Effects of the Rate of Impaired Insulin Secretion on Bone Mineral Density in Type 1 Diabetes

Effects of the Rate of Impaired Insulin Secretion on Bone Mineral Density in Type 1 Diabetes
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DOI:
10.1210/jendso/bvab048.557
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发表时间:
2021-05-03
影响因子:
4.1
通讯作者:
Wataru O
Wataru O
中科院分区:
其他
文献类型:
--
作者:
Suzuki M;Urai S;Fukuoka H;Hirota Y;Yamamoto M;Yamamoto N;Shichi H;Fujita Y;Kanie K;Iguchi G;Takahashi Y;Wataru O

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背景:1 型糖尿病 (T1DM) 是一种与低骨矿物质密度 (BMD) 和骨折相关的众所周知的疾病,其中危险因素之一是内源性胰岛素分泌受损。然而,T1DM 胰岛素分泌能力受损率与 BMD 之间的关联仍有待阐明。目的:阐明胰岛素分泌受损率对T1DM患者骨密度的影响。患者和方法:这是一项回顾性单中心横断面研究,连续登记了神户大学医院的 170 名日本 T1DM 患者。根据日本糖尿病协会的诊断标准,将患者分为三个亚型;急性发作(AO)(n = 51,男性 25%,39 ± 15 岁)、缓慢进展(n = 37,男性 37%,57 ± 14 岁)和暴发性(F)(n = 12,男性 33%,51 ± 15 岁)主要取决于 T1DM 发病时的胰岛素分泌能力。评估三组之间的腰椎(LS)和股骨颈(FN)BMD Z 评分。结果:AO 中的 LS BMD 低于 SP(p = 0.03),而与 F 相比没有观察到差异(SP/AO/F;0.38 ± 1.08/-0.25 ± 0.96/-0.35 ± 1.01)。 AO 中的 FN BMD 也往往低于 SP (p = 0.08) 和 F (p = 1.00) (SP/AO/F;0.03 ± 1.01/-0.44 ± 0.96/-0.35 ± 0.70)。为了确定与 BMD 降低相关的因素,使用 AO 和 SP 进行了多变量回归分析。 LS BMD 与致病组相关(p = 0.01)。由于 AO 组和 SP 组的持续时间和 CPR 之间均呈负相关(p <0.01,p <0.01),因此我们将这些受试者分为以下 5 组; 1到4年、5到9年、10到14年、15到19年、以及20多年。在这些组中,1 至 4 年内 AO 的 CPR 低于 SP (p <0.01)。有趣的是,LS BMD 在 5 至 9 年内开始下降(p = 0.03),并在 10 至 14 年内持续下降(p = 0.01)。在 FN 中,BMD 在 10 至 14 年内开始下降(p = 0.01),表明 BMD 下降后胰岛素分泌受损。然而,在15岁以上组中,AO组和SP组之间的BMD和CPR均未见差异,表明这种切线BMD差异与胰岛素分泌的差异有关。结论:本研究首次表明T1DM的致病亚型对BMD有不同的影响。对每个疾病时期的详细检查表明,由于胰岛素分泌受损,骨密度持续下降。
Background: Type 1 Diabetes mellitus (T1DM) is a well-known condition associated with low bone mineral density (BMD) and bone fracture, in which one of the risk factor is impaired endogenous insulin secretion. However, the association between the rate of impaired insulin secretory capacity in T1DM and BMD remains to be elucidated. Objective: To clarify the effect of the rate of impaired insulin secretion on BMD in T1DM. Patients and Methods: This a retrospective single-center cross-sectional study, in which consecutive one-hundred seventy Japanese patients with T1DM at Kobe University Hospital were registered. According to the diagnostic criteria of The Japan Diabetes Society, patients were stratified into three subtypes; acute-onset (AO) (n =51, male 25%, 39 ± 15 years), slowly-progressive (SP) (n =37, male 37%, 57 ± 14 years), and fulminant (F) (n =12, male 33%, 51 ± 15 years) mainly by insulin secretory capacity at onset of T1DM. Lumbar spine (LS) and femoral neck (FN) BMD Z-score between three groups were evaluated. Results: The LS BMD is lower in AO than SP (p =0.03), while no differences were observed compared to F (SP/AO/F; 0.38 ± 1.08/-0.25 ± 0.96/-0.35 ± 1.01). The FN BMD also tended to be lower in AO than in SP (p =0.08) and in F (p =1.00) (SP/AO/F;0.03 ± 1.01/-0.44 ± 0.96/-0.35 ± 0.70). To identify the factors associated with decreased BMD, the multivariate regression analysis was performed using AO and SP. The LS BMD was associated with the pathogenic group (p =0.01). Since a negative correlation was seen between durations and CPR both in AO and SP group (p <0.01, p <0.01), we divided these subjects into following 5 groups; 1 to 4, 5 to 9, 10 to 14, 15 to 19, and more than 20 years. In these groups, the CPR was lower in AO than in SP in 1 to 4 years (p <0.01). Intriguingly, LS BMD was started to decline in 5 to 9 years (p =0.03) and was still continued in 10 to 14 years (p =0.01). In FN, BMD was started to decline in 10 to 14 years (p =0.01), suggesting the BMD decline followed by impaired insulin secretion. However, the difference of both BMD and CPR between AO and SP groups were not seen in more than 15 years group, indicating this tangent BMD difference is link to the difference of insulin secretion. Conclusions: This study firstly showed that pathogenic subtypes of T1DM differently affected on BMD. A detailed examination of each disease period showed that BMD continued to decrease as impaired insulin secretion.