全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Bone Health in Type 1 Diabetes: Where We Are Now and How We Should Proceed

DOI: 10.1155/2014/982129

Full-Text   Cite this paper   Add to My Lib

Abstract:

Type 1 diabetes (T1D) is autoimmune disease with chronic hyperglycaemic state. Besides diabetic retinopathy, nephropathy, and neuropathy, T1D is characterized by poor bone health. The reduced bone mineralization and quality/strength, due to hyperglycemia, hypoinsulinemia, autoimmune inflammation, low levels of insulin growth factor-1 (IGF-1), and vitamin D, lead to vertebral/hip fractures. Young age of T1D manifestation, chronic poor glycemic control, high daily insulin dose, low BMI, reduced renal function, and the presence of complications can be helpful in identifying T1D patients at risk of reduced bone mineral density. Although risk factors for fracture risk are still unknown, chronic poor glycemic control and presence of diabetic complications might raise the suspicion of elevated fracture risk in T1D. In the presence of the risk factors, the assessment of bone mineral density by dual-energy X-ray absorptiometry and the search of asymptomatic vertebral fracture by lateral X-ray radiography of thorax-lumbar spine should be recommended. The improvement of glycemic control may have a beneficial effect on bone in T1D. Several experiments showed promising results on using anabolic pharmacological agents (recombinant IGF-1 and parathyroid hormone) in diabetic rodents with bone disorder. Randomized clinical trials are needed in order to test the possible use of bone anabolic therapies in humans with T1D. 1. Introduction Type 1 diabetes (T1D) is an autoimmune disease that precipitates in genetically susceptible individuals by environmental factors. The body’s own immune system attacks the beta-cells in the islets of Langerhans of the pancreas, destroying or damaging them sufficiently to reduce and eliminate insulin production, leading to the hypoinsulinemia and chronic hyperglycaemia [1]. T1D incidence has been globally rising during the past decades by as much as 3% annually, the cause of which is unknown. If these trends will continue, the total prevalence of people with type 1 diabetes will increase in coming years [2]. Chronic hyperglycaemia in T1D leads, in course of time, to chronic complications. Besides acute diabetic complications, nowadays, health providers give more attention to the prevention of disabling chronic complications, such as diabetic retinopathy, nephropathy, neuropathy, and precocious atherosclerosis with early cardiovascular disease. Recently, a major interest has been focused on poor bone metabolism in T1D that can represent an overlooked complication of diabetes. 2. What Do We Know? Bone Parameters and Fracture Risk in Type 1

References

[1]  T. L. van Belle, K. T. Coppieters, and M. G. von Herrath, “Type 1 diabetes: etiology, immunology, and therapeutic strategies,” Physiological Reviews, vol. 91, no. 1, pp. 79–118, 2011.
[2]  L. Guariguata, “Estimating the worldwide burden of type 1 diabetes,” Diabetes Voice, vol. 56, no. 2, pp. 6–8, 2011.
[3]  F. Albright and E. C. Reifenstein, “Bone development in diabetic children: a roentgen study,” The American Journal of the Medical Sciences, vol. 174, pp. 313–319, 1948.
[4]  M. E. Levin, V. C. Boisseau, and L. V. Avioli, “Effects of diabetes mellitus on bone mass in juvenile and adult onset diabetes,” The New England Journal of Medicine, vol. 294, no. 5, pp. 241–245, 1976.
[5]  J. Pascual, J. Argente, M. B. Lopez et al., “Bone mineral density in children and adolescents with diabetes mellitus type 1 of recent onset,” Calcified Tissue International, vol. 62, no. 1, pp. 31–35, 1998.
[6]  A. Salvatoni, G. Mancassola, R. Biasoli et al., “Bone mineral density in diabetic children and adolescents: a follow-up study,” Bone, vol. 34, no. 5, pp. 900–904, 2004.
