[Tumor-induced osteomalacia caused by an orbital tumor: a case report].

A 52-year-old patient was initially diagnosed as hypophosphatemic osteomalacia in the Department of Endocrinology due to knee, foot and lumbosacral pain. The symptoms were not significantly relieved after phosphorus and vitamin D supplementation. Later, the imaging examination showed an orbital tumor in the right eye. The tumor was surgically removed, and the symptoms of systemic bone pain were relieved.

Pulsed electromagnetic fields preserve bone architecture and mechanical properties and stimulate porous implant osseointegration by promoting bone anabolism in type 1 diabetic rabbits.

The effects of exogenous pulsed electromagnetic field (PEMF) stimulation on T1DM-associated osteopathy were investigated in alloxan-treated rabbits. We found that PEMF improved bone architecture, mechanical properties, and porous titanium (pTi) osseointegration by promoting bone anabolism through a canonical Wnt/ß-catenin signaling-associated mechanism, and revealed the clinical potential of PEMF stimulation for the treatment of T1DM-associated bone complications. INTRODUCTION: Type 1 diabetes mellitus (T1DM) is associated with deteriorated bone architecture and impaired osseous healing potential; nonetheless, effective methods for resisting T1DM-associated osteopenia/osteoporosis and promoting bone defect/fracture healing are still lacking. PEMF, as a safe and noninvasive method, have proven to be effective for promoting osteogenesis, whereas the potential effects of PEMF on T1DM osteopathy remain poorly understood. METHODS: We herein investigated the effects of PEMF stimulation on bone architecture, mechanical properties, bone turnover, and its potential molecular mechanisms in alloxan-treated diabetic rabbits. We also developed novel nontoxic Ti2448 pTi implants with closer elastic modulus with natural bone and investigated the impacts of PEMF on pTi osseointegration for T1DM bone-defect repair. RESULTS: The deteriorations of cancellous and cortical bone architecture and tissue-level mechanical strength were attenuated by 8-week PEMF stimulation. PEMF also promoted osseointegration and stimulated more adequate bone ingrowths into the pore spaces of pTi in T1DM long-bone defects. Moreover, T1DM-associated reduction of bone formation was significantly attenuated by PEMF, whereas PEMF exerted no impacts on bone resorption. We also found PEMF-induced activation of osteoblastogenesis-related Wnt/ß-catenin signaling in T1DM skeletons, but PEMF did not alter osteoclastogenesis-associated RANKL/RANK signaling gene expression. CONCLUSION: We reveal that PEMF improved bone architecture, mechanical properties, and pTi osseointegration by promoting bone anabolism through a canonical Wnt/ß-catenin signaling-associated mechanism. This study enriches our basic knowledge for understanding skeletal sensitivity in response to external electromagnetic signals, and also opens new treatment alternatives for T1DM-associated osteopenia/osteoporosis and osseous defects in an easy and highly efficient manner.

The preventive effects of pulsed electromagnetic fields on diabetic bone loss in streptozotocin-treated rats.

UNLABELLED: The present study was the first report demonstrating that pulsed electromagnetic field (PEMF) could partially prevent bone strength and architecture deterioration and improve the impaired bone formation in streptozotocin-induced diabetic rats. The findings indicated that PEMF might become a potential additive method for inhibiting diabetic osteopenia or osteoporosis. INTRODUCTION: Diabetes mellitus (DM) can cause various musculoskeletal abnormalities. Optimal therapeutic methods for diabetic bone complication are still lacking. It is essential to develop more effective and safe therapeutic methods for diabetic bone disorders. Pulsed electromagnetic field (PEMF) as an alternative noninvasive method has proven to be effective for treating fracture healing and osteoporosis in non-diabetic conditions. However, the issue about the therapeutic effects of PEMF on diabetic bone complication has not been previously investigated. METHODS: We herein systematically evaluated the preventive effects of PEMF on diabetic bone loss in streptozotocin-treated rats. Two similar experiments were conducted. In each experiment, 16 diabetic and eight non-diabetic rats were equally assigned to the control, DM, and DM + PEMF group. DM + PEMF group was subjected to daily 8-h PEMF exposure for 8 weeks. RESULTS: In experiment 1, three-point bending test suggested that PEMF improved the biomechanical quality of diabetic bone tissues, evidenced by increased maximum load, stiffness, and energy absorption. Microcomputed tomography analysis demonstrated that DM-induced bone architecture deterioration was partially reversed by PEMF, evidenced by increased Tb.N, Tb.Th, BV/TV, and Conn.D and reduced Tb.Sp and SMI. Serum OC analysis indicated that PEMF partially prevented DM-induced decrease in bone formation. In experiment 2, no significant difference in the bone resorption marker TRACP5b was observed. These biochemical findings were further supported by the dynamic bone histomorphometric parameters BFR/BS and Oc.N/BS. CONCLUSIONS: The results demonstrated that PEMF could partially prevent DM-induced bone strength and architecture deterioration and improve the impaired bone formation. PEMF might become a potential additive method for inhibiting diabetic osteoporosis.

Drosophila lacks C20 and C22 PUFAs.

Drosophila melanogaster has been considered a model organism for investigating human diseases and genetic pathways. Whether Drosophila is an ideal model for nutrigenomics, especially for FA metabolism, however, remains to be illustrated. The aim of this study was to examine the metabolism of C20 and C22 PUFAs in Drosophila. Analysis of FA composition revealed a complete lack of C20 and C22 PUFAs in the body tissue of larvae, pupae, and adult flies fed either a base or supplemented diet abundant in the PUFA precursors linoleic acid and α-linolenic acid. PUFA with >C20 could only be found in flies supplemented with specific FAs. Interestingly, the supplemented C22 PUFAs docosahexaenoic acid (22:6n-3) and docosatetraenoic acid (22:4n-6) were largely converted to the shorter chain C20 PUFAs eicosapentaenoic acid (20:5n-3) and arachidonic acid (20:4n-6), respectively. Furthermore, a genome sequence scan indicated that no gene encoding Δ-6/ Δ-5 desaturases, the key enzymes for the synthesis of C20/C22 PUFA, was present in Drosophila. These findings demonstrate that Drosophila lacks the capability to synthesize the biologically important C20 and C22 PUFAs, and thereby argue that Drosophila is not a valid model for the study of lipid metabolism and related diseases.