Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the role of AGEs in adynamic bone disease, we investigated the effect of these substances on cultured human osteoblasts and parathyroid cells. AGEs-BSA significantly inhibited parathyroid hormone secretion in response to the low calcium concentration. In HEK-293 cells, expressing calcium-sensing receptors, the same AGE concentration caused a significant potentiation of the extracellular Ca(2+) induced-intracellular calcium concentration. AGEs significantly inhibited the synthesis of type I collagen and osteocalcin in response to stimulation with 1,25(OH)(2)D(3). These data suggest that AGEs are involved in the pathogenesis of adynamic bone disease by inhibiting PTH secretion in response to hypocalcemia and by inhibiting osteoblastic activity.
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PMID:[Role of advanced glycation endproducts in adynamic bone disease]. 1577 14

Chronic kidney disease-mineral and bone disorder (CKD-MBD) develops as renal function deteriorates. The presence of diabetes mellitus as comorbidity modulates the severity of CKD-MBD. The prevalence of vascular calcification, which becomes higher in diabetic CKD patients than in non-CKD counterparts, increases cardiovascular mortality in diabetic patients. The main factor which causes vascular calcification in diabetic CKD patients is poor glycemic control, in contrast to hyperphosphatemia in non-diabetic CKD patients. Diabetes directly impairs osetoblasts to decrease bone mass, suppresses bone turnover to impair bone quality by impairing secretion of parathyroid hormone and increase AGE-modification of bone collagen. Therefore, therapeutic regimens for CKD-MBD should be considered specifically for diabetic CKD patients since the mode of its development differs between diabetic and non-diabetic CKD patients.
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PMID:[Chronic kidney disease (CKD) and bone. Impact of diabetes mellitus on the development of CKD-MBD]. 1932 28

A significant improvement in the knowledge of physiology, pathophysiology and pathobiochemistry of bone metabolism has enhanced the understanding not only of regulatory mechanisms of bone remodelation in adulthood but also of the dysfunction of such regulatory processes with other diseases. In the pathophysiology of metabolic bone disease in diabetic patients, attention is currently being focused on the method in which the differentiation of mesenchymal stem cells in osteoblasts, or adipocytes is regulated. The key role of PPAR-gamma, its activation or activity inhibition and thus also the directing of the differentiation in fat cells or osteoblasts is especially important in diabetic patients. Thiazolidinediones, in particular of the rosiglitazone type, have a positive impact on increased tissue sensitivity to insulin built on the activation of PPAR-gamma. Therefore, they can provoke the image of an aging bone in case of prolonged administration. Nevertheless, many factors contribute to the causes of increased fragility of bones in diabetic patients, both directly and indirectly--AGE, changes in insulin and IGF-I concentrations, renal dysfunctions, chronic inflammatory processes and impaired immunity. The treatment of osteoporosis in diabetic patients does not principally differ from the treatment of postmenopausal osteoporosis.
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PMID:[Drugs influencing bone metabolism in diabetic patients]. 1944 52