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Title:
Bone Loss in Diabetes: Use of Antidiabetic Thiazolidinediones and Secondary Osteoporosis | Current Osteoporosis Reports
Description:
Clinical evidence indicates that bone status is affected in patients with type 2 diabetes mellitus (T2DM). Regardless of normal or even high bone mineral density, T2DM patients have increased risk of fractures. One class of antidiabetic drugs, thiazolidinediones (TZDs), causes bone loss and further increases facture risk, placing TZDs in the category of drugs causing secondary osteoporosis. Risk factors for development of TZD-induced secondary osteoporosis are gender (women), age (elderly), and duration of treatment. TZDs exert their antidiabetic effects by activating peroxisome proliferator-activated receptor-γ (PPAR-γ) nuclear receptor, which controls glucose and fatty acid metabolism. In bone, PPAR-γ controls differentiation of cells of mesenchymal and hematopoietic lineages. PPAR-γ activation with TZDs leads to unbalanced bone remodeling: bone resorption increases and bone formation decreases. Laboratory research evidence points toward a possible separation of unwanted effects of PPAR-γ on bone from its beneficial antidiabetic effects by using selective PPAR-γ modulators. This review also discusses potential pharmacologic means to protect bone from detrimental effects of clinically used TZDs (pioglitazone and rosiglitazone) by using combinational therapy with approved antiosteoporotic drugs, or by using lower doses of TZDs in combination with other antidiabetic therapy. We also suggest a possible orthopedic complication, not yet supported by clinical studies, of delayed fracture healing in T2DM patients on TZD therapy.
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Keywords {🔍}

bone, article, google, scholar, pubmed, risk, tzds, diabetes, increased, rosiglitazone, cas, fractures, pparγ, studies, fracture, loss, type, tzd, effects, women, treatment, patients, formation, effect, tdm, pioglitazone, therapy, antidiabetic, number, levels, thiazolidinediones, leckaczernik, resorption, showed, diabetic, clinical, bmd, aging, decreased, research, marrow, osteoporosis, drugs, development, receptor, cells, osteoblasts, men, clin, evidence,

Topics {✒️}

aid=2e0a4c8c-af53-41a8-8155-8818183333bc tgf-beta/bmp signaling pathways tzd-induced secondary osteoporosis ppar-gamma regulates osteoclastogenesis estrogen-deprived rats treated tzd-induced bone loss ppar-gamma2 transcription factor selective ppar-γ modulators pparγ ligand-binding domain ppar-γ transcription factor nuclear factor-κb ligand unbalanced bone remodeling forming additional cross-links article download pdf ppar-γ controls differentiation ppar-γ controls production beata lecka-czernik org/meetings/annualmeeting/abstractdetail ppar-γ anti-inflammatory article lecka-czernik controlled case-series study ppar-gamma ligand transforming growth factor-β cross-sectional study based steroid receptor coactivator-2 ppar-γ include production related subjects ppargamma agonist brl49653 bone remodeling process bone resorption marker cellular mechanisms activated prevent secondary osteoporosis including receptor activator bone formation marker bone resorption increases distinct regulatory pathways ppar-γ proadipocytic activity privacy choices/manage cookies bone formation decreases open access prior tzd-unrelated fractures peptide-1 analog liraglutide metabolic status lazarenko op estrogen-deficient rats clinical research evidence polycystic ovary syndrome bone marrow structure/function research triangle park bone mineral density

Questions {❓}

Can We Prevent Secondary Osteoporosis in TZD Users?
Rosen CJ, Bouxsein ML: Mechanism of disease: is osteoporosis the obesity of bone?

Schema {🗺️}

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         headline:Bone Loss in Diabetes: Use of Antidiabetic Thiazolidinediones and Secondary Osteoporosis
         description:Clinical evidence indicates that bone status is affected in patients with type 2 diabetes mellitus (T2DM). Regardless of normal or even high bone mineral density, T2DM patients have increased risk of fractures. One class of antidiabetic drugs, thiazolidinediones (TZDs), causes bone loss and further increases facture risk, placing TZDs in the category of drugs causing secondary osteoporosis. Risk factors for development of TZD-induced secondary osteoporosis are gender (women), age (elderly), and duration of treatment. TZDs exert their antidiabetic effects by activating peroxisome proliferator-activated receptor-γ (PPAR-γ) nuclear receptor, which controls glucose and fatty acid metabolism. In bone, PPAR-γ controls differentiation of cells of mesenchymal and hematopoietic lineages. PPAR-γ activation with TZDs leads to unbalanced bone remodeling: bone resorption increases and bone formation decreases. Laboratory research evidence points toward a possible separation of unwanted effects of PPAR-γ on bone from its beneficial antidiabetic effects by using selective PPAR-γ modulators. This review also discusses potential pharmacologic means to protect bone from detrimental effects of clinically used TZDs (pioglitazone and rosiglitazone) by using combinational therapy with approved antiosteoporotic drugs, or by using lower doses of TZDs in combination with other antidiabetic therapy. We also suggest a possible orthopedic complication, not yet supported by clinical studies, of delayed fracture healing in T2DM patients on TZD therapy.
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      headline:Bone Loss in Diabetes: Use of Antidiabetic Thiazolidinediones and Secondary Osteoporosis
      description:Clinical evidence indicates that bone status is affected in patients with type 2 diabetes mellitus (T2DM). Regardless of normal or even high bone mineral density, T2DM patients have increased risk of fractures. One class of antidiabetic drugs, thiazolidinediones (TZDs), causes bone loss and further increases facture risk, placing TZDs in the category of drugs causing secondary osteoporosis. Risk factors for development of TZD-induced secondary osteoporosis are gender (women), age (elderly), and duration of treatment. TZDs exert their antidiabetic effects by activating peroxisome proliferator-activated receptor-γ (PPAR-γ) nuclear receptor, which controls glucose and fatty acid metabolism. In bone, PPAR-γ controls differentiation of cells of mesenchymal and hematopoietic lineages. PPAR-γ activation with TZDs leads to unbalanced bone remodeling: bone resorption increases and bone formation decreases. Laboratory research evidence points toward a possible separation of unwanted effects of PPAR-γ on bone from its beneficial antidiabetic effects by using selective PPAR-γ modulators. This review also discusses potential pharmacologic means to protect bone from detrimental effects of clinically used TZDs (pioglitazone and rosiglitazone) by using combinational therapy with approved antiosteoporotic drugs, or by using lower doses of TZDs in combination with other antidiabetic therapy. We also suggest a possible orthopedic complication, not yet supported by clinical studies, of delayed fracture healing in T2DM patients on TZD therapy.
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