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Type I Diabetic Bone Phenotype is Location but Not Gender Dependent

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Publisher Springer
Date 2007 Jul 5
PMID 17609971
Citations 27
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Abstract

Bone is highly dynamic and responsive. Bone location, bone type and gender can influence bone responses (positive, negative or none) and magnitude. Type I diabetes induces bone loss and increased marrow adiposity in the tibia. We tested if this response exhibits gender and location dependency by examining femur, vertebrae and calvaria of male and female, control and diabetic BALB/c mice. Non-diabetic male mice exhibited larger body, muscle, and fat mass, and increased femur BMD compared to female mice, while vertebrae and calvarial bone parameters did not exhibit gender differences. Streptozotocin-induced diabetes caused a reduction in BMD at all sites examined irrespective of gender. Increased marrow adiposity was evident in diabetic femurs and calvaria (endochondrial and intramembranous formed bones, respectively), but not in vertebrae. Leptin-deficient mice also exhibit location dependent bone responses and we found that serum leptin levels were significantly lower in diabetic compared to control mice. However, in contrast to leptin-deficient mice, the vertebrae of T1-diabetic mice exhibit bone loss, not gain. Taken together, our findings indicate that TI-diabetic bone loss in mice is not gender, bone location or bone type dependent, while increased marrow adiposity is location dependent.

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References
1.
Strotmeyer E, Cauley J, Orchard T, Steenkiste A, Dorman J . Middle-aged premenopausal women with type 1 diabetes have lower bone mineral density and calcaneal quantitative ultrasound than nondiabetic women. Diabetes Care. 2006; 29(2):306-11. DOI: 10.2337/diacare.29.02.06.dc05-1353. View

2.
Weiss L, Barrett-Connor E, von Muhlen D, Clark P . Leptin predicts BMD and bone resorption in older women but not older men: the Rancho Bernardo study. J Bone Miner Res. 2006; 21(5):758-64. DOI: 10.1359/jbmr.060206. View

3.
Hernandez C, Lecube A, Castellanos J, Segura R, Garat M, Garcia-Arumi J . Intravitreous leptin concentrations in patients with proliferative diabetic retinopathy. Retina. 2004; 24(1):30-5. DOI: 10.1097/00006982-200402000-00005. View

4.
Botolin S, Faugere M, Malluche H, Orth M, Meyer R, McCabe L . Increased bone adiposity and peroxisomal proliferator-activated receptor-gamma2 expression in type I diabetic mice. Endocrinology. 2005; 146(8):3622-31. PMC: 1242186. DOI: 10.1210/en.2004-1677. View

5.
Lo H, Lin S, Wang Y . The relationship among serum cytokines, chemokine, nitric oxide, and leptin in children with type 1 diabetes mellitus. Clin Biochem. 2004; 37(8):666-72. DOI: 10.1016/j.clinbiochem.2004.02.002. View