Effect of Glycemic Control on Calcium and Phosphorus Handling and Parathyroid Hormone Level in Patients with Non-Insulin-Dependent Diabetes Mellitus.

Nagasaka, Shoichiro; Murakami, Toru; Uchikawa, T.; Ishikawa, San‐e; Saito, Toshikazu

doi:10.1507/endocrj.42.377

Cited by 61 publications

(40 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…More recently, osteoporosis with an increased risk of fragility fractures has emerged as a complication in patients with long-standing or poorly controlled type 1 and type 2 diabetes mellitus (8). Several factors may contribute to poor bone health in patients with diabetes mellitus, including hypercalciuria in periods of glucosuria in type 1 and 2 diabetes mellitus (20), delayed bone mass accrual and a lower peak bone mass in type 1 diabetes mellitus (8), poor bone quality despite higher bone mineral density (BMD) in type 2 diabetes mellitus (26), and a higher propensity to falls and osteoporotic fractures in long-standing type 1 and 2 diabetes, in particular when neuropathy, retinopathy, or nephropathy are present (3). After sustaining fractures, patients with diabetes type 2 have a higher risk of wound infection, delayed fracture healing, a higher incidence of nonunion, and impaired osseointegration (22), which translate in prolonged hospitalization and decreased mobility.…”

mentioning

confidence: 99%

Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function

Hamann¹,

Goettsch

Mettelsiefen³

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

129

120

View full text Add to dashboard Cite

Hamann C, Goettsch C, Mettelsiefen J, Henkenjohann V, Rauner M, Hempel U, Bernhardt R, Fratzl-Zelman N, Roschger P, Rammelt S, Günther KP, Hofbauer LC. Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function. Am J Physiol Endocrinol Metab 301: E1220 -E1228, 2011. First published September 6, 2011; doi:10.1152/ajpendo.00378.2011.-Patients with diabetes mellitus have an impaired bone metabolism; however, the underlying mechanisms are poorly understood. Here, we analyzed the impact of type 2 diabetes mellitus on bone physiology and regeneration using Zucker diabetic fatty (ZDF) rats, an established rat model of insulin-resistant type 2 diabetes mellitus. ZDF rats develop diabetes with vascular complications when fed a Western diet. In 21-wk-old diabetic rats, bone mineral density (BMD) was 22.5% (total) and 54.6% (trabecular) lower at the distal femur and 17.2% (total) and 20.4% (trabecular) lower at the lumbar spine, respectively, compared with nondiabetic animals. BMD distribution measured by backscattered electron imaging postmortem was not different between diabetic and nondiabetic rats, but evaluation of histomorphometric indexes revealed lower mineralized bone volume/tissue volume, trabecular thickness, and trabecular number. Osteoblast differentiation of diabetic rats was impaired based on lower alkaline phosphatase activity (Ϫ20%) and mineralized matrix formation (Ϫ55%). In addition, the expression of the osteoblast-specific genes bone morphogenetic protein-2, RUNX2, osteocalcin, and osteopontin was reduced by 40 -80%. Osteoclast biology was not affected based on tartrate-resistant acidic phosphatase staining, pit formation assay, and gene profiling. To validate the implications of these molecular and cellular findings in a clinically relevant model, a subcritical bone defect of 3 mm was created at the left femur after stabilization with a four-hole plate, and bone regeneration was monitored by X-ray and microcomputed tomography analyses over 12 wk. While nondiabetic rats filled the defects by 57%, diabetic rats showed delayed bone regeneration with only 21% defect filling. In conclusion, we identified suppressed osteoblastogenesis as a cause and mechanism for low bone mass and impaired bone regeneration in a rat model of type 2 diabetes mellitus. bone defect; bone matrix mineralization; bone regeneration; type 2 diabetes mellitus; osteoblast; osteoclast DIABETES MELLITUS TYPE 2 AND the associated metabolic syndrome have become epidemic clinical and economic health problems (1). Morbidity and mortality of diabetes mellitus are determined by vascular complications, including cardiovascular disease, retinopathy, nephropathy, and polyneuropathy (11). Skeletal sequelae of long-standing diabetes mellitus include Charcot neuroarthropathy and the diabetic foot syndrome, which may require amputation. More recently, osteoporosis with an increased risk of fragility fractures has emerged as a complication in patients with long-stan...

show abstract

mentioning

confidence: 99%

Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function

Hamann¹,

Goettsch

Mettelsiefen³

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

129

120

View full text Add to dashboard Cite

show abstract

“…Hyperglycemia and its resultant glycosuria have been implicated in altered renal handling of calcium, phosphorus and uric acid. Studies have demonstrated an increase in urinary calcium and phosphorus excretion in patients with T2DM [15,16]. Recent investigations have also highlighted that stone formers with T2DM have increased urinary oxalate excretion [17,18].…”

Section: Discussionmentioning

confidence: 99%

66 Diabetic Severity and Risk of Kidney Stone Disease

Weinberg¹,

Patel²,

Chertow³

et al. 2013

Journal of Urology

View full text Add to dashboard Cite

show abstract

“…Serum PTH decreased from a mid-normal to a low-normal value. 18 Thus, in both type 1 and type 2 diabetes, there is a close correlation between the Pi concentration in plasma and an improvement in diabetes control and in intracellular phosphate with a stimulating influence on the rate of cell glycolysis.…”

Section: Raskin and Pakmentioning

confidence: 95%

Disturbance of inorganic phosphate metabolism in diabetes mellitus: temporary therapeutic intervention trials

Ditzel¹,

Lervang²

2009

DMSO

View full text Add to dashboard Cite

Effect of Glycemic Control on Calcium and Phosphorus Handling and Parathyroid Hormone Level in Patients with Non-Insulin-Dependent Diabetes Mellitus.

Cited by 61 publications

References 27 publications

Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function

Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function

66 Diabetic Severity and Risk of Kidney Stone Disease

Disturbance of inorganic phosphate metabolism in diabetes mellitus: temporary therapeutic intervention trials

Contact Info

Product

Resources

About