Effects of Glucagon-Like Peptide-1 Receptor Agonists on Bone Metabolism in Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.

IF 2.3 4区医学 Q3 ENDOCRINOLOGY & METABOLISM International Journal of Endocrinology Pub Date : 2024-09-14 eCollection Date: 2024-01-01 DOI:10.1155/2024/1785321

Xin Li, Yang Li, Chen Lei

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Abstract

Background: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are an intriguing class of antihyperglycemic drugs for type 2 diabetes mellitus (T2DM). Such drugs not only play a primary role in regulating blood glucose levels but also exhibit additional pleiotropic effects, including potential impacts on bone metabolism and fracture risk. However, the mechanism of such drugs is unclear. The purpose of this study was to evaluate the effect of GLP-1 RAs on bone metabolism in T2DM.

Methods: From database inception to May 1, 2023, the searches were conducted on multiple databases such as Web of Science, Embase, PubMed, CNKI, the Cochrane Library, Wanfang, and VIP. We systematically collected all randomized controlled trials of bone metabolism in patients with T2DM treated with GLP-1 RAs. The quality evaluation was performed according to the Cochrane Handbook for Systematic Reviews of Interventions. Data extraction was analyzed using Review Manager 5.4 software, and funnel plots were drawn to evaluate publication bias.

Results: Twenty-six randomized controlled trials that met the inclusion criteria were included, involving a total of 2268 participants. In this study, compared to other antidiabetic drugs or placebo, GLP-1 RAs were found to significantly increase serum calcium (mean difference (MD) = 0.05, 95% confidence interval (CI) (0.01, 0.09), P = 0.002], bone alkaline phosphatase [standardized MD (SMD) = 0.76, 95% CI (0.29, 1.24), and P = 0.001), and osteocalcin (SMD = 2.04, 95% CI (0.99, 3.08), and P = 0.0001) in T2DM. Specifically, liraglutide increased procollagen type 1 N-terminal propeptide (SMD = 0.45, 95% CI (0.01, 0.89), and P = 0.04). GLP-1 RAs were also associated with a reduction in cross-linked C-terminal telopeptides of type I collagen (SMD = -0.36, 95% CI (-0.70, -0.03), and P = 0.03). In additionally, GLP-1 RAs increased lumbar spine bone mineral density (BMD) (SMD = 1.04, 95% CI (0.60, 1.48), and P < 0.00001) and femoral neck BMD (SMD = 1.29, 95% CI (0.36, 2.23), and P = 0.007).

Conclusions: GLP-1 RAs can not only improve BMD in the lumbar spine and femoral neck of patients with T2DM but also protect bone health by inhibiting bone resorption and promoting bone formation. Systematic Review Registration. PROSPERO, identifier CRD42023418166.

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胰高血糖素样肽-1 受体激动剂对 2 型糖尿病患者骨代谢的影响：系统回顾与元分析》。

背景：胰高血糖素样肽-1 受体激动剂（GLP-1 RAs）是一类治疗 2 型糖尿病（T2DM）的降糖药物，其疗效令人瞩目。这类药物不仅在调节血糖水平方面发挥主要作用，而且还表现出其他多效应，包括对骨代谢和骨折风险的潜在影响。然而，这类药物的作用机制尚不清楚。本研究旨在评估 GLP-1 RAs 对 T2DM 骨代谢的影响：从数据库建立之初到 2023 年 5 月 1 日，我们在 Web of Science、Embase、PubMed、CNKI、Cochrane Library、万方和 VIP 等多个数据库中进行了检索。我们系统地收集了所有使用 GLP-1 RAs 治疗 T2DM 患者骨代谢的随机对照试验。根据《Cochrane干预措施系统综述手册》进行了质量评估。使用Review Manager 5.4软件对数据提取进行分析，并绘制漏斗图以评估发表偏倚：符合纳入标准的 26 项随机对照试验被纳入研究，共有 2268 人参与。在这项研究中，与其他抗糖尿病药物或安慰剂相比，GLP-1 RAs 能显著增加血清钙（平均差（MD）= 0.05，95% 置信区间（CI）（0.01, 0.09），P = 0.002]、骨碱性磷酸酶[标准化 MD（SMD）= 0.76，95% CI（0.29，1.24），P = 0.001]和骨钙素（SMD = 2.04，95% CI（0.99，3.08），P = 0.0001）。具体而言，利拉鲁肽可增加 1 型胶原蛋白 N 端肽（SMD = 0.45，95% CI (0.01，0.89)，P = 0.04）。GLP-1 RA 还与 I 型胶原交联 C 端端肽的减少有关（SMD = -0.36，95% CI (-0.70, -0.03)，P = 0.03）。此外，GLP-1 RAs还能增加腰椎骨矿物质密度（BMD）（SMD = 1.04，95% CI (0.60，1.48)，P < 0.00001）和股骨颈BMD（SMD = 1.29，95% CI (0.36，2.23)，P = 0.007）：结论：GLP-1 RAs 不仅能改善 T2DM 患者腰椎和股骨颈的 BMD，还能通过抑制骨吸收和促进骨形成保护骨骼健康。系统综述注册。PROSPERO，标识符 CRD42023418166。

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来源期刊

International Journal of Endocrinology ENDOCRINOLOGY & METABOLISM-

CiteScore

5.20

自引率

0.00%

发文量

147

审稿时长

1 months

期刊介绍： International Journal of Endocrinology is a peer-reviewed, Open Access journal that provides a forum for scientists and clinicians working in basic and translational research. The journal publishes original research articles, review articles, and clinical studies that provide insights into the endocrine system and its associated diseases at a genomic, molecular, biochemical and cellular level.