Serum osteocalcin level and its association with carotid atherosclerosis in patients with type 2 diabetes

Li, Sheng; Cao, Wenjie; Cha, Bingbing; Chen, Zhaoping; Wang, Fang; Liu, Jun

doi:10.1186/1475-2840-12-22

Cited by 40 publications

(31 citation statements)

References 35 publications

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“…In addition, measurement of plasma OC concentration has also been proposed as a potential biomarker of cardiometabolic risk, along with its established clinical significance as a biomarker of bone turnover [5]. Reduced plasma OC levels were indeed found to be associated with greater incidence of pathological CV changes, like arterial and valvular calcification [6,7], carotid atherosclerosis [8], and increased carotid intima-media thickness [9]. Moreover, reduced circulating OC levels have consistently been associated with the presence of insulin resistance, metabolic syndrome and type 2 diabetes mellitus (T2DM) [10,11], clearly linked to atherosclerosis development [8].…”

Section: Introductionmentioning

confidence: 99%

Osteocalcin as a potential risk biomarker for cardiovascular and metabolic diseases

Magni

Macchi

Sirtori

et al. 2016

Clinical Chemistry and Laboratory Medicine (CCLM)

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Clear evidence supports a role for circulating and locally-produced osteocalcin (OC) in the pathophysiology of cardiovascular (CV) lesions and CV risk, also in combination with metabolic changes, including type 2 diabetes mellitus (T2DM). Reduced plasma OC levels are associated with greater incidence of pathological CV changes, like arterial and valvular calcification, coronary and carotid atherosclerosis and increased carotid intima-media thickness. The actual relationship between OC levels and incidence of major CV events is, however, still unclear. Moreover, reduced circulating OC levels have been mostly associated with insulin resistance, metabolic syndrome or T2DM, indicating relevant OC actions on pancreatic β-cells and insulin secretion and activity. Based on these observations, this review article will attempt to summarize the current evidence on the potential usefulness of circulating OC as a biomarker for CV and metabolic risk, also evaluating the currently open issues in this area of research.

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Section: Introductionmentioning

confidence: 99%

Osteocalcin as a potential risk biomarker for cardiovascular and metabolic diseases

Magni

Macchi

Sirtori

et al. 2016

Clinical Chemistry and Laboratory Medicine (CCLM)

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“…In addition Sheng et al[15] observed that reduced osteocalcin is associated with increased risk of carotid atherosclerosis plaques in type 2 diabetes patients. They indicated decreased serum concentration of osteocalcin as a high risk for carotid atherosclerotic plaques and presented osteocalcin as a promising candidate for risk assessment of CVD.…”

Section: Discussionmentioning

confidence: 99%

Coronary Artery Calcium Score and Bone Metabolism: A Pilot Study in Postmenopausal Women

et al. 2017

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BackgroundSince 1991 many studies evaluated the link between cardiovascular diseases and osteoporosis, two age-related conditions, but the main common pathologic pathway has not been determined yet. The histological similarity between arterial calcified plaque and bone matrix and involvement of similar cells and mediators provide a special field of research. Therefore in the present study, we aimed to evaluate the relationship between coronary artery calcium score (CACS) as a surrogate marker of atherosclerosis and bone mediators and parameters in postmenopausal women.MethodsEleven postmenopausal women who had CACS higher than 80 were enrolled into the study and underwent bone densitometry. In addition, their serum and urine samples were taken for measuring osteoprotegerin, osteocalcin, and β cross laps. Patients' 10-year probability of fracture was calculated by the World Health Organization fracture-risk assessment tool (FRAX).ResultsThe regression analysis of our results showed the association between CACS and OC (std β=0.66, 95% confidence interval [CI] 5.47-72.27, P=0.027), femoral bone density (std β=−0.6, 95% CI -6864.34-14.27, P=0.05) and T-score (std β=−0.6, 95% CI −773.08-1.28, P=0.05) which remained significant after adjustment for age, weight, years since menopause and body mass index. No association was found between CACS and osteoprotegerin, spinal bone density and FRAX score.ConclusionsIn conclusion, this pilot study with small sample size showed the potential association between CACS and osteocalcin, femoral bone density and T-score. However, the relationship between CACS and osteoprotegerin, receptor activator of nuclear factor-kappa B ligand, FRAX score and other bone parameters remain to be clarified in larger sample size studies.

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“…However, in our study, elevated OCN levels were accompanied by decreased BMD. This result might be attributed to retarded growth and deficient glucose metabolism [50,51]. Several researches declare that BMD and osteocalcin level can be influenced by estrogen, calcium and fat mass, resulting in decreased BMD and increased osteocalcin level [52,53].…”

Section: Discussionmentioning

confidence: 99%

Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model

Zou

Xiong

Lai

et al. 2015

Sci. China Life Sci.

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Bone was reported as a crucial organ for regulating glucose homeostasis. In this study, we found that Phex mutant mice (PUG), a model of human X-linked hypophosphatemic rickets (XLH), displayed metabolic abnormality in addition to abnormal phosphate homeostasis, skeletal deformity and growth retardation. Glucose tolerance was elevated with enhanced insulin sensitivity in PUG, though circulating insulin level decreased. Interestingly, bone mineral density defects and glucose metabolic abnormality were both rescued by adding phosphorus-and calcium-enriched supplements in daily diet. Serum insulin level, glucose tolerance and insulin sensitivity showed no differences between PUG and wild-type mice with rescued osteocalcin (OCN) following treatment. Our study suggested that OCN is a potential mediator between mineral homeostasis and glucose metabolism. This investigation brings a new perspective on glucose metabolism regulation through skeleton triggered mineral homeostasis and provides new clues in clinical therapeutics of potential metabolic disorders in XLH patients. glucose metabolism, mineral homeostasis, bone, Phex, X-linked hypophosphatemic rickets Citation:Zou JH, Xiong XW, Lai BB, Sun M, Tu X, Gao X. Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model. [5,6]. In the past decades, bone was studied as an endocrinal organ [7,8]. Interactions between bone and energy metabolism aroused extensive interests and concerns [911]. Phex is mainly expressed in osteoblasts and odontoblasts [1214] and its mutations lead to reduced 1,25-(OH) 2 D 3 and elevated circulating FGF23 (fibroblast growth factor 23) [1517]. 1,25-(OH) 2 D 3 and its receptor could influence expression of uncoupling protein (UCP) in adipocytes [18,19]. In vitro studies demonstrate that the role of 1,25-(OH) 2 D 3 in lipid metabolism is regulator of peroxisome proliferator-activated receptor alpha (Ppara) [20]. Circulating FGF23 is also associated with fat mass and serum lipids [21]. In mouse models of XLH, like Hyp mice, decreased renal glucose reabsorption activity [22], increased glucose production in renal proximal tubules [23] and osteoblasts [24] were observed. The only known physiological substrate of PHEX protein, acidic serine aspartate-rich MEPE associated motif (ASARM peptide), could regulate glucose metabolism and insulin signaling [14]. The above findings indicate PHEXmediated association between skeletal function and energy

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Serum osteocalcin level and its association with carotid atherosclerosis in patients with type 2 diabetes

Cited by 40 publications

References 35 publications

Osteocalcin as a potential risk biomarker for cardiovascular and metabolic diseases

Osteocalcin as a potential risk biomarker for cardiovascular and metabolic diseases

Coronary Artery Calcium Score and Bone Metabolism: A Pilot Study in Postmenopausal Women

Glucose metabolic abnormality is associated with defective mineral homeostasis in skeletal disorder mouse model

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