[7]  F. R. Brandao, E. J. Vicente, C. H. Daltro, M. Sacramento, A. Moreira, and L. Adan, “Bone metabolism is linked to disease duration and metabolic control in type 1 diabetes mellitus,” Diabetes Research and Clinical Practice, vol. 78, no. 3, pp. 334–339, 2007.
[8]  E. Y. Liu, J. Wactawski-Wende, R. P. Donahue, J. Dmochowski, K. M. Hovey, and T. Quattrin, “Does low bone mineral density start in post-teenage years in women with type 1 diabetes?” Diabetes Care, vol. 26, no. 8, pp. 2365–2369, 2003.
[9]  L. D. Mastrandrea, J. Wactawski-Wende, R. P. Donahue, K. M. Hovey, A. Clark, and T. Quattrin, “Young women with type 1 diabetes have lower bone mineral density that persists over time,” Diabetes Care, vol. 31, no. 9, pp. 1729–1735, 2008.
[10]  S. Bechtold, I. Dirlenbach, K. Raile, V. Noelle, W. Bonfig, and H. P. Schwarz, “Early manifestation of type 1 diabetes in children is a risk factor for changed bone geometry: data using peripheral quantitative computed tomography,” Pediatrics, vol. 118, no. 3, pp. e627–e634, 2006.
[11]  A. B. R. Maggio, S. Ferrari, M. Kraenzlin et al., “Decreased bone turnover in children and adolescents with well controlled type 1 diabetes,” Journal of Pediatric Endocrinology and Metabolism, vol. 23, no. 7, pp. 697–707, 2010.
[12]  P. Gunczler, R. Lanes, V. Paz-Martinez et al., “Decreased lumbar spine bone mass and low bone turnover in children and adolescents with insulin dependent diabetes mellitus followed longitudinally,” Journal of Pediatric Endocrinology and Metabolism, vol. 11, no. 3, pp. 413–419, 1998.
[13]  G. Valerio, A. del Puente, A. Esposito-del Puente, P. Buono, E. Mozzillo, and A. Franzese, “The lumbar bone mineral density is affected by long-term poor metabolic control in adolescents with type 1 diabetes mellitus,” Hormone Research, vol. 58, no. 6, pp. 266–272, 2002.
[14]  K. Heilman, M. Zilmer, K. Zilmer, and V. Tillmann, “Lower bone mineral density in children with type 1 diabetes is associated with poor glycemic control and higher serum ICAM-1 and urinary isoprostane levels,” Journal of Bone and Mineral Metabolism, vol. 27, no. 5, pp. 598–604, 2009.
[15]  J. Léger, D. Marinovic, C. Alberti et al., “Lower bone mineral content in children with type 1 diabetes mellitus is linked to female sex, low insulin-like growth factor type I levels, and high insulin requirement,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 10, pp. 3947–3953, 2006.
[16]  M. T. Saha, H. Siev?nen, M. K. Salo, S. Tulokas, and H. H. Saha, “Bone mass and structure in adolescents with type 1 diabetes compared to healthy peers,” Osteoporosis International, vol. 20, no. 8, pp. 1401–1406, 2009.
[17]  J. Heap, M. A. Murray, S. C. Miller, T. Jalili, and L. J. Moyer-Mileur, “Alterations in bone characteristics associated with glycemic control in adolescents with type 1 diabetes mellitus,” Journal of Pediatrics, vol. 144, no. 1, pp. 56–62, 2004.
[18]  E. A. Hamed, N. H. Abu Faddan, H. A. Adb Elhafeez, and D. Sayed, “Parathormone—25(OH)-vitamin D axis and bone status in children and adolescents with type 1 diabetes mellitus,” Pediatric Diabetes, vol. 12, no. 6, pp. 536–546, 2011.
[19]  M. Mu?oz-Torres, E. Jódar, F. Escobar-Jiménez, P. J. López-Ibarra, and J. D. Luna, “Bone mineral density measured by dual X-ray absorptiometry in Spanish patients with insulin-dependent diabetes mellitus,” Calcified Tissue International, vol. 58, no. 5, pp. 316–319, 1996.
