Bone Mineral Density and Bone Metabolism in Diabetes Mellitus

Piepkorn, B.; Kann, Peter Herbert; Forst, Thomas; Andreas, J.; Pfützner, A.; Beyer, Jeannette

doi:10.1055/s-2007-979106

Cited by 124 publications

(102 citation statements)

References 14 publications

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“…In turn, the lack of metabolic control may potentially affect also the maintenance of bone mass, interfering not only with the equilibrium of mineral metabolism (19,20), but also with bone remodeling activity (21,22).…”

Section: Discussionmentioning

confidence: 99%

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Cutrim¹,

Pereira²,

Paula³

et al. 2007

Braz J Med Biol Res

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We assessed the effect of chronic hyperglycemia on bone mineral density (BMD) and bone remodeling in patients with type 2 diabetes mellitus. We investigated 42 patients with type 2 diabetes under stable control for at least 1 year, 22 of them with good metabolic control (GMC: mean age = 48.8 ± 1.5 years, 11 females) and 20 with poor metabolic control (PMC: mean age = 50.2 ± 1.2 years, 8 females), and 24 normal control individuals (CG: mean age = 46.5 ± 1.1 years, 14 females). We determined BMD in the femoral neck and at the L2-L4 level (DEXA) and serum levels of glucose, total glycated hemoglobin (HbA 1 ), total and ionic calcium, phosphorus, alkaline phosphatase, follicle-stimulating hormone, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor I (IGFI), osteocalcin, procollagen type I C propeptide, as well as urinary levels of deoxypyridinoline and creatinine. HbA 1 levels were significantly higher in PMC patients (12.5 ± 0.6 vs 7.45 ± 0.2% for GMC and 6.3 ± 0.9% for CG; P < 0.05). There was no difference in 25-OH-D, iPTH or IGFI levels between the three groups. BMD values at L2-L4 (CG = 1.068 ± 0.02 vs GMC = 1.170 ± 0.03 vs PMC = 1.084 ± 0.02 g/cm 2 ) and in the femoral neck (CG = 0.898 ± 0.03 vs GMC = 0.929 ± 0.03 vs PMC = 0.914 ± 0.03 g/cm 2 ) were similar for all groups. PMC presented significantly lower osteocalcin levels than the other two groups, whereas no significant difference in urinary deoxypyridine was observed between groups. The present results demonstrate that hyperglycemia is not associated with increased bone resorption in type 2 diabetes mellitus and that BMD is not altered in type 2 diabetes mellitus.

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Section: Discussionmentioning

confidence: 99%

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Cutrim¹,

Pereira²,

Paula³

et al. 2007

Braz J Med Biol Res

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show abstract

“…Although there were greater numbers of self-reported fractures, there was no association with BMD-defined osteoporosis. In larger-scale studies, type 1 diabetes increases the risk of fracture, especially in those with microvascular complications [2,14,41] and in females [42,43]. In type 2 diabetes, both lower [44] and higher [1] rates of fracture have been reported, with disease duration and use of insulin increasing the risk [42].…”

Section: Discussionmentioning

confidence: 99%

“…Several mechanisms may contribute to type 1 diabetesassociated osteopenia, including impaired vitamin D-para-thyroid hormone (PTH) regulation [9,13] and altered bone mineral metabolism [14]. Increased bone resorption and decreased formation have been observed in young poorly controlled patients with type 1 diabetes of long duration [15,16].…”

Section: Introductionmentioning

confidence: 99%

Bone mineral density and its determinants in diabetes: the Fremantle Diabetes Study

et al. 2006

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Aims/hypothesis: We assessed the effects of type 1 and type 2 diabetes on bone density and metabolism.Materials and methods: We analysed bone mineral density (BMD) measured at the hip, spine and forearm using dual energy X-ray absorptiometry in 34 patients with type 1 and 194 patients with type 2 diabetes. Patients were from the community-based Fremantle Diabetes Study, and findings for them were compared with those from normal age-and sex-matched control subjects from the local community. Biochemical and hormonal markers of bone metabolism were measured in a subset of 70 patients. Results: After adjusting for age and BMI, there was a lower BMD at total hip (p<0.001) and femoral neck (p=0.012) in type 1 men vs control subjects, but type 1 women and matched controls had similar BMD at each site. There was a higher BMD at total hip (p=0.006), femoral neck (p=0.026) and forearm (p<0.001) in type 2 women vs control subjects, but diabetes status was not associated with BMD in type 2 men after adjustment for age and BMI. Serum oestradiol, BMI, C-terminal telopeptide of collagen type 1 and male sex were consistently and independently associated with BMD at forearm, hip and femoral neck and explained 61, 55 and 50% of the total variance in BMD, respectively, at these sites. Spine BMD was independently associated with BMI and ln(oestradiol). Conclusions/interpretation: Men with type 1 diabetes may be at increased risk of osteoporosis, while type 2 women appear to be protected even after adjusting for BMI. Low serum oestradiol concentrations may predispose to diabetes-associated osteoporosis regardless of sex.

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“…Although the anabolic effect of insulin on bone may be primarily related to its ability to stimulate osteoblast proliferation, that on cartilage may involve the acceleration of chondrocyte differentiation (11,12). Patients with insulin deficiency as exemplified by type 1 diabetes mellitus are associated with osteoporosis (13,14). Diabetes has also been shown to impair fracture healing, which is restored by treatment with insulin in both humans and animals (2,15,16).…”

mentioning

confidence: 99%

Impairment of Bone Healing by Insulin Receptor Substrate-1 Deficiency

Shimoaka

Kamekura

Chikuda

et al. 2004

Journal of Biological Chemistry

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Insulin receptor substrate-1 (IRS-1) is an essential molecule for intracellular signaling of insulin-like growth factor (IGF)-I and insulin, both of which are potent anabolic regulators of bone and cartilage metabolism. To investigate the role of IRS-1 in bone regeneration, fracture was introduced in the tibia, and its healing was compared between wild-type (WT) mice and mice lacking the IRS-1 gene (IRS-1 ؊/؊ mice). Among 15 IRS-1 ؊/؊ mice, 12 remained in a non-union state even at 10 weeks after the operation, whereas all 15 WT mice showed a rigid bone union at 3 weeks. This impairment was because of the suppression of callus formation with a decrease in chondrocyte proliferation and increases in hypertrophic differentiation and apoptosis. Reintroduction of IRS-1 to the IRS-1 ؊/؊ fractured site using an adenovirus vector significantly restored the callus formation. In the culture of chondrocytes isolated from the mouse growth plate, IRS-1 ؊/؊ chondrocytes showed less mitogenic ability and Akt phosphorylation than WT chondrocytes. An Akt inhibitor decreased the IGF-Istimulated DNA synthesis of chondrocytes more potently in the WT culture than in the IRS-1 ؊/؊ culture. We therefore conclude that IRS-1 deficiency impairs bone healing at least partly by inhibiting chondrocyte proliferation through the phosphatidylinositol 3-kinase/Akt pathway, and we propose that IRS-1 can be a target molecule for bone regenerative medicine.

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Bone Mineral Density and Bone Metabolism in Diabetes Mellitus

Cited by 124 publications

References 14 publications

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Bone mineral density and its determinants in diabetes: the Fremantle Diabetes Study

Impairment of Bone Healing by Insulin Receptor Substrate-1 Deficiency

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