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Bone mass is maintained through the close microanatomical coupling of osteoblastic and osteoclastic activities, so we also detected the osteoclast formation using osteoblast:osteoclast co-culture system. The result showed that the number and size of osteoclasts co-cultured with ColI-CNN1 osteoblasts were increased compared with wild-type osteoblasts, which was caused by increased level of RANKL and decreased level of OPG in ColI-CNN1 osteoblasts. All the results indicated that the reduced bone mass of ColI-CNN1 was caused by impaired osteogenesis and enhanced osteoclastogenesis. [The work was supported by the Special Funds for Major State Basic Research Program of China (973 program) (No.2005CB522604), National Natural Science Foundation of China (No.30425023, No.30530410, No.30901527)] Disclosures: Lin Chen, None. SU0201 High Fat Diet-Induced Obesity Reduces Bone Formation through Activation of PPAR�� to Suppress Wnt/��-catenin Signaling in Prepubertal Rats.Jin-Ran Chen*1, Oxana P. Lazarenko2, Kartik Shankar2, Xianli Wu2, Thomas M. Badger2, Martin J. Ronis2. 1University of Arkansas for Medical Science, Arkansas Children's Nutrition Center, USA, 2University of Arkansas for Medical Sciences/Arkansas Children's Nutrition Center, USA The effects of a high fat diet (HFD) and of obesity on skeletal development, maturation and remodeling remain largely unclear particularly in children. In this report, we utilized a total enteral nutrition (TEN) model to examine the direct effect of HFD feeding on bone prior to puberty. We chronically fed HFD containing 25% or 45% fat calories via TEN to male Sprague-Dawley rats for 4 weeks beginning at weaning. Body weight gains were matched between HFD-fed rats and rats fed a low fat chow diet (LFD) ad libitum. Both gonadal and abdominal fat mass were increased in HFD-fed animals compared to the LFD group (P