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2016 ; 7
(6
): 122-33
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Metformin revisited: Does this regulator of AMP-activated protein kinase
secondarily affect bone metabolism and prevent diabetic osteopathy
#MMPMID27022443
McCarthy AD
; Cortizo AM
; Sedlinsky C
World J Diabetes
2016[Mar]; 7
(6
): 122-33
PMID27022443
show ga
Patients with long-term type 1 and type 2 diabetes mellitus (DM) can develop
skeletal complications 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 monophosphate-activated 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 anti-osteoporotic 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.
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