Abstract
Excessive fructose consumption inhibits adaptive increases in intestinal Ca2+ transport in lactating and weanling rats with increased Ca2+ requirements by preventing the increase in serum levels of 1,25(OH)2D3. Here we tested the hypothesis that chronic fructose intake decreases 1,25(OH)2D3 levels independent of increases in Ca2+ requirements. Adult mice fed for five wk a high glucose-low Ca2+ diet displayed expected compensatory increases in intestinal and renal Ca2+ transporter expression and activity, in renal CYP27B1 (coding for 1α-hydroxylase) expression as well as in serum 1,25(OH)2D3 levels, compared with mice fed isocaloric glucose- or fructose-normal Ca2+ diets. Replacing glucose with fructose prevented these increases in Ca2+ transporter, CYP27B1, and 1,25(OH)2D3 levels induced by a low Ca2+ diet. In adult mice fed for three mo a normal Ca2+ diet, renal expression of CYP27B1 and of CYP24A1 (24-hydroxylase) decreased and increased, respectively, when the carbohydrate source was fructose instead of glucose or starch. Intestinal and renal Ca2+ transporter activity and expression did not vary with dietary carbohydrate. To determine the time course of fructose effects, a high fructose or glucose diet with normal Ca2+ levels was fed to adult rats for three mo. Serum levels of 1,25(OH)2D3 decreased and of FGF23 increased significantly over time. Renal expression of CYP27B1 and serum levels of 1,25(OH)2D3 still decreased in fructose- compared to those in glucose-fed rats after three mo. Serum parathyroid hormone, Ca2+ and phosphate levels were normal and independent of dietary sugar as well as time of feeding. Thus, chronically high fructose intakes can decrease serum levels of 1,25(OH)2D3 in adult rodents experiencing no Ca2+ stress and fed sufficient levels of dietary Ca2+. This finding is highly significant because fructose constitutes a substantial portion of the average diet of Americans already deficient in vitamin D.
Highlights
Fructose is one of the key components of the American diet and represents more than 10% of daily calorie intake [1]
Since excessive fructose consumption and vitamin D deficiency are each associated with similar metabolic diseases [3,4,5], a better understanding of the interaction between fructose and vitamin D metabolism will contribute to better health recommendations
Active transepithelial Ca2+ transport rate was modest in mice fed fructose-based, normal Ca2+ diet and was similar to that in mice fed a glucose-based, normal Ca2+ diet (Fig. 1A)
Summary
Fructose is one of the key components of the American diet and represents more than 10% of daily calorie intake [1]. This remarkable and recent increase in fructose consumption coincides with an striking increase in prevalence of vitamin D deficiency or insufficiency in developed countries [2]. In the event of decreased Ca2+ levels in the serum due to low dietary intake or increased demand of Ca2+, the synthesis of the hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is enhanced, leading to adaptive increases in intestinal Ca2+ absorption. Active intestinal and renal Ca2+ transport involves Ca2+ entry through the apical Ca2+ channel transient receptor potential vanilloid 6 and 5 (TRPV6 and TRPV5) respectively, its intracellular diffusion via Ca2+-binding proteins
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