[20]  M. Rix, H. Andreassen, and P. Eskildsen, “Impact of peripheral neuropathy on bone density in patients with type 1 diabetes,” Diabetes Care, vol. 22, no. 5, pp. 827–831, 1999.
[21]  J. T. Tuominen, O. Impivaara, P. Puukka, and T. R?nnemaa, “Bone mineral density in patients with type 1 and type 2 diabetes,” Diabetes Care, vol. 22, no. 7, pp. 1196–1200, 1999.
[22]  M. M. Campos Pastor, P. J. López-Ibarra, F. Escobar-Jiménez, M. D. Serrano Pardo, and A. García-Cervigón, “Intensive insulin therapy and bone mineral density in type 1 diabetes mellitus: a prospective study,” Osteoporosis International, vol. 11, no. 5, pp. 455–459, 2000.
[23]  S. A. G. Kemink, A. R. M. M. Hermus, L. M. J. W. Swinkels, J. A. Lutterman, and A. G. H. Smals, “Osteopenia in insulin-dependent diabetes mellitus: prevalence and aspects of pathophysiology,” Journal of Endocrinological Investigation, vol. 23, no. 5, pp. 295–303, 2000.
[24]  A. Rozadilla, J. M. Nolla, E. Montana et al., “Bone mineral density in patients with type 1 diabetes mellitus,” Joint Bone Spine, vol. 67, no. 3, pp. 215–218, 2000.
[25]  P.-J. López-Ibarra, M. M. C. Pastor, F. Escobar-Jiménez et al., “Bone mineral density at time of clinical diagnosis of adult-onset type 1 diabetes mellitus,” Endocrine Practice, vol. 7, no. 5, pp. 346–351, 2001.
[26]  D. J. Hadjidakis, A. E. Raptis, M. Sfakianakis, A. Mylonakis, and S. A. Raptis, “Bone mineral density of both genders in type 1 diabetes according to bone composition,” Journal of Diabetes and its Complications, vol. 20, no. 5, pp. 302–307, 2006.
[27]  K. K. Danielson, M. E. Elliott, T. Lecaire, N. Binkley, and M. Palta, “Poor glycemic control is associated with low BMD detected in premenopausal women with type 1 diabetes,” Osteoporosis International, vol. 20, no. 6, pp. 923–933, 2009.
[28]  E. J. Hamilton, V. Rakic, W. A. Davis et al., “Prevalence and predictors of osteopenia and osteoporosis in adults with type 1 diabetes,” Diabetic Medicine, vol. 26, no. 1, pp. 45–52, 2009.
[29]  T. Miazgowski, S. Pynka, M. Noworyta-Zietara, B. Kryzanowska-?winiarska, and R. Pikul, “Bone mineral density and hip structural analysis in type 1 diabetic men,” European Journal of Endocrinology, vol. 156, no. 1, pp. 123–127, 2007.
[30]  O. Alexopoulou, J. Jamart, J. P. Devogelaer, S. Brichard, P. de Nayer, and M. Buysschaert, “Bone density and markers of bone remodeling in type 1 male diabetic patients,” Diabetes and Metabolism, vol. 32, no. 5, pp. 453–458, 2006.
[31]  G. Hampson, C. Evans, R. J. Petitt et al., “Bone mineral density, collagen type 1 α 1 genotypes and bone turnover in premenopausal women with diabetes mellitus,” Diabetologia, vol. 41, no. 11, pp. 1314–1320, 1998.
[32]  C.-M. Ingberg, M. Palmér, J. ?man, B. Arvidsson, E. Schvarcz, and C. Berne, “Body composition and bone mineral density in long-standing type 1 diabetes,” Journal of Internal Medicine, vol. 255, no. 3, pp. 392–398, 2004.
[33]  M. J. Bridges, S. H. Moochhala, J. Barbour, and C. A. Kelly, “Influence of diabetes on peripheral bone mineral density in men: a controlled study,” Acta Diabetologica, vol. 42, no. 2, pp. 82–86, 2005.
