Malak Faraj, Giulia Leanza, Johannes Krug, Francesca Cannata, Viola Viola, Biagio Zampogna, Fabrizio Russo, Giuseppe Banfi, Giovanni Lombardi, Gianluca Vadalà, Laura Mangiavini, Rocco Papalia, Vincenzo Denaro, Björn Busse, Nicola Napoli
{"title":"高纤维饮食会减少 2 型糖尿病患者的骨骼形成,但不会影响骨骼的微结构。","authors":"Malak Faraj, Giulia Leanza, Johannes Krug, Francesca Cannata, Viola Viola, Biagio Zampogna, Fabrizio Russo, Giuseppe Banfi, Giovanni Lombardi, Gianluca Vadalà, Laura Mangiavini, Rocco Papalia, Vincenzo Denaro, Björn Busse, Nicola Napoli","doi":"10.1093/jbmrpl/ziae111","DOIUrl":null,"url":null,"abstract":"<p><p>Bone fragility is a recognized complication of type 2 diabetes mellitus (T2DM), increasing patient morbidity. Thus, the development of an effective intervention to prevent diabetic bone fragility is urgently needed. As lifestyle intervention represents an effective option for diabetes management, it may have an impact on bone health. While studies have shown a beneficial effect of dietary fiber in T2DM management, its effect on bone health is still unclear. Thus, we investigated the impact of a high-fiber diet on bone and glucose control in men and women with T2DM. Forty-five T2DM patients (HbA1c: 6.5% ± 0.49%, age: 74 ± 7.29 yr) scheduled for hip arthroplasty were randomly assigned to follow a high-fiber diet (38 g/day) or to make no diet changes for 12 wk. Interestingly, BMI decreased by 4% (<i>p</i> <.0001) and HbA1c by 3.4% (<i>p</i> <.0001) in the high-fiber diet group, but did not decrease in the control group. However, serum concentration of the bone formation marker procollagen type 1 amino-terminal propeptide (P1NP) decreased by 8.6 % in the high-fiber diet group (<i>p</i> =.0004), whereas it remained unchanged in the control group. In contrast, similar to the control group, serum concentration of the bone resorption marker C-terminal telopeptide of type I collagen (CTX) concentrations did not change in the high-fiber diet group. Bone microCT analysis revealed no changes in trabecular and cortical bone parameters between the high-fiber diet and control groups. Similarly, real-time (RT)-PCR analysis in bone tissue showed no changes in the gene expression of Wnt pathway-related genes (Sost, Dkk-1, Wnt10b, and Lef-1), bone formation markers (Runx2, Col1a1, and Ocn), and inflammatory cytokines (IL-6, IL-8, TNF-α, and IL-10) between the two groups. Our findings suggest that 12-wk high-fiber diet intervention improves metabolic outcomes in patients with T2DM. 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However, serum concentration of the bone formation marker procollagen type 1 amino-terminal propeptide (P1NP) decreased by 8.6 % in the high-fiber diet group (<i>p</i> =.0004), whereas it remained unchanged in the control group. In contrast, similar to the control group, serum concentration of the bone resorption marker C-terminal telopeptide of type I collagen (CTX) concentrations did not change in the high-fiber diet group. Bone microCT analysis revealed no changes in trabecular and cortical bone parameters between the high-fiber diet and control groups. Similarly, real-time (RT)-PCR analysis in bone tissue showed no changes in the gene expression of Wnt pathway-related genes (Sost, Dkk-1, Wnt10b, and Lef-1), bone formation markers (Runx2, Col1a1, and Ocn), and inflammatory cytokines (IL-6, IL-8, TNF-α, and IL-10) between the two groups. Our findings suggest that 12-wk high-fiber diet intervention improves metabolic outcomes in patients with T2DM. 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引用次数: 0
摘要
骨质脆弱是公认的 2 型糖尿病(T2DM)并发症,会增加患者的发病率。因此,迫切需要开发一种有效的干预措施来预防糖尿病患者骨质脆弱。生活方式干预是糖尿病管理的有效选择,可能会对骨骼健康产生影响。虽然有研究表明膳食纤维对 T2DM 的控制有益处,但其对骨骼健康的影响仍不明确。因此,我们研究了高纤维饮食对男性和女性 T2DM 患者骨骼和血糖控制的影响。45名计划接受髋关节置换术的T2DM患者(HbA1c:6.5% ± 0.49%,年龄:74 ± 7.29岁)被随机分配到高纤维饮食(38克/天)或不改变饮食12周。有趣的是,对照组的体重指数下降了 4%(p p p =.0004),而对照组则保持不变。相反,与对照组相似,高纤维饮食组血清中骨吸收标志物 I 型胶原蛋白 C 端端肽(CTX)的浓度没有变化。骨显微 CT 分析显示,高纤维饮食组和对照组的骨小梁和骨皮质参数没有变化。同样,骨组织中的实时(RT)-PCR 分析显示,两组之间 Wnt 通路相关基因(Sost、Dkk-1、Wnt10b 和 Lef-1)、骨形成标志物(Runx2、Col1a1 和 Ocn)和炎症细胞因子(IL-6、IL-8、TNF-α 和 IL-10)的基因表达没有变化。我们的研究结果表明,为期 12 周的高纤维饮食干预可改善 T2DM 患者的代谢结果。但是,它可能会减少骨形成,而不会影响骨的微结构或 Wnt 通路调节。
High-fiber diet reduces bone formation but does not affect bone microarchitecture in type 2 diabetes individuals.
Bone fragility is a recognized complication of type 2 diabetes mellitus (T2DM), increasing patient morbidity. Thus, the development of an effective intervention to prevent diabetic bone fragility is urgently needed. As lifestyle intervention represents an effective option for diabetes management, it may have an impact on bone health. While studies have shown a beneficial effect of dietary fiber in T2DM management, its effect on bone health is still unclear. Thus, we investigated the impact of a high-fiber diet on bone and glucose control in men and women with T2DM. Forty-five T2DM patients (HbA1c: 6.5% ± 0.49%, age: 74 ± 7.29 yr) scheduled for hip arthroplasty were randomly assigned to follow a high-fiber diet (38 g/day) or to make no diet changes for 12 wk. Interestingly, BMI decreased by 4% (p <.0001) and HbA1c by 3.4% (p <.0001) in the high-fiber diet group, but did not decrease in the control group. However, serum concentration of the bone formation marker procollagen type 1 amino-terminal propeptide (P1NP) decreased by 8.6 % in the high-fiber diet group (p =.0004), whereas it remained unchanged in the control group. In contrast, similar to the control group, serum concentration of the bone resorption marker C-terminal telopeptide of type I collagen (CTX) concentrations did not change in the high-fiber diet group. Bone microCT analysis revealed no changes in trabecular and cortical bone parameters between the high-fiber diet and control groups. Similarly, real-time (RT)-PCR analysis in bone tissue showed no changes in the gene expression of Wnt pathway-related genes (Sost, Dkk-1, Wnt10b, and Lef-1), bone formation markers (Runx2, Col1a1, and Ocn), and inflammatory cytokines (IL-6, IL-8, TNF-α, and IL-10) between the two groups. Our findings suggest that 12-wk high-fiber diet intervention improves metabolic outcomes in patients with T2DM. However, it may reduce bone formation without affecting bone microarchitecture or Wnt pathway regulation.