Bone Mineral Density in Diabetes

Jc, Krakauer; McKenna, Malachi J.; Ds, Rao; Fw, Whitehouse

doi:10.2337/diacare.20.8.1339b

Cited by 19 publications

(16 citation statements)

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“…Insulin deficiency as exemplified by IDDM patients is also associated with decreased bone mass (5-7). However, the change of bone mass in non-insulin-dependent diabetes mellitus (NIDDM) patients is controversial (5)(6)(7)(34)(35)(36). Although previous reports demonstrated a decrease in bone mass in NIDDM patients (5,35), accumulating evidence has shown that obese NIDDM patients have normal or even increased bone mass (6,7,34,36).…”

Section: Discussionmentioning

confidence: 98%

Insulin receptor substrate-1 in osteoblast is indispensable for maintaining bone turnover

Ogata¹,

Chikazu²,

Kubota³

et al. 2000

J. Clin. Invest.

243

185

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Section: Discussionmentioning

confidence: 98%

Insulin receptor substrate-1 in osteoblast is indispensable for maintaining bone turnover

Ogata¹,

Chikazu²,

Kubota³

et al. 2000

J. Clin. Invest.

243

185

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“…Insulin is known to play important anabolic roles in bone (30), and deficiency of insulin signaling is associated with osteopenia both in mice and humans (27,(50)(51)(52). A series of reports demonstrated that leptin, a well-known anorexigenic hormone secreted by adipocytes (53), also shows antiosteogenic action centrally through the hypothalamic and sympathetic nervous systems (11,13,31).…”

Section: Discussionmentioning

confidence: 99%

PPAR γ insufficiency enhances osteogenesis through osteoblast formation from bone marrow progenitors

Akune¹,

Ohba²,

Kamekura³

et al. 2004

J. Clin. Invest.

739

336

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Based on the fact that aging is associated with a reciprocal decrease of osteogenesis and an increase of adipogenesis in bone marrow and that osteoblasts and adipocytes share a common progenitor, this study investigated the role of PPARγ γ, a key regulator of adipocyte differentiation, in bone metabolism. Homozygous PPARγ γ-deficient ES cells failed to differentiate into adipocytes, but spontaneously differentiated into osteoblasts, and these were restored by reintroduction of the PPARγ γ gene. Heterozygous PPARγ γ-deficient mice exhibited high bone mass with increased osteoblastogenesis, but normal osteoblast and osteoclast functions, and this effect was not mediated by insulin or leptin. The osteogenic effect of PPARγ γ haploinsufficiency became prominent with aging but was not changed upon ovariectomy. The PPARγ γ haploinsufficiency was confirmed to enhance osteoblastogenesis in the bone marrow cell culture but did not affect the cultures of differentiated osteoblasts or osteoclast-lineage cells. This study demonstrates a PPARγ γ-dependent regulation of bone metabolism in vivo, in that PPARγ γ insufficiency increases bone mass by stimulating osteoblastogenesis from bone marrow progenitors.Nonstandard abbreviations used: alkaline phosphatase (ALP); bone morphogenetic protein-2 (BMP-2); bone volume (BV); CCAAT enhancer-binding proteins (C/EBPs); computed tomography (CT); LDL receptor-related protein 5 (LRP5); leukemia inhibitory factor (LIF); M-CSF-dependent bone marrow macrophage (M-BMMφ); receptor activator of nuclear factor κB ligand (RANKL); ovariectomy (OVX); PPAR responsive element (PPRE); tartrate-resistant acid phosphatase (TRAP); tissue volume (TV); type I collagen α1 chain (COL1A1).

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“…This possibility is also supported by the observation that fractures take a longer time to heal in diabetes. 58 Krakauer et al 59 have proposed the possibility of a low turnover state due to functional hypoparathyroidism and hyperglycemia to account for the differences between type 1 and type 2 diabetes, but this has yet to be investigated. The heterogeneity of types of diabetes, as well as variable contributions from associated conditions affecting BMD, make it difficult to designate one underlying mechanism for diabetic osteopenia.…”

Section: Diabetes-associated Risk Factorsmentioning

confidence: 99%

Osteoporosis: An Under-appreciated Complication of Diabetes

Brown¹,

Sharpless²

2004

Clinical Diabetes

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In Brief Care of patients with diabetes should include an assessment of bone health. It is now clear that patients with type 1 diabetes have lower bone mineral density (BMD) and higher risk of fractures. Evidence is accumulating that patients with type 2 diabetes who have complications are also at increased risk of certain types of osteoporotic fractures despite having a higher BMD when compared to patients with type 1 diabetes. Therapeutic interventions are key to preventing fractures, both by improving bone density and decreasing the risk for falls.

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Bone Mineral Density in Diabetes

Cited by 19 publications

References 0 publications

Insulin receptor substrate-1 in osteoblast is indispensable for maintaining bone turnover

Insulin receptor substrate-1 in osteoblast is indispensable for maintaining bone turnover

PPAR γ insufficiency enhances osteogenesis through osteoblast formation from bone marrow progenitors

Osteoporosis: An Under-appreciated Complication of Diabetes

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