[34]  P. Vestergaard, “Discrepancies in bone mineral density and fracture risk in patients with type 1 and type 2 diabetes—a meta-analysis,” Osteoporosis International, vol. 18, no. 4, pp. 427–444, 2007.
[35]  C. Eller-Vainicher, V. V. Zhukouskaya, Y. V. Tolkachev et al., “Low bone mineral density and its predictors in type 1 diabetic patients evaluated by the classic statistics and artificial neural network analysis,” Diabetes Care, vol. 34, no. 10, pp. 2186–2191, 2011.
[36]  M. J. Silva, M. D. Brodt, M. A. Lynch et al., “Type 1 diabetes in young rats leads to progressive trabecular bone loss, cessation of cortical bone growth, and diminished whole bone strength and fatigue life,” Journal of Bone and Mineral Research, vol. 24, no. 9, pp. 1618–1627, 2009.
[37]  J. S. Nyman, J. L. Even, C. Jo et al., “Increasing duration of type 1 diabetes perturbs the strength-structure relationship and increases brittleness of bone,” Bone, vol. 48, no. 4, pp. 733–740, 2011.
[38]  N. Erdal, S. Gürgül, C. Demirel, and A. Yildiz, “The effect of insulin therapy on biomechanical deterioration of bone in streptozotocin (STZ)-induced type 1 diabetes mellitus in rats,” Diabetes Research and Clinical Practice, vol. 97, no. 3, pp. 461–467, 2012.
[39]  S. Bechtold, S. Putzker, W. Bonfig, O. Fuchs, I. Dirlenbach, and H. P. Schwarz, “Bone size normalizes with age in children and adolescents with type 1 diabetes,” Diabetes Care, vol. 30, no. 8, pp. 2046–2050, 2007.
[40]  I. Roggen, I. Gies, J. Vanbesien, O. Louis, and J. de Schepper, “Trabecular bone mineral density and bone geometry of the distal radius at completion of pubertal growth in childhood type 1 diabetes,” Hormone Research in Paediatrics, vol. 79, no. 2, pp. 68–74, 2013.
[41]  L. A. G. Armas, M. P. Akhter, A. Drincic, and R. R. Recker, “Trabecular bone histomorphometry in humans with type 1 diabetes mellitus,” Bone, vol. 50, no. 1, pp. 91–96, 2012.
[42]  T. Neumann, A. S?mann, S. Lodes et al., “Glycaemic control is positively associated with prevalent fractures but not with bone mineral density in patients with type1 diabetes,” Diabetic Medicine, vol. 28, no. 7, pp. 872–875, 2011.
[43]  V. V. Zhukouskaya, C. Eller-Vainicher, V. V. Vadzianava et al., “Prevalence of morphometric vertebral fractures in patients with type 1 diabetes,” Diabetes Care, vol. 36, no. 6, pp. 1635–1640, 2013.
[44]  J. Starup-Linde, “Diabetes, biochemical markers of bone turnover, diabetes control and bone,” Frontiers in Endocrinology, vol. 4, article 21, 2013.
[45]  A. Patti, L. Gennari, D. Merlotti, F. Dotta, and R. Nuti, “Endocrine actions of osteocalcin,” International Journal of Endocrinology, vol. 2013, Article ID 846480, 10 pages, 2013.
[46]  L. R. McCabe, J. Zhang, and S. Raehtz, “Understanding the skeletal pathology of type 1 and 2 diabetes mellitus,” Critical Reviews in Eukaryotic Gene Expression, vol. 21, no. 2, pp. 187–206, 2011.
[47]  M. Hie, N. Iitsuka, T. Otsuka, and I. Tsukamoto, “Insulin-dependent diabetes mellitus decreases osteoblastogenesis associated with the inhibition of Wnt signaling through increased expression of Sost and Dkk1 and inhibition of Akt activation,” International Journal of Molecular Medicine, vol. 28, no. 3, pp. 455–462, 2011.
[48]  Y. F. Zhao, D. L. Zeng, L. G. Xia et al., “Osteogenic potential of bone marrow stromal cells derived from streptozotocin-induced diabetic rats,” International Journal of Molecular Medicine, vol. 31, no. 3, pp. 614–620, 2013.
