Gender differences in sclerostin and clinical characteristics in type 1 diabetes mellitus

Catalano, Antonino; Pintaudi, Basilio; Morabito, Nunziata; Vieste, Giacoma Di; Giunta, Loretta; Bruno, Maria Lucia; Cucinotta, Domenico; Lasco, Antonino; Benedetto, A. Di

doi:10.1530/eje-14-0106

Cited by 40 publications

(29 citation statements)

References 39 publications

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“…Our finding of no association of sclerostin with PTH was consistent with the similar finding in healthy children and healthy adults . In adult T1DM studies, no significant correlation of sclerostin with PTH was found in two studies , while Gennari et al reported a negative correlation in controls and a positive trend in T1DM patients, which has been attributed to a secondary raise in PTH levels due to lower 25(OH)D levels. Although we have evidence that PTH suppresses SOST gene, thus lowering sclerostin levels and leading to a negative correlation , the association of PTH with sclerostin in health and disease remains to be clarified with further investigation.…”

Section: Discussionsupporting

confidence: 91%

Sclerostin distribution in children and adolescents with type 1 diabetes mellitus and correlation with bone metabolism and bone mineral density

et al. 2015

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Section: Discussionsupporting

confidence: 91%

Sclerostin distribution in children and adolescents with type 1 diabetes mellitus and correlation with bone metabolism and bone mineral density

et al. 2015

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“…Increased sclerostin levels have also been reported in some [70, 71] but not all [72] clinical studies of adults with longstanding T1D, but not in children [73], possibly indicative of an exaggerated age-related increase in sclerostin levels in T1D [70]. Interestingly, this is similar to studies in adult patients with T2D, and with prediabetes, which also demonstrate increased serum sclerostin levels [72] [74-77]; in T2D, specifically, sclerostin levels correlate positively with glycated hemoglobin levels and with measures of insulin resistance [74, 76, 77], but negatively with bone-specific alkaline phosphatase (BSAP) [74].…”

Section: Effects Of Type 1 Diabetes On Osteocytesmentioning

confidence: 90%

Effects of Type 1 Diabetes on Osteoblasts, Osteocytes, and Osteoclasts

Kalaitzoglou

Popescu

Bunn

et al. 2016

Curr Osteoporos Rep

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Purpose of review To describe the effects of Type 1 diabetes on bone cells. Recent findings Type 1 diabetes (T1D) is associated with low bone mineral density, increased risk of fractures and poor fracture healing. Its effects on the skeleton were primarily attributed to impaired bone formation, but recent data suggests that bone remodeling and resorption are also compromised. The hyperglycemic and inflammatory environment associated with T1D impacts osteoblasts, osteocytes and osteoclasts. The mechanisms involved are complex; insulinopenia, pro-inflammatory cytokine production and alterations in gene expression are a few of the contributing factors leading to poor osteoblast activity and survival and, therefore, poor bone formation. In addition, the observed sclerostin level increase accompanied by decreased osteocyte number and enhanced osteoclast activity in T1D results in uncoupling of bone remodeling. Summary T1D negatively impacts osteoblasts and osteocytes whereas its effects on osteoclasts are not well characterized, although the limited studies available indicate increased osteoclast activity, favoring bone resorption.

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“…Metabolic alterations, like insulin resistance, can contribute to explain the rising of sclerostin. Patients with Type 1 diabetes do not have insulin resistance, and serum sclerostin does not differ from controls [12, 34]. …”

Section: Discussionmentioning

confidence: 99%

Normal bone density and trabecular bone score, but high serum sclerostin in congenital generalized lipodystrophy

Lima

Nóbrega

Lima

et al. 2017

Bone

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Context Berardinelli-Seip Congenital Lipodystrophy (BSCL) is a rare autosomal recessive syndrome characterized by a difficulty in storing lipids in adipocytes, low body fat mass, hypoleptinemia, and hyperinsulinemia. Sclerostin is a product of SOST gene that blocks the Wnt/β-catenin pathway, decreasing bone formation and enhancing adipogenesis. There are no data about sclerostin in people with BSCL. Objective We aimed to evaluate serum sclerostin, bone mineral density (BMD), and L1-L4 Trabecular Bone Score (TBS) in BSCL patients, generating new knowledge about potential mechanisms involved in the bone alterations of these patients. Design, Setting, and Patients In this cross-sectional study, we included 11 diabetic patients with BSCL (age 24.7±8.1 years; 6 females). Sclerostin, leptin, L1-L4 TBS, BMD were measured. Potential pathophysiological mechanisms have been suggested. Results Mean serum sclerostin was elevated (44.7±13.4 pmol/L) and was higher in men than women (55.3±9.0 vs. 35.1±8.4 pmol/L, p=0.004). Median of serum leptin was low [0.9 ng/mL (0.5-1.9) ]. Seven out of 11 patients had normal BMD, while four patients had high bone mass (defined as Z-score>+2.5SD). Patients on insulin had lower sclerostin (37.3±9.2 vs. 52.6±13.4 pmol/L, p=0.05). The mean TBS was 1.402±0.106, and it was higher than 1.300 in nine patients. Conclusions Patients with lipoatrophic diabetes (BSCL) have high serum concentrations of sclerostin, normal or high BMD, and reasonable trabecular bone mass measured by TBS. This is the first report of high sclerostin and good bone microarchitecture (TBS) in BSCL patients.

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Gender differences in sclerostin and clinical characteristics in type 1 diabetes mellitus

Cited by 40 publications

References 39 publications

Sclerostin distribution in children and adolescents with type 1 diabetes mellitus and correlation with bone metabolism and bone mineral density

Sclerostin distribution in children and adolescents with type 1 diabetes mellitus and correlation with bone metabolism and bone mineral density

Effects of Type 1 Diabetes on Osteoblasts, Osteocytes, and Osteoclasts

Normal bone density and trabecular bone score, but high serum sclerostin in congenital generalized lipodystrophy

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