ECEESPE2025 ePoster Presentations Bone and Mineral Metabolism (142 abstracts)
Bridging osteoporosis and glucose metabolism: the insulin sensitivity benefits of denosumab
Marta Vaz Lopes 1 , José Vicente Rocha 1,2 , Carolina Peixe 1,2 , Mariana de Griné Severino 1 , Catarina Isabel Lopes 1 , Miguel António Duarte 1 , Mariana Agapito Fonseca 1 , Ines Cosme 1,2 , Maria Inês Alexandre 1,2 , Ana Gomes 1,2 , Francisca Costa 2,3 , Eva Alves 2,3 , Francisco Sampaio 2,3 , EMA PAula Ricca Lacerda Nobre M Caetano 1,2 & Ana Paula Barbosa 1,2,3
1Serviço de Endocrinologia, Diabetes e Metabolismo - Hospital de Santa Maria, Lisbon, Portugal; 2Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal; 3Consulta Multidisciplinar de Osteoporose Fraturária - Hospital de Santa Maria, Lisbon, Portugal
JOINT3951
Introduction: Denosumab is a monoclonal antibody used in osteoporosis treatment because of its role in reduction of bone turnover through the inhibition of the RANKL/RANK pathway. While this pathway is primarily found in bone tissue, it is also expressed in the liver. Recent research suggests that inhibition of this pathway with denosumab therapy may lead to enhanced insulin sensitivity. However, data is still limited on this topic.
Methods: This retrospective study included patients with severe osteoporosis treated with denosumab in a tertiary center. Data at most recent follow-up were compared with data before denosumab treatment initiation, via paired-samples t-tests. Insulin resistance was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR).
Results: A total of 59 patients were included, with a mean age of 73.5±10.5 years; 89.9% (n =53) were female. Mean denosumab treatment duration was 37.9±16.9 months. Before denosumab treatment, 18.6% (n =11) of patients had type 2 diabetes (T2D), 61% (n =36) were prediabetic and 20.4% (n =12) had no glucose metabolism abnormalities. Out of the patients with T2D, all but one had good glycemic control before initiating denosumab therapy: 10 patients had HbA1c levels <7.5%, and 1 patient had a HbA1c level of 8.8%. At most recent follow-up, both mean fasting insulinemia (13.8±1.8mg/dL vs 9.1±0.9mg/dL, P=0.016) and mean HOMA-IR (4.01±1.5 vs 2.38±0.9, P = 0.019) significantly decreased compared to pre-denosumab treatment levels. However, this was not accompanied by a significant decrease in mean fasting plasma glucose levels (111.7±28mg/dL vs 100.5±25mg/dL, P = 0.35) nor in mean HbA1c levels (6.1±0.8% vs 5.9±0.6%, P = 0.064).
Discussion and conclusions: Denosumab was associated with significant reductions in insulin resistance in this population of patients with severe osteoporosis. These results are particularly relevant considering insulin resistance is a known risk factor for osteoporotic fractures. However, it is still unclear whether this reduction in insulin resistance can lead to actual improvement of clinical outcomes in T2D and prediabetes. The fact that most patients included in this study either did not have diabetes or had good glycemic control pre-denosumab may have contributed to the lack of significant decrease in HbA1c and fasting plasma glucose levels. Further studies including a larger sample of patients with T2D may help show whether the effects of denosumab on insulin resistance could improve glycemic control.
Volume 110
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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