[49]  S. Portal-Nú?ez, D. Lozano, L. Fernández de Castro, A. R. de Gortázar, X. Nogués, and P. Esbrit, “Alterations of the Wnt/β-catenin pathway and its target genes for the N- and C-terminal domains of parathyroid hormone-related protein in bone from diabetic mice,” FEBS Letters, vol. 584, no. 14, pp. 3095–3100, 2010.
[50]  L. J. Moyer-Mileur, H. Slater, K. C. Jordan, and M. A. Murray, “IGF-1 and IGF-binding proteins and bone mass, geometry, and strength: relation to metabolic control in adolescent girls with type 1 diabetes,” Journal of Bone and Mineral Research, vol. 23, no. 12, pp. 1884–1891, 2008.
[51]  B. J. van Sickle, J. Simmons, R. Hall, M. Raines, K. Ness, and A. Spagnoli, “Increased circulating IL-8 is associated with reduced IGF-1 and related to poor metabolic control in adolescents with type 1 diabetes mellitus,” Cytokine, vol. 48, no. 3, pp. 290–294, 2009.
[52]  K. M. Thrailkill and J. L. Fowlkes, “The role of vitamin d in the metabolic homeostasis of diabetic bone,” Clinical Reviews in Bone and Mineral Metabolism, vol. 11, no. 1, pp. 28–37, 2013.
[53]  S. Botolin and L. R. McCabe, “Chronic hyperglycemia modulates osteoblast gene expression through osmotic and non-osmotic pathways,” Journal of Cellular Biochemistry, vol. 99, no. 2, pp. 411–424, 2006.
[54]  P. Odetti, S. Rossi, F. Monacelli et al., “Advanced glycation end products and bone loss during aging,” Annals of the New York Academy of Sciences, vol. 1043, pp. 710–717, 2005.
[55]  J. L. Fowlkes, R. C. Bunn, and K. M. Thrailkill, “Contributions of the insulin/insulin-like growth factor-1 axis to diabetic osteopathy,” Journal of Diabetes and Metabolism, vol. 1, no. 3, p. S1-003, 2011.
[56]  S. F. Ahmed and C. Farquharson, “The effect of GH and IGF1 on linear growth and skeletal development and their modulation by SOCS proteins,” Journal of Endocrinology, vol. 206, no. 3, pp. 249–259, 2010.
[57]  L. M. Coe, R. Irwin, D. Lippner, and L. R. McCabe, “The bone marrow microenvironment contributes to type I diabetes induced osteoblast death,” Journal of Cellular Physiology, vol. 226, no. 2, pp. 477–483, 2011.
[58]  K. J. Motyl, S. Botolin, R. Irwin et al., “Bone inflammation and altered gene expression with type Idiabetes early onset,” Journal of Cellular Physiology, vol. 218, no. 3, pp. 575–583, 2009.
[59]  S. Botolin, M. Faugere, H. Malluche, M. Orth, R. Meyer, and L. R. McCabe, “Increased bone adiposity and peroxisomal proliferator-activated receptor-γ2 expression in type I diabetic mice,” Endocrinology, vol. 146, no. 8, pp. 3622–3631, 2005.
[60]  S. Botolin and L. R. McCabe, “Bone loss and increased bone adiposity in spontaneous and pharmacologically induced diabetic mice,” Endocrinology, vol. 148, no. 1, pp. 198–205, 2007.
[61]  M. F. Holick, N. C. Binkley, H. A. Bischoff-Ferrari et al., “Evaluation, treatment, and prevention of vitamin D deficiency: an endocrine society clinical practice guideline,” Journal of Clinical Endocrinology and Metabolism, vol. 96, no. 7, pp. 1911–1930, 2011.
[62]  K. M. Thrailkill, T. Nimmo, R. C. Bunn et al., “Microalbuminuria in type 1 diabetes is associated with enhanced excretion of the endocytic multiligand receptors megalin and cubilin,” Diabetes Care, vol. 32, no. 7, pp. 1266–1268, 2009.
