title: Octreotide abolishes the acute decrease in bone turnover in response to oral glucose.
abstract: Feeding or oral intake of glucose results in an acute suppression of bone turnover. This does not appear to be mediated by insulin. Several gastrointestinal hormones modulate bone turnover in vitro and may mediate this response. We examined whether inhibiting the production of gastrointestinal hormones using octreotide could block glucose-mediated suppression of bone turnover. Fifteen subjects were each studied on four occasions in a randomized, single-blind, crossover study after receiving 1) oral placebo, iv saline; 2) oral glucose, iv saline; 3) oral glucose, iv octreotide; or 4) iv octreotide alone. We measured serum C-terminal telopeptide of type I collagen, urinary N-terminal telopeptide of type I collagen, osteocalcin, procollagen type I N-terminal propeptide, PTH, insulin, ionized calcium, and glucose over 4 h. All bone turnover markers decreased significantly after oral glucose (P < 0.001). At 120 min serum C-terminal telopeptide decreased by 45 +/- 2%, urinary N-terminal telopeptide by 31 +/- 7%, osteocalcin by 16 +/- 1%, and procollagen type I N-terminal propeptide by 8 +/- 1%. There was no significant decrease in bone turnover in response to oral glucose during octreotide infusion. Octreotide alone resulted in a significant increase in all bone turnover markers (P < 0.05) and PTH (P < 0.01). We conclude that octreotide completely abolishes the bone turnover response to glucose intake and increases PTH secretion. The apparent bone turnover response to feeding is probably mediated by an octreotide-inhibitable endocrine factor.
authors.affiliation: Bone Metabolism Group, Clinical Sciences (North), University of Sheffield, Sheffield, United Kingdom S5 7AU. j.a.clowes@sheffield.ac.uk
authors.forename: Jackie A
authors.initials: JA
authors.lastname: Clowes
authors.forename: Heather C
authors.initials: HC
authors.lastname: Allen
authors.forename: Donna M
authors.initials: DM
authors.lastname: Prentis
authors.forename: Richard
authors.initials: R
authors.lastname: Eastell
authors.forename: Aubrey
authors.initials: A
authors.lastname: Blumsohn
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism*; D002118:Calcium / Q000097:blood; D003094:Collagen / Q000097:blood / Q000652:urine; D024042:Collagen Type I; D018592:Cross-Over Studies; D004347:Drug Interactions; D005260:Female; D005947:Glucose / Q000008:administration & dosage*; D006728:Hormones / Q000008:administration & dosage*; D006801:Humans; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood; D008297:Male; D015282:Octreotide / Q000008:administration & dosage*; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood / Q000652:urine; D011347:Procollagen / Q000097:blood; D016037:Single-Blind Method
chemical_list: D001786:Blood Glucose; D024042:Collagen Type I; D006728:Hormones; D007328:Insulin; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide; D015675:Osteocalcin; D003094:Collagen; D005947:Glucose; D015282:Octreotide; D002118:Calcium