Correlations between bone mineral density and circulating bone metabolic markers in diabetic patients

Suzuki, Kiyoshi; Sugimoto, Chieko; Takizawa, Makoto; Ishizuka, Seiichi; Kikuyama, Munetsugu; Togawa, Haruo; Taguchi, Yoshitaka; Nosaka, Kenziro; Seino, Yutaka; Ishida, Hideyuki

doi:10.1016/s0168-8227(00)00119-4

Cited by 42 publications

(26 citation statements)

References 24 publications

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“…The effect of diabetes on BMD is still not clear. BMD in patients with T2DM was reported to be decreased [18], unchanged [19] or even increased [7,11].…”

Section: Discussionmentioning

confidence: 99%

The relationship between insulin resistance and osteoporosis in elderly male type 2 diabetes mellitus and diabetic nephropathy

Xia

Zhong

Huang

et al. 2012

Annales d'Endocrinologie

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“…The effect of diabetes on BMD is still not clear. BMD in patients with T2DM was reported to be decreased [18], unchanged [19] or even increased [7,11].…”

Section: Discussionmentioning

confidence: 99%

The relationship between insulin resistance and osteoporosis in elderly male type 2 diabetes mellitus and diabetic nephropathy

Xia

Zhong

Huang

et al. 2012

Annales d'Endocrinologie

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“…A number of studies have reported that type 1 diabetes changes bone remodeling by impairing bone formation, leading to osteopenia (2,5). By contrast, bone loss in T2DM is less accepted, with reports of bone mineral density (BMD) ranging from low to high in T2DM (6)(7)(8). Therefore, the present study investigated whether T2DM causes osteoporosis and explored the underlying mechanisms involved in this process by performing histological, cellular and biomechanical experiments on male KK/Upj-Ay/J (KK-Ay) mice.…”

Section: Introductionmentioning

confidence: 99%

Decreased osteoclastogenesis, osteoblastogenesis and low bone mass in a mouse model of type 2 diabetes

Dong

Huang

et al. 2014

Molecular Medicine Reports

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Abstract. The effect of type 2 diabetes mellitus (T2DM) on bone is controversial. Therefore, the present study investigated whether T2DM causes osteoporosis and explored the underlying mechanisms involved in this process. The effects of T2DM on bone physiology were analyzed in a mouse model of T2DM; KK/Upj-Ay/J (KK-Ay) mice develop diabetes after 8 weeks and exhibit stable diabetes symptoms and signs after 10 weeks when fed a KK-Ay mouse maintenance fodder. Diabetic mice exhibited hyperglycemia, hyperinsulinemia and increased body and fat pad weight in comparison with C57BL/6 non-diabetic mice. Furthermore, diabetic mice demonstrated low bone weight and bone mineral density in the femur, tibia and fifth lumbar vertebra. Using von Kossa and tartrate-resistant acid phosphatase (TRAP) staining, alkaline phosphatase and TRAP activity analyses and gene profiling it was demonstrated that osteoblastogenesis and osteoclastogenesis were impaired in diabetic mice. To evaluate the bone biomechanics, the ultimate load of the bone was analyzed. It was found that the ultimate load of the tibia in diabetic mice was lower than that in the controls. The results from the present study suggest that bone metabolism is impaired in T2DM, resulting in decreased osteoblastogenesis, osteoclastogenesis and bone mass.

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“…Recently, increasing attention has been paid to the relationship between diabetes and osteoporotic fractures [Barrett-Connor and Holbrook, 1992]. Many clinical studies have reported that osteoporosis is one of the chronic complications associated with diabetes mellitus [Krakauer et al, 1995;Suzuki et al, 2000;Patel et al, 2008]. A higher risk of fractures was found in both type 1 and type 2 diabetes compared to the non diabetic population [Rakel et al, 2008;Khazai et al, 2009].…”

mentioning

confidence: 99%

Metformin stimulates osteoprotegerin and reduces RANKL expression in osteoblasts and ovariectomized rats

et al. 2011

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Anti-diabetic drug metformin has been shown to enhance osteoblasts differentiation and inhibit osteoclast differentiation in vitro and prevent bone loss in ovariectomized (OVX) rats. But the mechanisms through which metformin regulates osteoclastogensis are not known. Osteoprotegerin (OPG) and receptor activator of nuclear factor κB ligand (RANKL) are cytokines predominantly secreted by osteoblasts and play critical roles in the differentiation and function of osteoclasts. In this study, we demonstrated that metformin dose-dependently stimulated OPG and reduced RANKL mRNA and protein expression in mouse calvarial osteoblasts and osteoblastic cell line MC3T3-E1. Inhibition of AMP-activated protein kinase (AMPK) and CaM kinase kinase (CaMKK), two targets of metformin, suppressed endogenous and metformin-induced OPG secretion in osteoblasts. Moreover, supernatant of osteoblasts treated with metformin reduced formation of tartrate resistant acid phosphatase (TRAP)-positive multi-nucleated cells in Raw264.7 cells. Most importantly, metformin significantly increased total body bone mineral density, prevented bone loss and decreased TRAP-positive cells in OVX rats proximal tibiae, accompanied with an increase of OPG and decrease of RANKL expression. These in vivo and in vitro studies suggest that metformin reduces RANKL and stimulates OPG expression in osteoblasts, further inhibits osteoclast differentiation and prevents bone loss in OVX rats.

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Correlations between bone mineral density and circulating bone metabolic markers in diabetic patients

Cited by 42 publications

References 24 publications

The relationship between insulin resistance and osteoporosis in elderly male type 2 diabetes mellitus and diabetic nephropathy

The relationship between insulin resistance and osteoporosis in elderly male type 2 diabetes mellitus and diabetic nephropathy

Decreased osteoclastogenesis, osteoblastogenesis and low bone mass in a mouse model of type 2 diabetes

Metformin stimulates osteoprotegerin and reduces RANKL expression in osteoblasts and ovariectomized rats

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