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Osteoporosis, bone metabolism and obesityNutrition is critical to normal growth and maintenance of skeletal tissue. This research program focuses on the nutritional regulation of skeletal tissues by examining the biochemistry and gene expression within the extracellular matrix (proteoglycans and collagen). Importantly, there are clinical trials of bone turnover and bone mass to determine how nutritional intake influences the development of osteoporosis. The major focus in the laboratory is to determine how loss of body weight contributes to the risk of osteoporosis. Evidence shows that subjects who diet and lose weight also lose bone. Our goal is to determine mechanisms that regulate the rate of bone turnover and bone loss during caloric restriction. Bone turnover is measured in the urine and blood (e.g., pyridinium cross-links, serum osteocalcin) using techniques of spectrophotometry, HPLC, and radioimmunoassay. Calcium absorption (using stable isotopes) and bone-regulating hormones are examined in these studies to address mechanisms of regulation. In addition, studies examining gastric bypass patients are in progress to understand how obesity surgery influences calcium homeostatsis and bone mass. Due to the high rate of morbidity and mortality associated with osteoporotic fractures, we also use a rat model to better understand how nutrition regulates bone turnover, composition, and biomechanical properties. We also examine the regulation of bone turnover in disease states associated with changes in bone mass. For example, we have studied how glycemic control and hormones regulate bone turnover in insulin-dependent patients with diabetes. We have used biochemical markers of bone turnover to estimate the rate of growth in clinical and equine studies. In addition, the regulation of lipids in bone and connective tissue is an ongoing interest in the laboratory. Selected PublicationsRiedt CS, Buckley BT, Brolin RE, Ambia-Sobhan H, Rhoads GG, Shapses SA. (2008) Blood lead levels and bone turnover with weight reduction in women. J Expo Sci Environ Epidemiol. Mar 5. [Epub ahead of print] Levitt DG, Heymsfield SB, Pierson RN Jr, Shapses SA, Kral JG. (2007) Physiological models of body composition and human obesity. Nutr Metab (Lond). 4:19. Fishbein KW, Gluzband YA, Kaku M, Ambia-Sobhan H, Shapses SA, Yamauchi M, Spencer RG. (2007) Effects of formalin fixation and collagen cross-linking on T2 and magnetization transfer in bovine nasal cartilage. Magn Reson Med. 57(6):1000-11. Riedt CS, Schlussel Y, von Thun N, Ambia-Sobhan H, Stahl T, Field MP, Sherrell RM, Shapses SA. (2007) Premenopausal overweight women do not lose bone during moderate weight loss with adequate or higher calcium intake. Am J Clin Nutr. 85(4):972-80. Riedt CS, Brolin RE, Sherrell RM, Field MP, Shapses SA. (2006) True fractional calcium absorption is decreased after Roux-en-Y gastric bypass surgery. Obesity (Silver Spring). 14(11):1940-8. Shapses SA, Riedt CS. (2006) Bone, body weight, and weight reduction: what are the concerns?
J Nutr. 136(6):1453-6. Review. Cifuentes M, Advis JP, Shapses SA. (2004) Estrogen prevents the reduction in fractional calcium absorption due to energy restriction in mature rats. J Nutr. 134(8):1929-34. Cifuentes M, Riedt CS, Brolin RE, Field MP, Sherrell RM, Shapses SA. (2004) Weight loss and calcium intake influence calcium absorption in overweight postmenopausal women. Shapses SA, Heshka S, Heymsfield SB. (2004) Effect of calcium supplementation on weight and fat loss in women. J Clin Endocrinol Metab. 89(2):632-7. Goode LR, Brolin RE, Chowdhury HA, Shapses SA. (2004) Bone and gastric bypass surgery: effects of dietary calcium and vitamin D. Obes Res. 12(1):40-7. |