Osteologie 2020; 29(01): 7-12
DOI: 10.1055/a-1076-1523
Originalarbeit

Knochen und Diabetes mellitus

Bone and Diabetes mellitus
Stephan H. Scharla
1   Praxis Innere Medizin, Endokrinologie & Diabetologie,, Bad Reichenhall, Germany
2   Medizinische Fakultät, Ludwig-Maximilians-Universität,, München, Germany
› Author Affiliations

Zusammenfassung

Diabetes mellitus ist mit einem erhöhten Risiko für Osteoporose und Frakturen assoziiert. Patienten mit Diabetes mellitus Typ 1 sind stärker betroffen, mit einem relativen Risiko für Hüftfrakturen von 2,5 bis 12. Das Risiko für Wirbelfrakturen ist bis 2-fach erhöht. Bei Patienten mit Diabetes mellitus Typ 2 ist das Frakturrisiko nicht so deutlich erhöht und mit der Zeitdauer der Diabetes-Erkrankung, dem Vorliegen von vaskulären Schäden, einer Neuropathie und mit einer Insulintherapie assoziiert. Ursachen für das gesteigerte Frakturrisiko sind toxische Effekte von hohen Glukosekonzentration auf Osteoblasten, die Glykierung von Knochenmatrixproteinen mit Veränderung der Kollagenstruktur, hormonelle Veränderungen und eine Störung der Knochenarchitektur. Das Frakturrisiko kann auch schon ohne deutliche Knochendichte-Minderung bereits erhöht sein. Die therapeutische Interventionsschwelle bei der Knochendichtemessung sollte deshalb in Richtung höhere Werte angepasst werden. Der Knochen als endokrines Organ moduliert aber auch den Zuckerstoffwechsel. Das aus dem Knochen freigesetzte untercarboxylierte Osteocalcin stimuliert die Insulinsekretion im Pankreas, verbessert die Insulinsensitivität und ist mit dem Risiko für die Manifestation des Diabetes mellitus assoziiert.

Abstract

Diabetes mellitus is associated with an increased risk for osteoporosis and fractures. Patients with diabetes mellitus type 1 are more severely affected (relative risk for hip fracture reaching from 2.5 to 12). The relative risk for vertebral fractures is doubled. In contrast, patients with diabetes mellitus 2 exhibit only a moderately increased fracture risk, which is associated with duration of diabetic disease, vascular disease, neuropathy, and insulin treatment. The causes for the increased fracture risk are toxic effects of high glucose concentrations on osteoblasts, the glycation of bone matrix proteins leading to changes in collagen structure, endocrine alterations, and changes in bone architecture. The fracture risk may be increased, even without significant loss of measured bone mineral density (BMD). Therefore, the therapeutic intervention threshold of BMD measurements has to be increased. Bone tissue is an endocrine organ and modulates sugar metabolism. Undercarboxylated osteocalcin released from bone stimulates insulin secretion in the pancreatic gland, improves insulin sensitivity and modulates the risk of diabetes manifestation.



Publication History

Received: 05 December 2019

Accepted: 12 December 2019

Article published online:
25 February 2020

© Georg Thieme Verlag KG
Stuttgart · New York

 
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