Incretins and bone: evolving concepts in nutrient-dependent regulation of bone turnover.
Postprandial variation of bone turnover markers and the closed relationship between bone remodeling and nutrient supply has been extensively studied in the past few years, but the underlying pathophysiologic mechanisms remain largely unknown. Recent studies have shown that the acute regulation of bone turnover induced by feeding is probably mediated by gastrointestinal (GI) peptides. The greater response of bone remodeling during oral versus intravenous glucose administration and the inhibition of this response after administration of octreotide, that inhibits the release of GI peptides, further support the existence of a gutbone axis. Glucose-dependent insulinotropic peptide and glucagon-like peptides-1 and -2 are released from K and L cells of the gastrointestinal tract, respectively, and are considered the main mediators of the postprandial response of bone turnover. In this review we outline the most recent evidence that demonstrates the role of incretins in nutrient-dependent regulation of bone metabolism. Further elucidation of the underlying mechanisms can be exploited therapeutically in the future.
Division of Endocrinology and Metabolism, Bone Metabolic Unit, AHEPA University Hospital, Thessaloniki, Greece. margia@med.auth.gr
Maria P
MP
Yavropoulou
John G
JG
Yovos
D000818:Animals; D001846:Bone Development; D016723:Bone Remodeling; D001842:Bone and Bones / Q000378:metabolism*; D002940:Circadian Rhythm; D004032:Diet / Q000009:adverse effects; D019858:Enteroendocrine Cells / Q000378:metabolism*; D005749:Gastric Inhibitory Polypeptide / Q000378:metabolism; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism; D053767:Glucagon-Like Peptide 2 / Q000378:metabolism; D006801:Humans; D054795:Incretins / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D008954:Models, Biological
D053767:Glucagon-Like Peptide 2; D054795:Incretins; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1