Orthopaedic Hospital | Endocrinology Laboratory

Scope

The main research program in this laboratory has been directed toward assessing the role of dietary magnesium deficiency as a risk factor for osteoporosis. The investigators in the lab have recently completed a NIH-sponsored study in which dietary restriction to only 50 percent of dietary requirement resulted in bone loss. They are currently exploring the mechanisms by which this might occur and hypothesize that the release of inflammatory cytokines are involved in stimulation osteoclastic bone resorption and as well as changes in hormones regulating bone and mineral metabolism.

Metabolic bone diseases are another focus of study in this laboratory. Mononuclear cells obtained and cultured from whole blood have been used in investigating the molecular genetics of Paget's disease with the In-Situ-Hybridization system.

The etiology of fibrous dysplasia has been studied by investigating possible cell signaling errors which produce abnormal fibro-osseous tissue.

Research

Current projects include:

Breeding mice with gene knock-out for TNFα, IL1β, and substance P to assess if these inflammatory cytokines play a role in magnesium deficiency-induced bone loss.
Conducting a double blind trial of the effect of soy protein versus estrogen on bone mineral density in women in order to assess the effectiveness of soy protein with hormone replacement therapy in preventing bone loss.

Apparatus

Full immunohistochemistry (IHC) capabilities; two laminar flow cabinets for tissue culture and other sterile techniques; CO₂ incubators and a cryogenic tank containing stock cell lines and human bone cells; Zeiss photomicroscope with Ultraviolet light source and filters, adapted with a Spot 2 cool color digital (CCD) camera; an atomic absorption spectrometer, a standard refrigerator, a -20°C freezer, a -80°C ultra low freezer, a Vac-Elut vacuum manifold, centrifuges.

Staff

The Endocrinology Laboratory is under the direction of Robert K. Rude, M.D..

Selected Publications

Rude RK, Gruber HE, Norton, HJ, Wei LY, Frausto A, Mills BG: Bone Loss Induced by Dietary Magnesium Reduction to 10% of Nutrition Requirement in the Rats is associated with increased release of substance P and tumor necrosis factor-a. J Nutrition, 134:79-85, 2004.
Rude RK, Gruber HE. Magnesium Deficiency and osteoporosis: animal and human observations. J Nutr Biochem 15(12):710-716, 2004
Rude RK, Gruber HE, Norton HJ, Wei LY, Frausto A and Kilburn J. Dietary Magnesium Reduction to 25% of Nutrient Requirement Disrupts Bone and Mineral Metabolism in the Rat, Bone, 37: 211-219, 2005.
Rude RK, Gruber HE, Wei LY, Frausto A. Immunolocalization of RANKL is Increased and OPG Decreased During Dietary Magnesium Deficiency in the Rat, Nutrition and Metabolism 2:24-31, 2005.
Rude RK, Gruber HE, Norton HJ, Wei LY, Frausto A and Kilburn. Nutrient Requirement Reduction of Dietary Magnesium by Only 50% in the Rat Disrupts Bone and Mineral Metabolism Osteoporosis Int 17:1022-1032, 2006.

Contacts

Robert Rude, M.D., rrude60075@aol.com, tel. (213) 742-1376

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Osteoclasts