Stan R Ursem1, Marc G Vervloet2, Rahel M Büttler1, Mariëtte T Ackermans3, Mirjam M Oosterwerff4, Elisabeth M V Eekhoff5, Paul Lips5, Mireille J Serlie6, Susanne E la Fleur7, Annemieke C Heijboer8. 1. Department of Clinical Chemistry, Endocrine Laboratory, VU University Medical Center, Amsterdam, the Netherlands. 2. Department of Nephrology, VU University Medical Center, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences (ACS), VU University Medical Center, Amsterdam, the Netherlands. 3. Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. 4. Department of Internal Medicine, Section of Endocrinology, Catharina Hospital, Eindhoven, the Netherlands. 5. Department of Internal Medicine, Section of Endocrinology, VU University Medical Center, Amsterdam, the Netherlands. 6. Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. 7. Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Metabolism and Reward group, Netherlands Institute for Neuroscience, KNAW, Amsterdam, the Netherlands. 8. Department of Clinical Chemistry, Endocrine Laboratory, VU University Medical Center, Amsterdam, the Netherlands; Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Electronic address: a.heijboer@vumc.nl.
Abstract
AIMS: Different studies point to a link between glucose metabolism and Fibroblast Growth Factor 23 (FGF23), an osteocyte-derived phosphaturic hormone. We aimed to investigate in humans the effect of (I) a glucose load and (II) a hyperinsulinemic-euglycemic clamp on FGF23 concentrations and conversely (III) the effect of a diet-induced increase in FGF23 concentration on glucose and insulin concentrations. METHODS: Plasma cFGF23 concentrations were measured during: I. an oral glucose tolerance test in eight adults with impaired glucose tolerance and vitamin D deficiency and II. a hyperinsulinemic-euglycemic clamp in nine healthy adults. III. Serum glucose and insulin concentrations were measured in nine healthy adults receiving a single-day phosphate-enriched or -restricted diet. RESULTS: I. A glucose load decreased FGF23 and phosphate concentrations. II. The hyperinsulinemic-euglycemic clamp decreased phosphate concentrations, but did not affect FGF23 concentrations. III. Fasting insulin and glucose concentrations remained unchanged after a diet-induced increase in FGF23 concentration. CONCLUSIONS: An oral glucose load in vitamin D deficient patients with impaired glucose metabolism decreased FGF23 concentrations, which cannot be attributed to changes in insulin concentration. Thus, bone may react rapidly after glucose loading by alternating FGF23 secretion. A diet-induced increase in FGF23 concentrations did not affect fasting glucose or insulin levels.
AIMS: Different studies point to a link between glucose metabolism and Fibroblast Growth Factor 23 (FGF23), an osteocyte-derived phosphaturic hormone. We aimed to investigate in humans the effect of (I) a glucose load and (II) a hyperinsulinemic-euglycemic clamp on FGF23 concentrations and conversely (III) the effect of a diet-induced increase in FGF23 concentration on glucose and insulin concentrations. METHODS: Plasma cFGF23 concentrations were measured during: I. an oral glucose tolerance test in eight adults with impaired glucose tolerance and vitamin Ddeficiency and II. a hyperinsulinemic-euglycemic clamp in nine healthy adults. III. Serum glucose and insulin concentrations were measured in nine healthy adults receiving a single-day phosphate-enriched or -restricted diet. RESULTS: I. A glucose load decreased FGF23 and phosphate concentrations. II. The hyperinsulinemic-euglycemic clamp decreased phosphate concentrations, but did not affect FGF23 concentrations. III. Fasting insulin and glucose concentrations remained unchanged after a diet-induced increase in FGF23 concentration. CONCLUSIONS: An oral glucose load in vitamin D deficient patients with impaired glucose metabolism decreasedFGF23 concentrations, which cannot be attributed to changes in insulin concentration. Thus, bone may react rapidly after glucose loading by alternating FGF23 secretion. A diet-induced increase in FGF23 concentrations did not affect fasting glucose or insulin levels.
Authors: Stefanie Krick; Eric Scott Helton; Samuel B Hutcheson; Scott Blumhof; Jaleesa M Garth; Rebecca S Denson; Rennan S Zaharias; Hannah Wickham; Jarrod W Barnes Journal: Front Endocrinol (Lausanne) Date: 2018-11-27 Impact factor: 5.555
Authors: Stan R Ursem; Charlene Diepenbroek; Vesna Bacic; Unga A Unmehopa; Leslie Eggels; Clarissa M Maya-Monteiro; Annemieke C Heijboer; Susanne E la Fleur Journal: Eur J Neurosci Date: 2021-07-20 Impact factor: 3.386