evidence that leptin deficiency has a significant impact on the length of long bones in ob/ob mice by affecting growth plate cartilage [9,10,11, 21]
Our study supports the hypothesis that growth plate morphology in long bones is altered in obese, leptin-deficient mice
Summary
Obesity and type 2 diabetes mellitus (T2DM) are on the rise worldwide in children and adolescents [1, 2]. T2DM accounts for 45% of all new onset diabetes cases in juveniles, up from 3% just two decades ago [1] This is a serious health concern as T2DM adversely affects growth and development, resulting in long-term, disabling complications [1]. Once such complication is impaired bone formation and mineralization, which is associated with decelerated bone growth, increased risk of bone fracture, Longitudinal growth of long bones occurs via endochondral ossification. During this process, growth plate cartilage expands and is replaced with bone tissue. We tested the hypothesis that leptin deficiency affects the microstructure of growth plate cartilage in juvenile ob/ob mice
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