Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?

• Autores: McCarthy, Antonio Desmond; Cortizo, Ana María; Sedlinsky, Claudia
• Año de publicación: 2016
• Idioma: español castellano
• Tipo de recurso: artículo
• Materia: Ciencias Químicas; Diabetes Mellitus; Osteoporosis; Bone fractures; Metformin; AMP-activated kinase
• Institución: Comisión de Investigaciones Científicas de la Provincia de Buenos Aires

Patients with long-term type 1 and type 2 diabetes or “diabetic osteopathy”. These include osteopenia, osteoporosis and an increased incidence of low-stress fractures. In this context, it is important to evaluate whether current anti-diabetic treatments can secondarily affect bone metabolism. Adenosine monophosphateactivated protein kinase (AMPK) modulates multiple metabolic pathways and acts as a sensor of the cellular energy status; recent evidence suggests a critical role for AMPK in bone homeostasis. In addition, AMPK activation is believed to mediate most clinical effects of the insulin-sensitizer metformin. Over the past decade, several research groups have investigated the effects of metformin on bone, providing a considerable body of pre-clinical (in vitro , ex vivo and in vivo ) as well as clinical evidence for an anabolic action of metformin on bone. However, two caveats should be kept in mind when considering metformin treatment for a patient with type 2 DM at risk for diabetic osteopathy. In the first place, metformin should probably not be considered an antiosteoporotic drug; it is an insulin sensitizer with proven macrovascular benefits that can secondarily improve bone metabolism in the context of DM. Secondly, we are still awaiting the results of randomized placebo-controlled studies in humans that evaluate the effects of metformin on bone metabolism as a primary endpoint.