Comparison of insulin-like growth factor-1 and sclerostin levels between premenopausal women with and without diabetes mellitus

Abstract

Objectives This study assesses the serum levels of insulin-like growth factor-1 (IGF-1) and sclerostin as markers of decreased bone formation in premenopausal women with type 2 diabetes mellitus. Methods A cross-sectional study was conducted to measure serum levels of IGF-1 and sclerostin in 40 premenopausal women with and without diabetes mellitus using an enzyme-linked immunosorbent assay. The levels of IGF-1 and sclerostin were compared between the groups using the Mann Whitney test and unpaired t-test, respectively. Results The median IGF-1 serum levels were 40.60 ng/mL and 42.7 ng/mL in the diabetic and non-diabetic groups, respectively, with no significant difference. The serum levels of sclerostin were significantly higher in the diabetic group than in the non-diabetic group (132.1 pg/mL and 96.0 pg/mL, respectively; p < 0.001). Conclusion The levels of sclerostin were significantly higher in premenopausal women with diabetes mellitus than in the non-diabetic group. Since sclerostin influences the differentiation and maturation of osteoblasts, serum sclerostin might potentially be useful as a marker of decreased bone formation in premenopausal women with diabetes.

Links among Obesity, Type 2 Diabetes Mellitus, and Osteoporosis: Bone as a Target

“…Many studies suggest that due to chronic hyperglycemia, the formation of ROS may be associated with collagen glycation, which is an important factor [4,5]. Overall, bone damage in T2DM can be caused by multiple mechanisms: accumulation of advanced glycation end products (AGEs) [79], increased levels of pro-inflammatory cytokines (e.g., IL-6, TNF-α) [80], sclerostin [81], leptin [80], lower levels of OC [11,82]), procollagen I N-terminal propeptide (P1NP) [83,84], parathyroid hormone (PTH) [85], and impairment of osteoblastogenesis [86]. The status of low bone turnover in T2DM is also reflected in lower levels of bone resorption markers (e.g., TRAP5b and C-telopeptide of type I collagen (CTx)) [82,85].…”

Organokines, Sarcopenia, and Metabolic Repercussions: The Vicious Cycle and the Interplay with Exercise

“…Hyperglycemia leads to a decrease in bone formation, as it directly increases sclerostin production, inhibiting bone formation by downregulating the Wnt pathway (a signaling pathway that affects bone modeling and remodeling). In addition, there is a relationship between elevated sclerostin levels with the increase in the risk of spinal fracture [ 75 , 112 , 116 , 117 ].…”

“…Its excess is related to metabolic disorders, while insulin increases the number and function of osteoblasts, which indirectly controls blood glucose levels. Therefore, it is being argued that sclerostin has great potential to directly implicate sarcopenia and other metabolic implications [ 73 , 75 , 76 , 112 ].…”

The complex pathophysiology of bone fragility in obesity and type 2 diabetes mellitus: therapeutic targets to promote osteogenesis

“…Furthermore, Jain et al.,studies confirmed that visceral adipose tissue (VAT) is negatively associated with bone mineral density ( 23 ). On the other hand, in T2D BMD is normal or above normal,likely protective against vertebral fractures ( 24 ), but some studies show reduced BMD ( 25 , 26 ) due to accumulation of advanced glycation end products (AGEs) ( 27 , 28 ) increased proinflammatory cytokines such as TNF-a, IL-6 ( 28 , 29 ) high sclerostin levels ( 30 ) leading to reduction in bone formation, OCN ( 31 ) and (Procollagen I N-terminal propeptide) P1NP levels in T2DM ( 31 , 32 ) and impairment in osteoblastogenesis ( 33 – 35 ). There is also reduction in bone resorption markers (CTX and TRAP5b) ( 28 ) though bone turnover markers are not as predictive of fractures compared to BMD and maybe difficult to interpret,.…”