[63]  K. M. Thrailkill, C. Jo, G. E. Cockrell, C. S. Moreau, and J. L. Fowlkes, “Enhanced excretion of vitamin D binding protein in type 1 diabetes: a role in vitamin D deficiency?” Journal of Clinical Endocrinology and Metabolism, vol. 96, no. 1, pp. 142–149, 2011.
[64]  A. Joshi, P. Varthakavi, M. Chadha, and N. Bhagwat, “A study of bone mineral density and its determinants in type 1 diabetes mellitus,” Journal of Osteoporosis, vol. 2013, Article ID 397814, 8 pages, 2013.
[65]  M. O. ?amurdan, P. Ciaz, A. Bideci, and F. Demirel, “Role of hemoglobin A1c, duration and puberty on bone mineral density in diabetic children,” Pediatrics International, vol. 49, no. 5, pp. 645–651, 2007.
[66]  T. J. Wilkin, “Is autoimmunity or insulin resistance the primary driver of type 1 diabetes?” Current Diabetes Reports, vol. 13, no. 5, pp. 651–656, 2013.
[67]  S. A. Jamal, V. J. D. Swan, J. P. Brown et al., “Kidney function and rate of bone loss at the hip and spine: the Canadian multicentre osteoporosis study,” The American Journal of Kidney Diseases, vol. 55, no. 2, pp. 291–299, 2010.
[68]  V. Morelli, C. Eller-Vainicher, A. S. Salcuni et al., “Risk of new vertebral fractures in patients with adrenal incidentaloma with and without subclinical hypercortisolism: a multicenter longitudinal study,” Journal of Bone and Mineral Research, vol. 26, no. 8, pp. 1816–1821, 2011.
[69]  P. Vestergaard, L. Rejnmark, and L. Mosekilde, “Diabetes and its complications and their relationship with risk of fractures in type 1 and 2 diabetes,” Calcified Tissue International, vol. 84, no. 1, pp. 45–55, 2009.
[70]  S. Ferrari, M. L. Bianchi, J. A. Eisman et al., “Osteoporosis in young adults: pathophysiology, diagnosis, and management,” Osteoporosis International, vol. 23, no. 12, pp. 2735–2748, 2012.
[71]  K. J. Motyl, L. K. McCauley, and L. R. McCabe, “Amelioration of type I diabetes-induced osteoporosis by parathyroid hormone is associated with improved osteoblast survival,” Journal of Cellular Physiology, vol. 227, no. 4, pp. 1326–1334, 2012.
[72]  A. B. R. Maggio, R. R. Rizzoli, L. M. Marchand, S. Ferrari, M. Beghetti, and N. J. Farpour-Lambert, “Physical activity increases bone mineral density in children with type 1 diabetes,” Medicine and Science in Sports and Exercise, vol. 44, no. 7, pp. 1206–1211, 2012.
[73]  D. Hans, N. Barthe, S. Boutroy, L. Pothuaud, R. Winzenrieth, and M. Krieg, “Correlations between trabecular bone score, measured using anteroposterior dual-energy X-ray absorptiometry acquisition, and 3-dimensional parameters of bone microarchitecture: an experimental study on human cadaver vertebrae,” Journal of Clinical Densitometry, vol. 14, no. 3, pp. 302–312, 2011.
[74]  W. D. Leslie, B. Aubry-Rozier, O. Lamy, and D. Hans, “TBS (trabecular bone score) and diabetes-related fracture risk,” Journal of Clinical Endocrinology and Metabolism, vol. 98, no. 2, pp. 602–609, 2013.
[75]  C. Eller-Vainicher, V. Morelli, F. M. Ulivieri et al., “Bone quality, as measured by trabecular bone score in patients with adrenal incidentalomas with and without subclinical hypercortisolism,” Journal of Bone and Mineral Research, vol. 27, no. 10, pp. 2223–2230, 2012.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133

WeChat 1538708413