Dr. Cao's research focuses on how dietary factors influence inflammatory processes related to bone metabolism particularly in obesity.
The skeleton serves as both a structural function and a homeostatic function. Bone is constantly remodeling itself throughout life and normally its mass is maintained through balanced bone formation and resorption. In osteoporosis, the balance is disrupted in favor of bone resorption resulting in decreasing bone mass and strength. Osteoporosis and obesity are interrelated diseases. Both osteoblasts (bone forming cells) and adipocytes (energy storing cells) are derived from common mesenchymal stem cells, and normal aging is associated with high incidence of osteoporosis and bone marrow adiposity. Both diseases are associated with elevated production of inflammatory cytokines.
Current research projects:
Investigating how dietary protein and acid-base balance affect calcium retention, markers of bone metabolism, and pro-inflammatory cytokine production in postmenopausal women. General approach: In a cross-over design, postmenopausal women will consume diets varying in meat protein and potential renal acid load for 7 weeks. Calcium retention will be measured by whole body scintillation counting for 4 weeks after ingestion of the radio-labeled meals. Blood and urine samples will be collected to assess the effects of the diet on biomarkers of bone metabolism and pro-inflammatory cytokines.
Studying how obesity and/or physical activity affect(s) calcium absorption, inflammatory cytokine production, osteoblast and osteoclast activity in diet-induced obesity animal model.
Determining whether and how food antioxidants can affect inflammation status to reduce bone loss in animal model.
Demonstrated that decreased IGF-1 receptor activation and impaired IGF-1 signaling in aging are responsible for reduced responsiveness to IGF-1 and decreased bone formation.
Demonstrated high-fat diet decrease bone mineral density despite positive effect of increased body weight on bone formation.
Demonstrated that aging significantly increases stromal/osteoblastic cell-induced osteoclastogenesis, promotes expansion of the osteoclast precursor pool and alters the relationship between osteoblasts and osteoclasts in cancellous bone.
Showed that with aging the expression of RANKL is increased and OPG is decreased in whole bone and in cultured primary osteoblasts. These changes are responsible for the imbalance in bone formation and resorption associated with aging.
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