The effects of increasing serum calcitriol on energy and fat metabolism and gene expression.
OBJECTIVE
Evidence from a number of investigations indicates that calcium intake could be inversely related to body weight through alterations in the 1,25-OH(2)-D(3) metabolism. The objective of this study was to test whether energy and substrate metabolism and adipose tissue enzyme mRNA expression can be altered by changes in serum 1,25-OH(2)-D(3) through oral cholecalciferol supplementation in non-obese human subjects.


METHODS
An intervention study was used with a treatment period of 7 days. During this intervention, energy expenditure (EE) and substrate metabolism were measured using indirect calorimetry at t = 0, 1, 3, and 7 days, and blood samples were obtained at t = -1, 0, 1, 2, 3, 5 and 7 days. Fat biopsies were obtained at t = 0 and 7 days for determination of expression of genes involved in lipolytic and lipogenic pathways. Subjects from the general community were studied in an ambulatory setting at a university hospital. Ten healthy young men (age, 28 +/- 3 years; BMI, 25.5 +/- 0.5 kg/m(2)) were recruited by local announcement, and all completed the study. All subjects received 2000 IU cholecalciferol/d for 7 days, and they were instructed to consume a low-cholecalciferol, low-calcium diet. EE, fat oxidation, and adipose tissue enzyme mRNA were the main outcome measures.


RESULTS
Despite a significant increase in serum 1,25-OH(2)-D(3) concentration at t = 5 and 7 days, no significant differences in substrate and energy metabolism nor mRNA concentrations of different lipid metabolism-related proteins were observed.


CONCLUSIONS
Seven-day supplementation with 2000 IU cholecalciferol/d together with a decrease in dietary calcium intake does not affect EE or substrate metabolism nor gene expression of proteins related to fat metabolism, despite a significant increase in serum 1,25-OH(2)-D(3) concentration.
Boon
Niels
N
Nutrition and Toxicology Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
Hul
Gabby B J
GB
Sicard
Audrey
A
Kole
Eveline
E
Van Den Berg
Elisa R
ER
Viguerie
Nathalie
N
Langin
Dominique
D
Saris
Wim H M
WH
D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000328:Adult; D000704:Analysis of Variance; D001786:Blood Glucose / Q000378:metabolism; D002117:Calcitriol / Q000097:blood*; D002118:Calcium / Q000097:blood; D002762:Cholecalciferol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D019587:Dietary Supplements; D004734:Energy Metabolism / Q000187:drug effects*; D064429:Fatty Acid Synthases / Q000235:genetics; D005230:Fatty Acids, Nonesterified / Q000097:blood; D015870:Gene Expression / Q000187:drug effects* / Q000235:genetics; D005990:Glycerol / Q000097:blood; D005993:Glycerolphosphate Dehydrogenase / Q000235:genetics; D006801:Humans; D007473:Ion Channels / Q000235:genetics; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics; D047495:PPAR gamma / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D002787:Sterol Esterase / Q000235:genetics; D013997:Time Factors; D000071246:Uncoupling Protein 2; D014815:Vitamins / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007473:Ion Channels; D024101:Mitochondrial Proteins; D047495:PPAR gamma; D012333:RNA, Messenger; D000071246:Uncoupling Protein 2; D014815:Vitamins; D002762:Cholecalciferol; D005993:Glycerolphosphate Dehydrogenase; D064429:Fatty Acid Synthases; D002787:Sterol Esterase; D002117:Calcitriol; D005990:Glycerol; D002118:Calcium