Y Fujita1, K Watanabe, K Maki. 1. Division of Developmental Stomatognathic Function Science, Department of Growth and Development of Functions, Kyushu Dental College, Kitakyushu, Japan.
Abstract
OBJECTIVES: This study evaluated the influence of diet-induced obesity on bone tissue quantity and quality in the proximal tibiae of growing mice and also examined the relationships between the serum total cholesterol, leptin, and adiponectin levels and trabecular and cortical bone mineral parameters. METHODS: Six-week-old male C57BL/6J mice were divided into two groups; one received a control diet, and the other received a high-fat-diet. After treatment for 4, 8, or 12 weeks, the bone quantity and quality were analyzed using peripheral quantitative computed tomography (pQCT), micro-computed tomography and histomorphometry. RESULTS: In the early stages, trabecular bone density decreased with an increase in the number of adipocytes and the deterioration of trabeculae. In contrast, although cortical bone formation was slower in obese mice compared with control mice, bone formation on the periosteal surface increased with age. Serum leptin levels were correlated with trabecular, but not cortical bone density, whereas neither the adiponectin nor total cholesterol level was correlated with bone mass in mice with diet-induced obesity. CONCLUSIONS: We conclude that bone loss at these two sites is differentially regulated in mice. Furthermore, we demonstrate that serum leptin may be a useful indicator of risk for osteoporosis associated with diet-induced obesity.
OBJECTIVES: This study evaluated the influence of diet-induced obesity on bone tissue quantity and quality in the proximal tibiae of growing mice and also examined the relationships between the serum total cholesterol, leptin, and adiponectin levels and trabecular and cortical bone mineral parameters. METHODS: Six-week-old male C57BL/6J mice were divided into two groups; one received a control diet, and the other received a high-fat-diet. After treatment for 4, 8, or 12 weeks, the bone quantity and quality were analyzed using peripheral quantitative computed tomography (pQCT), micro-computed tomography and histomorphometry. RESULTS: In the early stages, trabecular bone density decreased with an increase in the number of adipocytes and the deterioration of trabeculae. In contrast, although cortical bone formation was slower in obesemice compared with control mice, bone formation on the periosteal surface increased with age. Serum leptin levels were correlated with trabecular, but not cortical bone density, whereas neither the adiponectin nor total cholesterol level was correlated with bone mass in mice with diet-induced obesity. CONCLUSIONS: We conclude that bone loss at these two sites is differentially regulated in mice. Furthermore, we demonstrate that serum leptin may be a useful indicator of risk for osteoporosis associated with diet-induced obesity.
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