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Chronic high fructose intake impairs renal calcitriol metabolism
Author(s) -
Douard Veronique,
Patel Chirag,
Sabbagh Yves,
Lee Jacklyn,
Ferraris Ronaldo P.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.703.2
Subject(s) - calcitriol , endocrinology , medicine , weanling , chemistry , metabolism , vitamin d and neurology , biology
We recently showed that excessive fructose (F) consumption inhibits adaptive increases in intestinal Ca transport in lactating and weanling rats with enhanced Ca needs, by preventing the increase in blood levels of the biologically active vitamin D, calcitriol. Here we tested the hypothesis that chronic F intake decreases calcitriol levels independent of Ca status. In the control study, adult mice fed for 5 wk a 40% glucose (G)‐low Ca diet displayed expected adaptive increases in intestinal and renal Ca transporter expression and activity as well as in serum calcitriol levels, compared with mice fed G‐ or F‐normal Ca diets. However, dietary F clearly prevented increases in calcitriol and Ca transporter expression to Ca deficiency. When the 40% F‐normal Ca diet was fed to adult rats for 3 mo, calcitriol levels and expression of CYP27B1 that synthesizes calcitriol decreased markedly compared to those in G‐fed mice. Ca status and Ca transporter expression were normal and independent of dietary sugar. Expression of CYP27B1 also decreased and of CYP24A1 increased in adult mice fed for 3 mo a 60% F‐normal Ca diet. Thus, chronic F intakes stimulate renal catabolism and impair synthesis of calcitriol, regardless of Ca status. This finding is highly significant because F constitutes a substantial portion of the average diet of Americans now highly vulnerable to F‐induced deficiencies in calcitriol